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S258 Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2)
Herbal therapy: A review of emerging pharmacological
tools in the management of diabetes mellitus in Africa
Cromwell Mwiti Kibiti, Anthony Jide Afolayan
Department of Botany, Medicinal Plants and Economic Development (MPED) Research Centre, University of Fort Hare, Alice, 5700, South Africa
Submitted: 14-08-2014 Revised: 26-09-2014 Published: 24-09-2015
Address for correspondence:
Prof. Anthony Jide Afolayan, Department of Botany, Medicinal
Plants and Economic Development (MPED) Research Centre,
University of Fort Hare, Alice, 5700, South Africa.
E-mail: aafolayan@ufh.ac.za
Background: Diabetes mellitus is a chronic physiological glucose metabolic disorder. It has affected
millions of people all over the world thereby having a signicant impact on quality of life. The
management of diabetes includes both nonpharmacological and conventional interventions.
Drawbacks in conventional therapy have led to seeking alternative therapy in herbal medicine.
Therefore, the need to review, elucidate and classify their mode of action in therapy for diabetes
disease arises. Materials and Methods: Comprehensive literature reports were used to review all
conventional agents and herbal therapy used in the management of diabetes. An online database
search was conducted for medicinal plants of African origin that have been investigated for
their antidiabetic therapeutic potentials. Results: The results showed that of the documented
sixty ve plants used, fourteen inhibit intestinal absorption of glucose, three exhibit insulin‑mimetic
properties, seventeen stimulate insulin secretion from pancreatic beta cells, twelve enhance
peripheral glucose uptake, one promotes regeneration of beta-cell of islets of Langerhans, thirteen
ameliorate oxidative stress and twenty induces hypoglycemic effect (mode of action is still
obscure). Thirteen of these plants have a duplicate mode of actions while one of them has three
modes of actions. These agents have a similar mechanism of action as the conventional drugs.
Conclusion: In conclusion, antidiabetic activities of these plants are well established; however,
the molecular modulation remains unknown. It is envisaged that the use of herbal therapy will
promote good health and improve the status of diabetic patients.
Key words: Antidiabetic, diabetes, herbal therapy, in vitro, in vivo
Access this article online
Website:
www.phcog.com
DOI:
10.4103/0973-1296.166046
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INTRODUCTION
Diabetes mellitus is a chronic metabolic disorder caused
by abnormal metabolism of carbohydrate, promoted by
factors such as insulin deciency and/or insulin resistance.[1]
The prevalence of diabetes globally was estimated to be
4.0% in 1995 and is projected to rise to 5.4% (300 million)
by the year 2025. In 2010, 12.1 million people were
estimated to be living with diabetes in Africa, and this is
projected to increase to 23.9 million by 2030.[2] Diabetes
mellitus has affected several millions of people all over
the world, thereby signicantly impacting on the economy,
health, quality of life and life expectancy of patients, as
well as on the health care systems.[3]
There are two major forms of diabetes mellitus;
insulin‑dependent diabetes mellitus (IDDM) also known
as type I diabetes and non‑insulin‑dependent diabetes
mellitus (NIDDM) also known as type II diabetes.[4] IDDM
is caused by failure to release insulin from the β‑cells
of the islets of Langerhans in the pancreas. NIDDM is
caused by insulin resistance probably due to too few insulin
receptors.[5]
The major causes of IDDM include genetic predisposition,
environmental factors such as nutrition, exposure to viruses
and allergens and autoimmunity leading to destruction of
insulin‑producing pancreatic β‑cells.[6] The major causes
of NIDDM include genetic and environmental factors.
IDDM requires insulin injection to prevent ketosis and
other complications as well as maintenance of life.[6]
The complications of IDDM and NIDDM include;
retinopathy, neuropathy, angiopathy, nephropathy,
infection and diabetic ketoacidosis.[4] Diabetic foot
disease which is due to changes in blood vessels and
nerves, often leads to ulceration and subsequent limb
amputation. Skin disorders are also more common in
diabetics. Bacterial (mycobacterium and anaerobic) and
fungal infections are common in diabetics.[4]
ABSTRACT
PHCOG MAG. ORIGINAL ARTICLE
Kibiti and Afolayan: Anti‑diabetic plants in Africa
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Various approaches have been used in the management
of diabetes mellitus. These are nonpharmacological
interventions including; diet therapy, physical
activity, acupuncture and hydrotherapy and mineral
supplementation.[5‑7] The conventional management
of diabetes mellitus includes; insulin therapy, oral
glucose‑lowering agents such as sulfonylurea, biguanides,
alpha‑glucosidase inhibitors, thiazolidinediones, and
meglitinides.[8‑13] Another approach which has been
tried is the prevention of autoimmune attack using
immunosuppressive compounds.[14‑18] Transplantation of
either the pancreas or preparations of islet tissues has
also been tried.[17,18] Regardless of the efciency of the
above‑mentioned methods used in the management of the
disease, they have several drawbacks. These include; adverse
side effects, cost (expensive) and inaccessible to many
communities. This has led to the use of herbal therapy as
an alternative method in the management of the disease.
Therefore, this review has chronicled the nonpharmacological
and pharmacological interventions used in the management
of diabetes mellitus and their drawbacks leading to sourcing
for herbal therapy.
Nonpharmacological interventions in the management
of diabetes mellitus
Diet therapy
Given the heterogeneous nature of type 2 diabetes, no
single dietary approach is appropriate for all patients. Meal
plans and diet modications are generally individualized by
a registered dietician to meet patient needs and lifestyle.
A typical conventional approach would recommend a diet
composed of 60–65% carbohydrate, 25–35% fat, and
10–20% protein with limited or no alcohol consumption.[5]
Vegetables
Vegetables are among the numerous plant adjuncts tried on
the treatment of diabetes mellitus. Bitter gourd (Momordica
charantia) and Ivy gourd (Coccinia indica) are hypoglycemic
when administered orally. Other vegetables such as
cabbage (Brassicia oleracia) green leafy vegetables, beans,
and tubers are hypoglycemic in both experimental animals
and humans.[19]
Mineral supplementation
The treatment of diabetes requires nutritional
supplementation, as these patients have a greatly increased
need for many nutrients. These improve blood sugar
control and prevent many major complications of diabetes.
The mineral supplements include:
Chromium (Cr) is an essential element required for
normal lipid and carbohydrate metabolism. Brewers yeast
appears to be the richest source of GTF‑chromium,
followed closely by black pepper, wheat germ, rye bread,
mushrooms, prunes, wine, and beer. Most meats, fresh
fruits, and cheeses are fair sources of chromium. Cereals
are poorer sources, their chromium decreasing with rening
and processing.[20]
Vanadium is known to play a role in the regulation of
intracellular signaling and as a cofactor of enzymes essential
in energy metabolism hence reduces gluconeogenesis and
increases glycogen deposition.[21] A reasonable amount
of supplemental vanadium is 20 µg/day. Vanadyl sulfate
at a dose of 100 mg/day is effective in improving insulin
sensitivity. Good sources of vanadium include seafood,
mushrooms, olives, whole grain bread, carrots and
vegetable oils.[22]
Magnesium (Mg) is one of the major mineral constituents
of the human body. Its functions include strengthening
cell membrane structure, cofactor to several enzymes like
kinase, which participate in energy production processes
and participation in deoxyribonucleic acid (DNA)
replication.[23] A reasonable amount of supplemental
magnesium is 450 mg/day.[23]
Zinc is an important trace element in diabetes. It is a
cofactor for insulin. Although its real mechanisms in
carbohydrate metabolism is not clear, zinc has inuence
in carbonic anhydrase, alkaline phosphatase, alcohol
dehydrogenase, pancreatic carboxypeptidases A and
B, lactate dehydrogenase, glutamate dehydrogenase,
glyceraldehyde‑3‑phosphate dehydrogenase and maltose
dehydrogenase. Zinc plays a vital role in the biosynthesis
of nucleic acids, RNA polymerases, and DNA polymerases;
hence its involvement in the healing processes of body
tissues. Other physiological processes that require zinc
include hormone metabolism, immune responses and
stabilization of ribosomes and membranes.[24]
Manganese (Mn) is a trace metal in the body. It is both
an activator and a constituent of several enzymes. It is
necessary for the normal activity of hydrolyases, kinases,
decarboxylases, transferases, leucine aminopeptidase,
alkaline phosphatase and of the enzymes of oxidative
phosphorylation. Manganese metalloenzymes include
pyruvate decarboxylase, arginase, glutamate synthetase,
and manganese superoxide dismutase.[25]
Molybdenum (Mo) affects glucose metabolism. In the
hepatocytes, molybdenum stimulates glycolysis and
accelerates glycogen degradation.[26] Mo also increases
insulin receptor autophosphorylation and phosphorylation
of its substrate and augments glucose transport, oxidation
and lipogenesis in adipocytes.[26]
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Molybdate is an effective antihyperglycemic agent in
diabetics with severe insulin resistance. It is associated
with a substantial reduction of hyperinsulinemia and an
increase in pancreatic insulin stores. The glucose‑lowering
effect of Mo may be partly related to attenuation of
hepatic glucose production. Hence, Mo proves to be an
effective blood glucose‑lowering agent in severely diabetic
patients.[27]
Iron is an important element, it is found in the portion of
the cell involved in energy production and as a cofactor
for several enzymes such as succinic dehydrogenase,
catalase, and cytochromes.[28] Insulin is known to cause a
rapid and marked stimulation of iron uptake by fat cells,
redistributing transferrin receptors from an intracellular
membrane compartment to the cell surface. Insulin is
also responsible for the increased ferritin synthesis.[29]
Reciprocally, iron inuences insulin action. Iron interferes
with insulin inhibition of glucose production by the
liver. Hepatic excretion and metabolism of insulin is
reduced with increasing iron stores, leading to peripheral
hyperinsulinemia.[30] In fact, the initial and most common
abnormality seen in iron overload conditions is liver insulin
resistance. Iron overload also affects skeletal muscle, the
main effector of insulin action.[31]
Physical activity
In well‑controlled diabetes, physical activity improves
the body’s ability to use glucose and lowers the insulin
requirement. Exercise should start at a low level and
gradually increase to avoid adverse effects such as injury,
hypoglycemia, or cardiac problems.[32]
Acupuncture and hydrotherapy
Acupuncture is the best‑known alternative therapy in the
United States of America for chronic pain and is used in the
treatment of diabetes. Acupuncture is effective in treating
not only diabetes, but also in preventing and managing
complications of the diseases.[7] Acupuncture activates
glucose‑6‑phosphatase an important enzyme in carbohydrate
metabolism and affects the hypothalamus. Acupuncture
acts on the pancrease to enhance insulin synthesis, increase
the number of receptors on target cells, and accelerate
the utilization of glucose, resulting in lowering of blood
sugar. Acupuncture also has an antiobesity effect, which
is the most modiable risk factor for type 2 diabetes. The
therapeutic effect of acupuncture on diabetes is not the result
of its action on one single organ but on multiple systems.[7]
Acupuncture can be effective in treating complications of
diabetes and is promising in patients with dietary control,
physical exercise, breathing exercises and massage. Although
acupuncture shows some effectiveness in treating diabetes,
its mechanisms are still obscure.[7]
Since hot‑tub therapy can increase blood ow to skeletal
muscles, it has been recommended for patients with type 2
diabetes who are unable to exercise. Hot‑tub therapy
decreases weight, mean plasma glucose level and mean
glycosylated hemoglobin.[6,7,33] However, caution should
be taken that the water is not too hot as neuropathy may
prevent the patient from noticing that they are burning
themselves; proper water sanitation and appropriate
guidance should be considered.[6]
Conventional management of diabetes mellitus
Insulin therapy (exogenous insulin)
Insulin therapy restores normoglycemia, suppressing
ketogenesis, delaying or arresting diabetic complications.
Insulin also stimulates the synthesis of glucokinase and
moderates the degree of gluconeogenesis.[9] Weight
gain, hypoglycemia, skin reactions, insulin resistance
due to antibody reaction, insulin lipidystrophy, visual
disturbance and allergy are common side‑effects of
insulin therapy. Insulin therapy is also unavailable
to many communities in developing countries due
to inaccessible health facilities and socioeconomic
factors.[2]
Oral glucose – lowering agents
Sulfonylurea
These include sulfonylurea such as tolbutamide and
glyburide. The mode of action of sulfonylureas could be
chiey explained by inhibition of KATP channels initiating
insulin secretion from the pancreatic β‑cells. This enhances
the glycolytic ux and inhibits glucose output from the
liver inhibiting gluconeogenesis.[34] Thus, these drugs
could be used only in patients with type 2 diabetes having
functional beta cells for endogenous insulin production.
A signicant side effect is hypoglycemia and weight gain
due to hyperinsulinemia. The weight gain is implicated as
a cause of secondary drug failure.[13]
Biguanides
These reduce hepatic glucose output, fasting glucose
output and fasting glucose levels by increasing hepatic
insulin sensitivity. They reduce intestinal absorption of
glucose. These include the drug metformin derived from a
medicinal plant, Galega ofcinalis.[11] Metformin is a biguanide
agent that lowers blood glucose primarily by decreasing
hepatic glucose production and increases muscle glucose
uptake. It also reduces plasma triglyceride and low‑density
lipoprotein (LDL)‑cholesterol levels and reducing insulin
resistance. Metformin is used as monotherapy or in
combination with sulfonylureas for the management of
type 2 diabetes. The side‑effects include weakness, fatigue,
shortness of breath, nausea, dizziness, lactic acidosis, and
kidney toxicity.[11]
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Alpha‑glucosidase inhibitors
Alpha‑glucosidase inhibitors, such as acarbose (Precose)
and miglitol (Glyset), are indicated as monotherapy or
in combination with sulfonylureas for management
of type 2 diabetes. These are inhibitors of intestinal
α‑glycosidase.[10] These agents inhibit the breakdown
of complex carbohydrates and delay the absorption of
monosaccharide from the gastrointestinal tract. The major
side‑effects are gas, bloating and diarrhoea.[10]
Thiazolidinediones
These are represented by troglitazone, rosiglitazone and
pioglitazone. The thiazolidinediones are a unique drug
class of “insulin sensitizers” that promote skeletal muscle
glucose uptake and to a much lesser extent, in the liver.[35]
Troglitazone is the rst agent of this drug class to be
introduced in the United States of America market and
like metformin, it reduces insulin resistance. Troglitazone
is benecial in patients requiring large daily amounts of
insulin (more than 30 units/day) whose diabetes is still
uncontrolled. Troglitazone is also effective when used in
combination with other oral agents thereby potentially
delaying the need to start insulin therapy.[36]
Molecular mechanisms of action of these agents are
through binding avidly to peroxisome proliferator‑activated
receptor gamma (PPARγ). Thiazolidinediones are selective
agonists of PPARγ. When activated by a ligand, such as a
thiazolidinedione, PPARγ binds to the 9‑cis retinoic acid
receptor retinoid X receptor to form a heterodimer. This
binds to DNA to regulate the genetic transcription and
translation of a variety of proteins involved in cellular
differentiation and glucose and lipid metabolism.[37]
The potential role of the thiazolidinediones in reducing
hepatic lipid content in non‑alcoholic steatohepatitis
is still under investigation. The thiazolidinediones
do not increase insulin secretion. On the contrary,
thiazolidinediones reduce insulin levels acutely, which may
be a consequence of improved insulin sensitivity and/
or reduced circulating fatty acids (as fatty acids stimulate
insulin secretion). In the longer term, thiazolidinediones
arrest the decline in β‑cell function that occurs in type 2
diabetes, perhaps by protecting the β‑cell from lipotoxicity.
The thiazolidinediones are of no use in type 1 diabetes or in
the occasional lean insulin‑decient (but insulin‑sensitive)
patient with type 2 diabetes.[37]
In addition to promoting adipogenesis and fatty acid
uptake, thiazolidinediones improve insulin sensitivity by
altering hormone production by adipocytes. Adipocytes
secrete a number of important hormones, referred to as
“adipokines,” including leptin, adiponectin, resistin and
tumor necrosis factor‑α.[38,39] The disadvantage of these
drugs is that they are expensive oral agents. These drugs
decrease plasma triglyceride levels, but such decrease
may be associated with weight gain and an increase in
LDL – cholesterol levels.[40] Hepatotoxicity is a concern
requiring monthly monitoring of liver function every
month for the rst 8 months of treatment and every other
month for 4 months thereafter.[35]
Meglitinides
One of the meglitinides is repaglinide. Repaglinide is an
insulin secretagogue, the rst of the meglitinide class.
It is a member of the carbamoyl methyl benzoic acid
family (glinides) introduced in early 1998. It is structurally
different from the traditional sulfonylureas, but shows
chemical resemblance to the nonsulfonylurea moiety of
the glibenclamide molecule.[12] Nateglinide, the newest
member of the class has recently become available. The
meglitinides stimulate the release of insulin from the
pancreatic β‑cells. However, this action is mediated through
a different binding site on the “sulfonylurea receptor”
of the β‑cells and the drugs have somewhat different
characteristics when compared with sulfonylureas. In
contrast to glibenclamide, meglitinides do not stimulate
calcium‑dependent exocytosis.[12] Unlike commonly used
sulfonylureas, the meglitinides have a very quick onset of
action and a short half‑life. Repaglinide is a suitable option
for patients with severe sulfa allergy who are not candidates
for sulfonylurea therapy. The drug is used as monotherapy
or in combination with metformin. The major side
effects are weight gain, gastrointestinal disturbances and
hypoglycaemia.[41]
Advancements in diabetes management
Prevention of autoimmune attack
There are several attempts made to control autoimmune
attack on the β‑cells and there are several on‑going
diabetes prevention trials worldwide. In general, it
is preferable to start a specific immuno‑modulatory
treatment while substantial β‑cells mass remains; that’s
during the prediabetic phase.[14,42] The vitamin B‑complex
nicotinamide is currently undergoing a multicentre trial
in Europe. Nicotinamide is thought to protect against
damage acting as an antioxidant and thus inhibits the
deleterious effects of free radicals. It also inhibits the
enzyme Poly (ADP‑ribose) polymerase, thereby saving
the cellular stores of nicotinamide adenosine diphosphate.
Furthermore, it stimulates islet cell proliferation.[16] Another
interesting immunosuppressive compound, which has
shown encouraging results in newly diagnosed patients,
is cyclosporine A, which acts by inhibiting T‑helper
lymphocyte function.[43] Unfortunately cyclosporin A must
be given early and it has potentially serious side effects,
including a toxic action on the β‑cell itself.[16] Newer
immunosuppressive drugs, such as FK‑506Transpl, are
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under investigation, and some of these side effects may be
avoided. Moreover, Bacillus Calmette‑Guerin, a nonspecic
immunostimulant, has been shown to induce extended
remission in newly diagnosed patients by unknown
mechanism.[15]
Transplantation
Transplanting technology of either the pancreas or
preparations of islet tissues is limited by the problem
of obtaining donor tissue and preventing immune
rejection of the graft.[17] Nevertheless, transplanting
is as yet the only available treatment that can lead to
insulin independence. Human allograft transplantation
cannot be used on a large scale in clinical practice.
After whole pancreas transplantation the graft
survival after 1‑year is 85–90%. Islet transplants are
much more vulnerable. Many of them fail within few
weeks or months after engraftment and most islet
transplants.[17] The reasons for these functional failures
are largely unknown, although insufcient numbers of
islets, engraftment difculties, chronic rejection and
recurrence of autoimmune disease have been suggested
to be contributing factors. Moreover, hyperglycemia in
the recipient after transplantation deteriorates islet graft
survival and function.[18]
One of the major obstacles for clinical islet transplantation
is a lack of donors. Therefore, it is important to optimize
the number of β‑cells harvested from each donor,
stimulate the growth and/or differentiation of β‑cells or
to genetically manipulate insulin‑producing cell lines for
transplantation.[17] The differentiated β‑cells have the ability
to proliferate at a low pace. The proliferation rate can be
affected in many ways, for example, by growth stimulating
hormones like growth hormone and prolactin. Also, the
size and composition of the graft and the blood glucose
level in the recipient are of crucial importance for β‑cell
replication.[17]
Herbal management
The drawbacks of conventional therapy though effective,
have led to seeking alternative therapy in herbal medicine.
Many pharmaceutical drugs are derived from plants
that were rst used in traditional systems of medicine,
and according to WHO, about 25% of medicines are
plant‑derived.[44] Traditional knowledge has proven a
useful tool in the search for new plant‑based medicines.
Less than a quarter of the estimated 250,000 medicinal
plant species have been investigated for hypoglycemic
activity.[45] Moreover, only a small number of these have
received a scientic medicinal evaluation to establish their
efcacy. Examples of plants that have been documented
for diabetic therapy in Africa have been reviewed and
discussed subsequently.
METHODOLOGY
This review was carried out using comprehensive and
systematic literature reports on the use of traditional
and conventional therapy in the management of diabetes
and emergence of herbal therapy. Empirical searches
were conducted using Google Scholar (http://www.
scholar. google.com), and Science Direct (http://www.
science direct.com), PubMed and Medline for medicinal
plants of African origin that have been studied and
investigated for their antidiabetic therapeutic potentials
both in vivo and in vitro. In addition to these databases, the
University of Fort Hare’s online database was also used.
Some articles were found through tracking citations from
other publications or by directly accessing the journals’
website. The keyword combinations for the search were
antidiabetic, antihyperglycemia, hypoglycemia, mode of
action, medicinal plant, and Africa. Following the search,
the antidiabetic plants were categorized and presented
based on their mode of actions and parts of Africa they
are used including East, West, North and Southern Africa.
Plants used in the management of diabetes mellitus
in Africa
Green tea (Camellia sinensis)
Green tea (leaves of Camellia sinensis, Theaceae) is
a popular beverage in Kenya and East Asia, and
also used as a herbal remedy in Europe and North
America. Green tea is considered to be antiinammatory,
antioxidative, antimutagenic, and anticarcinogenic and can
prevent cardiac disorders. Epidemiologically, it has been
suggested that green tea consumption prevents type 2
diabetes.[46] Green tea extract contains polyphenols like
catechin, epicatechin, epigallocatechin, and their gallates,
tannin, and caffeine. Furthermore, the polyphenols in
green tea extract have epigllo‑catechin‑3‑gallate as the
main constituent with anti‑diabetic activity.[47] The extract
also has pyrroloquinoline quinone, a newly discovered
vitamin.[48] Some constituent components enhance the basal
and insulin‑stimulated glucose uptake, inhibit intestinal
glucose uptake by inhibiting the sodium‑dependent
glucose transporter in the intestinal epithelial cells, and
reduce serum glucose level in alloxan‑diabetic rats.[49]
Controversially, caffeine acutely lowers insulin sensitivity
in humans.[50]
Onion (Allium cepa) and garlic (Allium sativum)
Onion (A. cepa) and garlic (A. sativum) contains active
hypoglycemic constituents. Garlic (A. sativum) also contains
hypoglycemic organic sulfur compounds.[51] Volatile
oils in raw onion and garlic cloves lower fasting glucose
concentration in both diabetic animals and human subjects.
The active components are believed to be sulfur‑containing
compounds such as allyl propyl disulde in onions and
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diallyl disulde (allicin) in garlic. These active ingredients
lower glucose levels by competing with insulin (which is
also a disulde) for insulin‑inactivating sites in the liver,
resulting in an increase of free insulin. Onion extracts
reduce blood sugar levels in a dose‑dependent manner.
A typical dosage of A. cepa is one 400 mg capsule daily
while the general dosage of garlic is 4 g fresh garlic or 8 mg
of the essential oil.[52]
Panax ginseng (Panax quinquefolius)
Panax ginseng (P. quinquefolius) is widely used in Chinese
medicine for over 2000 years. The root of ginseng has
been used for over 2000 years in the Far East for its health
promoting properties. It is also used in Northern Africa,
especially in Egypt.[53] Of the several species of ginseng,
P. ginseng (Asian ginseng) and P. quinquefolius (American
ginseng) are commonly used. Constituents of all
ginseng species include ginsenosides, polysaccharides,
peptides, polyacetylenic alcohol, and fatty acids. Most
pharmacological actions of ginseng are attributed to
ginsenosides, a family of steroids named steroidal
saponins.[54] The chemical composition of ginseng products
and potency may vary with the plant extract derivative,
the age of the root, the location where grown, the season
when harvested, and the methods of drying. Both Asian
and American ginseng has signicant hypoglycemic action.
The blood lowering effect appears to be attributed to
ginsenoside Rb‑2 and more specically to panaxans I, J,
K and L But whether these constituents have a similar
effect on type 2 diabetes is yet unknown.[55] The ginseng’s
mechanisms of action are thought to be: Slowing the
digestion of food, decreasing the rate of carbohydrate
absorption into portal hepatic circulation; ginseng may
affect glucose transport, which is mediated by nitric
oxide (NO); and lastly, ginseng may modulate NO‑mediated
insulin secretion and NO stimulates glucose‑dependent
secretion of insulin. However, the side‑effects of ginseng
are nervousness and excitation. The recommended daily
ginseng dosage is 1–3 g of the crude root, or 200–600 mg
of a standardized extract.[56]
Bitter Gourd (Momordica charantia)
Bitter Gourd (M. charantia), also known as balsam pear
is a tropical vegetable widely cultivated in parts of Asia,
Africa, and South America, which has been extensively used
in folk medicine as a remedy for diabetes.[57] The active,
hypoglycemic constituents include charantin, obtained
from an alcohol extract of the fruit, and a polypeptide called
p‑insulin (plant insulin or polypeptide‑p) isolated from the
fruit and seeds of the plant. The p‑insulin consists of 166
residues containing 17 amino acids and has a molecular
weight of 11,000. It is structurally and pharmacologically
comparable to bovine insulin, and is composed of two
polypeptide chains with disulde bonds. p‑insulin has an
onset of action similar to bovine insulin (30–60 min) and
a peak hypoglycemic effect after 4 h in type I diabetics,
compared with 2–3 h for regular insulin. Although the
precise mechanism of action remains to be fully elucidated,
M. charantia stimulates insulin release or possibly glycogen
synthesis in the liver.[57] In addition, the plant is believed to
contain several anti‑diabetic principles. The hypoglycemic
effects of this plant appears to be due to extra‑pancreatic
activity, including increased glucose utilization by the
liver;[58] decreased glucose synthesis by depression of key
gluconeogenic enzymes like glucose‑6‑phosphatase and
fructose‑1,6‑biphosphatase; and enhancement of glucose
oxidation through the shunt pathway via activation of
glucose‑6‑phosphate dehydrogenase.[59] Interestingly,
these herbs on an individual basis are reported to possess
a variety of healthful properties, including blood glucose
regulating, immunomodulation, liver detoxifying, and
anti‑inflammatory properties. These properties are
signicant to the diabetic as autoimmune processes are
believed to play a role in the destruction of β‑cells, and
inammation mediated by free radicals is also characteristic
of the diabetic condition.[60]
The recommended dose of bitter melon depends on the
form it is being consumed. Dosage for tincture ranges from
5 mL 2–3 times daily to as high as 50 ml/day. However,
bitter melon juice is very difcult to make palatable since,
as the name implies, it is quite bitter. To avoid the bitter
taste, the Indians and Chinese crush the herbs and form
tablets. In Central America, it is prepared as an extract or
decoction.[60] Dosage of capsulized dried powder range
from 3 to 15 g daily. That is quite a large dose so to avoid the
necessity of taking so many capsules; a standardized extract
may be used at dosages of 100–200 mg 3 times daily.[60]
Ackee fruit (Blighia sapida)
Ackee is the National fruit of Jamaica and was imported
from West Africa in the 18th century. It is a tall, leafy tree (up
to 12 m) that produces clusters of fruits widely used for
human consumption and for industrial purposes. The
fruit is yellow in color and shaped like an oblong capsule
that contains three cream‑colored arils. The arils may be
consumed safely when the fruit becomes red and opens
under the light of the sun. It is then commonly boiled in
water or milk and eaten alone or in meat or sh dishes. It is
also consumed raw in some African countries. Ackee fruit
contains hypoglycin, a natural toxin. It exists as a cyclic
amino acid, hypoglycin A (HG‑A), and its gamma‑glutamyl
derivative, HG‑B. When the fruit is consumed unripe, it
produces an acute toxic effect within 2–3 h with symptoms
including nausea, vomiting, headache, and drowsiness.
Coma and death may occur within 12 h in severe cases.
The most toxic is HG‑A, which is found in the unripe
arils. HG‑A is a water‑soluble liver toxin that produces
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hypoglycemia through the inhibition of gluconeogenesis,
secondary to the limitation of cofactors (CoA and
carnitine) that are essential for the oxidation of long‑chain
fatty acids.[61] The concentration of HG‑A in the unripe
ackee is 20 times greater than in the mature fruit. However
the level of concentration of the toxin lowers rapidly after
its exposure to the sun. The seeds contain HG‑B and are
always poisonous. An important factor seems to be the
nutritional status of the person consuming ackee since
diagnosed patients often present chronic malnutrition and
vitamin deciencies. When ingested unripe, ackee produces
vomiting and fatal cases of poisoning.[61]
Khat (Catha edulis)
Catha edulis popularly called khat is an evergreen shrub of
the tropics. The fresh leaf is traditionally chewed by some
people in East Africa and the Arabian Peninsula to attain
a state of euphoria and stimulation. Since the leaf rapidly
loses its effect upon wilting, the chewing habit has remained
endemic to the areas where the plant is cultivated.[62]
In South Africa, the plant has found its way to the
country due to influence of availability of this plant
through improved road networks, and the availability of
air transport, and the habit has spread considerably in
those regions and countries where the plant does not.[62]
Although it has been reported that there is moderate in vitro
antidiabetic property of C. edulis,[63] there is no published
scientic article substantiating this claim in animal models.
Fenugreek (Trigonella foenum graecum)
Trigonella foenum graecum has been used as a remedy
for diabetes, particularly in India and Africa. The
active principal is in the defatted portion of the seed,
which contains the alkaloid trigonelline, nicotinic acid
and coumarin. Administration of the defatted seed
(1.5–2.0 g/kg daily) reduces fasting and postprandial blood
levels of glucose, glycagon, somatostatin, insulin, total
cholesterol, and triglycerides and increased high‑density
lipoprotein‑cholesterol levels.[60] Human studies have
conrmed the glucose and lipid‑lowering effects. The ber
constitutes potential mechanisms of fenugreek’s benecial
effect in diabetic patients. Dosages of the ber range from
10 to 100 g daily in divided dosages. The major side‑effect is
that the urine may have a maple syrup smell after fenugreek
consumption.[60]
Gurmar (Gymnema sylvestre)
Gymnema sylvestre, a plant native in the tropical forests
of Africa and India, has long been used as a treatment
for diabetes. It is postulated that G. sylvestre enhances
the production of endogenous insulin. A typical dosage
of G. sylvestre extract is 400–600 mg/day. One of its
side‑effects may be a reduction or loss of the taste sensation
of sweetness and bitterness although this occurs only if
the plant is directly exposed to the tongue.[60]
Bitter leaf (Vernonia amygdalina)
Vernonia amygdalina commonly known as bitter leaf is
a small tree growing up to 3 m high. It occurs wild in
most countries of tropical Africa. In South Africa, the
plant is found in KwaZulu Natal, Mpumalanga, Eastern
and Northern Cape Provinces. It is probably the most
used plant in the genus Vernonia. The common and
documented medicinal uses include treatment of malaria,
venereal diseases, wounds, hepatitis, and diabetes. The
leaves may be consumed either as a vegetable or aqueous
extracts as tonics for the treatment of various illnesses. It
has been reported that chloroform extract of the plant
has hypoglycemic activity in both normoglycemic and
alloxan‑induced hyperglycemic rats. Ebong et al.,[64] also
reported the anti‑diabetic efcacy of combined ethanolic
extracts of Azadirachta indica (neem) and V. amygdalina in
rats. Also V. amygdalina extract alone shows hypoglycemic
activity in diabetic rats.[65]
Aloe vera
The dried sap (uid) of A. vera is a traditional remedy
used for diabetes in the Arabian peninsula and Africa.
A. vera juice is prepared from A. vera gel, a mucilaginous
preparation obtained from the leaves of the plant. Oral
administration of the juice reduces fasting blood glucose
and triglyceride levels in type 2 diabetic patients with or
without combination of a conventional antidiabetic agent.
The amount used is one tablespoon of A. vera juice with
no signicant adverse effects reported.[60]
Marula (Sclerocarya birrea)
Sclerocarya birrea commonly known as marula is one of the
most highly valued indigenous trees in southern Africa.
It grows up to 15 m high with gray ssured bark, stout
branchlets, and pale foliage. The leaves are compound,
pinnate and the owers greenish‑white or reddish. The
fruits are yellow and closely resemble the mango fruits.
The pulp of the fruit is delicious, and the large nut is also
edible. In Africa, the tree is commonly found in savannah
regions, and its geographical distribution stretches from
Gambia in the west across to Nigeria and Cameroon, in
Central Africa, and to Ethiopia and Sudan in the east. In
South Africa, the plant is commonly found in the Northern
Province.[62] The Zulu people use the bark decoction to
treat diarrhea, dysentery, fevers, stomach ailments, ulcers
and bacterial‑related diseases. Traditional Zulu healers
wash in bark decoctions before treating patients with
gangrenous rectitis and also administer the decoction to
the patient.[62] Dimo et al.[66] has shown that a methanol/
methylene chloride (1:1) extract of the plant reduces blood
glucose and increases plasma insulin levels in diabetic rats.
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Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2) S265
The extract also prevents body weight loss and reduces
plasma cholesterol, while the triglyceride and urea levels
normalized with controls. It has also been reported that an
aqueous stem‑bark extract of the plant has hypoglycemic
effect in normal and streptozotocin (STZ) treated diabetic
rats.[67] These observations thus lend condence to the
folkloric use of the plant in the management and/or control
of adult‑onset diabetes in some African communities.
Wild cucumber (Momordica foetida)
Momordica foetida is a perennial climbing herb with tendrils
and popularly known as Wild cucumber. It is commonly
found in Gabon, Malawi, Ghana, Sudan, and Tanzania.
The owers are cream, often with a reddish or orange
center, having the male and female owers on the same
plant. The characteristic fruit is bright orange with prickles,
and the plant has a strong unpleasant smell. The herb is
used to treat a number of ailments including hypertension,
diabetes mellitus, fever and symptoms of malaria.[62] In
diabetes management, the information is still obscure.
An isolate from the plant, fetidin, has shown the exhibit
hypoglycaemic effect in normal and not in diabetic rats.[68]
Moreover, the mechanism of action of the plant has not
been elucidated. These are classical examples of plants used
in traditional medicine in the management of diabetes in
Africa with different cultural background. Other plants
used in East, West, North or Southern Africa are outlined
in Tables 1‑4.
These antidiabetic plants have been reported in different
parts of the Africa for the treatment of diabetes
with different therapeutic targets.[128] Some have been
investigated in STZ and alloxan induced diabetic rats at
different dosages to evaluate their antidiabetic potentials.
The majority of these plants displayed hypoglycemic
effect. Some of the mechanisms of action reported are
related to inhibition of mitochondrial function, stimulation
of glycolysis, activation of adenosine mono‑phosphate
kinase (AMPK) pathway, suppression of adipogenesis,
uptake of glucose and induction of LDL. Also, some
plants with anti‑diabetic properties have also been
reported to inhibit carbohydrate digestive enzymes such
as α‑glucosidase and α‑amylase.[129] Antioxidant properties
and modication of insulin structure or insulin receptor
sensitivity, as well as up‑regulation of glucose transporter
of some plants, have been reported in several studies.[130]
In this review, it has been noted that there are several
possible mechanisms through which these herbs can act
to control the blood glucose level.[130] The mechanisms of
action can be related, generally, to the ability of the plant
in question (or its active principle) to lower plasma glucose
level by interfering with one or more of the processes
involved in glucose homeostasis.[8,130,131]
In a nutshell, the reported mechanisms whereby medicinal
plants act as anti‑diabetic therapies can be summarized as
follows:
Table 1: Some of the plants that are documented to be used in Southern Africa to manage diabetes mellitus
Scientic name Parts of the
plant used
Mechanisms of actions Type (class)
of herb
Region
commonly used
References
Artemisia afra (Asteraceae) Leaf Induces hypoglycemic effect;
ameliorates oxidative stress
G, F South Africa [62,69]
Aloe vera (L.) Burm (Asphodelaceae) Whole plant Ameliorates oxidative stress F South Africa [70,71]
Aloe arborescens (Asphodelaceae) Leaf Inhibits glucokinase and
G6Pase activities
ASouth Africa [72]
Artemisia roxburghiana (Asteraceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [73]
Allium sativum (Alliaceae) Garlic gloves Possess insulin mimetic
properties; regulates GLUT4
translocation
B, D South Africa [74]
Allium cepa (Alliaceae) Bulbs Possess insulin mimetic
properties; regulates GLUT4
translocation
B, D South Africa [75]
Brachylaena discolor (Asteraceae) Leaves, roots
and stems
Stimulates glucose utilization in
adipocytes
DSouth Africa [63]
Cissampelos capensis (Menispermaceae) Leaves Induces hypoglycemic effect G South Africa [63]
Salvia coccinia (Lamiaceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [73]
Monstera deliciosa (Araceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [73]
Abies pindrow (Pinaceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [73]
Catharanthus roseus (Apocynaceae) Juice leaf Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [76-78]
Contd...
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S266 Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2)
• Stimulation of insulin synthesis and/or secretion from
pancreatic beta‑cells
• Regeneration/revitalization of damaged pancreatic
beta cells
• Improvement of insulin sensitivity (enhancement of
glucose uptake by fat and muscle cells)
• Mimicking the action of insulin (acting like insulin)
• Slowing down the absorption of carbohydrates from
the gut and altering glucose metabolizing enzymes
• Ameliorating oxidative stress.
Therefore, in this review, different medicinal plants used in
Africa for management of diabetes have been classied based
on their modes of action [Figure 1] including; inhibiting
intestinal absorption of glucose and altering glucose
metabolizing enzymes (type A herbs); having insulin mimetic
properties (type B herbs); potentiating glucose‑induced
insulin release (type C herbs); enhance peripheral glucose
uptake (type D herbs); promote regeneration of β‑cell
of islets of Langerhans (type E herbs); and ameliorating
oxidative stress (type F herbs). Some of the plants have
been shown to induce hypoglycemic effect, but the mode
of action still remains obscure, hence, they have been
classied as type G herbs [Tables 1‑4].
It is noted that, of the documented 65 plants used in treatment
of diabetes in Africa as listed in Tables 1‑4, 14 inhibit intestinal
absorption of glucose and altering glucose metabolizing
enzymes, three exhibit insulin‑mimetic properties, seventeen
stimulate insulin secretion from pancreatic beta cells, twelve
enhance peripheral glucose uptake, one promotes regeneration
of beta‑cell of islets of Langerhans, 13 ameliorate oxidative
stress and twenty induce hypoglycemic effect (mode of action
is still obscure). Of these plants, thirteen of them have been
identied to have duplicate mode of actions while one of
them has three modes of actions.
Table 1: Contd...
Scientic name Parts of the
plant used
Mechanisms of actions Type (class)
of herb
Region
commonly used
References
Clausena anisata (Rutaceae) Root Induces hypoglycemic effect G South Africa [79]
Ficus lutea (Moracea) Leaves Actsasα‑amylaseinhibitorin
the gut
ASouth Africa [80]
Ginkgo biloba (Ginkgoaceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [81]
Gymnema sylvestre (Asclepiadaceae) Leaves Inhibit carbohydrate absorption
in the gut
ASouth Africa [82]
Gynura procumbens (Asteraceae) Leaves Lowers intestinal absorption of
glucose; increase hepatic insulin
sensitivity
A, D South Africa [83,84]
Harpagophytum procumbens (Pedaliaceae) Root Induces hypoglycemic effect G South Africa [85]
Hypoxis hemerocallidea (Hypoxidaceae) Tuber Induces hypoglycemic effect G South Africa [86]
Leonotis leonurus (Lamiaceae) Leaf Induces hypoglycemic effect G South Africa [87]
Momordia foetida (Cucurbitaceae) Whole plant Induce hypoglycemic effect G South Africa [68]
Nelumbo nucifera (Nymphaeaceae) Rhizomes Improves glucose uptake into
the cells
DSouth Africa [88]
Olea europaea (Oleaceae) Leaves Regulate GLUT4 translocation D South Africa [89]
Opuntia streptacantha L. (Cactaceae) Fruits, stems Stimulates insulin release from
β‑cellsofLangerhans
CSouth Africa [90]
Psidium guajava (Myrtaceae) Leaves, roots Increases glucose utilization in
the liver and the muscles
A, D South Africa [63]
Sclerocarya birrea (Anacardiaceae) Stem bark Increases glucose utilization in
the liver and the muscles
A, D South Africa [63,91,92]
Solanum lycocarpum (Solanaceae) Fruits Induces hypoglycemic effect G South Africa [92]
Strychnos henningsii (Loganiaceae) Leaves and
bark
Induces hypoglycemic effect;
ameliorates oxidative stress
G, F South Africa [93]
Sutherlandia frutescens (Fabaceae) Plant shoot Decreases intestinal glucose
uptake; increases glucose uptake
in muscle and adipose tissue;
ameliorates oxidative stress
A, D, F South Africa [94]
Syzygium cordatum (Myrtaceae) Leaves Induces hypoglycemic effect;
stimulates hepatic glycogenesis
ASouth Africa [95]
Vernonia amygdalina (Asteraceae) Leaves Induces hypoglycemic effect;
ameliorates oxidative stress
GSouth Africa [63,65,66]
Vinca major (Myrtaceae) Leaves, roots
and stems
Increases glucose utilization in
the liver and the muscles
CSouth Africa [64]
The herbs have been classied into type A, type B, type C, type D, type E, type F and type G herbs. G6Pase: Glucose 6 phosphatase
Kibiti and Afolayan: Anti‑diabetic plants in Africa
Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2) S267
Table 2: Some of the plants that are documented to be used in West Africa to manage diabetes mellitus
Scientic name Parts of the
plant used
Mechanisms of actions Type (class)
of herb
Region
commonly used
References
Aloe vera (L.) Burm (Asphodelaceae) Whole plant Ameliorates oxidative stress F West Africa [70,71]
Artemisia roxburghiana (Asteraceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [73]
Achyranthes aspera L. (Amaranthaceae) Whole plant Ameliorates oxidative stress F West Africa [96]
Azadirachta indica (Meliaceae) Roots Promotesregenerationofβ‑cells
and stimulates insulin release
fromtheβ‑cells
C, E West Africa [97,98]
Allium sativum (Alliaceae) Garlic gloves Possess insulin mimetic properties;
regulates GLUT4 translocation
B, D West Africa [74]
Allium cepa (Alliaceae) Bulbs Possess insulin mimetic properties;
regulates GLUT4 translocation
B, D West Africa [75]
Abroma augusta (Sterculiaceae) Leaves Ameliorates oxidative stress F West Africa [99]
Salvia coccinia (Lamiaceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [73]
Monstera deliciosa (Araceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [73]
Abies pindrow (Pinaceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [73]
Camellia sinensis (Theaceae) Leaves Inhibits rate-limiting
gluconeogenic enzymes, PEPCK
and G6Pase
AWest Africa [76]
Catharanthus roseus (Apocynaceae) Juice leaf Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [76-78]
Cinnamomum cassia (Lauraceae) Bark Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [100]
Garcinia kola Heckel (Clusiaceae) Stem bark Inhibit carbohydrate absorption
in the gut
FWest Africa [101]
Ginkgo biloba (Ginkgoaceae) Whole plant Stimulates insulin release from
β‑cellsofLangerhans
CWest Africa [81]
Gongronema latifolium (Asclepiadaceae) Whole plant Activates hepatic hexokinase
and decreases the activities
of glucokinase; ameliorates
oxidative stress
A, F Nigeria [102,103]
Gymnema sylvestre (Asclepiadaceae) Leaves Inhibit carbohydrate absorption
in the gut
AWest Africa [82]
Gynura procumbens (Asteraceae) Leaves Lowers intestinal absorption of
glucose; Increase hepatic insulin
sensitivity
A, D West Africa [83,84]
Irvingia gabonesis (Irvingiaceae) Tuber Exerts hypolipidaemic effects
to alleviate hyperglcaemia;
ameliorates oxidative stress
F Nigeria [104]
Juniperus communis (Cupressaceae) Whole plant Potentiates glucose induced
insulin secretion; potentiates
peripheral glucose utilization
C, D West Africa [105]
Loranthus begwensis (Loranthaceae) Whole plants Induces hypoglycemic effect G Nigeria [106]
Mangifera indica (Anacardiaceae) Leaves Reduce the intestinal absorption
of glucose
A Nigeria [107]
Ocimum canum (Lamiaceae) Whole plant Enhances insulin release from
β‑cellsofpancrease
C Ghana [108]
Olea europaea (Oleaceae) Leaves Regulate GLUT4 translocation D West Africa [89]
Opuntia streptacantha L. (Cactaceae) Fruits, stems Stimulates insulin release from
β‑cellsofLangerhans
C Africa [90]
Opuntia megacantha (Cactaceae) Fruits, stems Inhibit carbohydrate absorption
in the gut
AWest Africa [109]
Pycnanthus angolensis (Myristicaceae) Leaves, stems Induces hypoglycemic effect G West Africa [110]
Sclerocarya birrea (Anacardiaceae) Stem bark Increases glucose utilization in
the liver and the muscles
A, D Gambia, Nigeria
and Cameroon
[63,91,92]
Tetrapleura tetraptera (Fabaceae) Fruit Induces hypoglycemic effect G West Africa [111]
The herbs have been classied into type A, type B, type C, type D, type E, type F and type G herbs. G6Pase: Glucose 6 phosphatase; PEPCK: Phosphoenolpyruvate carboxykinase
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S268 Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2)
Table 3: Some of the plants that are documented to be used in East Africa to manage diabetes mellitus
Scientic name Parts of the
plant used
Mechanisms of actions Type (class)
of herb
Region
commonly used
References
Aloe vera (L.) Burm (Asphodelaceae) Whole plant Ameliorates oxidative stress F East Africa [70,71]
Artemisia roxburghiana (Asteraceae) Whole plant Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [73]
Aspilia pluriseta (Compositae) Roots Induces hypoglycemic effect G Kenya [112]
Allium sativum (Alliaceae) Garlic gloves Possess insulin mimetic
properties; regulates GLUT4
translocation
B, D East Africa [74]
Allium cepa (Alliaceae) Bulbs Possess insulin mimetic
properties; regulates GLUT4
translocation
B, D East Africa [75]
Caesalpinia volkensii (Caesalpiniaceae) Leaves Induces hypoglycemic effect G Kenya [113]
Salvia coccinia (Lamiaceae) Whole plant Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [73]
Monstera deliciosa (Araceae) Whole plant Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [73]
Abies pindrow (Pinaceae) Whole plant Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [73]
Camellia sinensis (Theaceae) Leaves Inhibits rate-limiting
gluconeogenic enzymes,
PEPCK and G6Pase
A West and East
Africa
[76]
Catha edulis (Celastraceae) Leaves Induces hypoglycemic effect G East Africa [63]
Catharanthus roseus (Apocynaceae) Juice leaf Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [76-78]
Cinnamomum zeylanicum (Lauraceae) Bark Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [100]
Olea europaea (Oleaceae) Leaves Potentiate glucose-induce
insulin release; increase
peripheral uptake of glucose
C, D East Africa [89]
Cogniauxia podoleana Baillon (Cucurbitaceae) Leaves Induces hypoglycemic effect G Democratic
Republic of
Congo
[114]
Erythinia abbyssinica (Fabaceae) Stem bark Induces hypoglycemic effect G Kenya [115]
Ficus sycomorus (Moracea) Stem bark Induces hypoglycemic effect G Kenya [80,116]
Ginkgo biloba (Ginkgoaceae) Whole plant Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [81]
Gymnema sylvestre (Asclepiadaceae) Leaves Inhibit carbohydrate
absorption in the gut
AEast Africa [82]
Gynura procumbens (Asteraceae) Leaves Lowers intestinal absorption
of glucose; Increase hepatic
insulin sensitivity
A, D East Africa [83,84]
Kleinia squarrosa (Asteraceae) Stem bark Induces hypoglycemic effect G Kenya [117]
Maesa lancelata (Myrsinaceae) Fresh fruit Ameliorates oxidative stress F East Africa [118]
Olea europaea (Oleaceae) Leaves Regulate GLUT4 translocation D East Africa [89]
Opuntia robusta (Cactaceae) Fruits Ameliorates oxidative stress F East Africa [119]
Opuntia streptacantha L. (Cactaceae) Fruits, stems Stimulates insulin release
fromβ‑cellsofLangerhans
CEast Africa [90]
Pycnanthus angolensis (Myristicaceae) Leaves,
stems
Induces hypoglycemic effect G East Africa [110]
Solanum lycocarpum (Solanaceae) Fruits Induces hypoglycemic effect G Kenya [92]
Strychnos henningsii (Loganiaceae) Leaves and
bark
Induces hypoglycemic effect;
ameliorates oxidative stress
G, F East Africa [93]
Tetrapleura tetraptera (Fabaceae) Fruit Induces hypoglycemic effect G East Africa [ 111]
The herbs have been classied into type A, type B, type C, type D, type E, type F and type G herbs. G6Pase: Glucose 6 phosphatase; PEPCK: Phosphoenolpyruvate carboxykinase
CONCLUSION
It can be concluded on the basis of the above mentioned
reviews that the majority of anti‑diabetic medicinal
plants exert their blood glucose lowering effect through
stimulation of insulin release from pancreatic beta‑cells
or through alteration of some hepatic enzymes involved
in glucose metabolism and decreasing intestinal glucose
Kibiti and Afolayan: Anti‑diabetic plants in Africa
Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2) S269
absorption. Another point of note in the above‑mentioned
reviews is that a given plant and/or its product may exert
its blood glucose lowering effect through a combination of
more than one mechanism.[131‑133] These plants also have a
similar mode of action as the conventional drugs used in
the management of diabetes mellitus hence due to their
advantages and accessibility; herbal therapy has surpassed
conventional therapy. Moreover, traditional knowledge
has proven a useful tool in the search for new plant‑based
medicines.
A review of literature suggests that most researchers utilize
strategies that are more or less similar to one another to
study medicinal plants with alleged anti‑diabetic potential.
That is, candidate plants are collected, extracted and
screened for hypoglycemic activity using either in vitro or
in vivo bioassay techniques. Then, active compounds are
isolated and identied from plants through fractionation
guided bioassays. Then blood glucose lowering mechanism
of action of the crude plant extract and/or active
ingredients is investigated. Therefore, these studies have
led to ndings which are still obscure. Therefore, while the
metabolic activities of these plants are well established, the
molecular mechanism underlying their biological activities
remains unknown.
There is a need to use molecular tools to determine
genes that act as molecular signatures to be involved
in the diagnosis of the disease, monitor the herbal
therapeutic progress and determine the effectiveness of
the bioactive compounds in efcient manner. It is vital
to embrace computational biology tools to study the
identied compounds in relation to existing anti‑diabetic
drugs in order to improve potency and efcacy of bioactive
Table 4: Some of the plants that are documented to be used in North Africa to manage diabetes mellitus
Scientic name Parts of the
plant used
Mechanisms of actions Type (class)
of herb
Region
commonly used
References
Aloe vera (L.) Burm (Asphodelaceae) Whole plant Ameliorates oxidative stress F North Africa [70,71]
Artemisia roxburghiana (Asteraceae) Whole plant Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [73]
Allium sativum (Alliaceae) Garlic gloves Possess insulin mimetic properties;
regulates GLUT4 translocation
B, D North Africa [74]
Allium cepa (Alliaceae) Bulbs Possess insulin mimetic properties;
regulates GLUT4 translocation
B, D North Africa [75]
Psacalium decompositum (Asteraceae) Roots Induces hypoglycemic effect G North Africa [120]
Salvia coccinia (Lamiaceae) Whole plant Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [73]
Monstera deliciosa (Araceae) Whole plant Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [73]
Abies pindrow (Pinaceae) Whole plant Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [73]
Catharanthus roseus (Apocynaceae) Juice leaf Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [76-78]
Coriandrum sativum (Apiaceae) Seeds Possess insulin like activity; potentiates
insulin releasing
B, C North Africa [121]
Eruca sativa (Cruciferae) Seeds Ameliorates oxidative stress F Egypt [122]
Foeniculum vulgar (Apiaceae) Whole plant Inhibit carbohydrate absorption in the gut F Morocco [123]
Ginkgo biloba (Ginkgoaceae) Whole plant Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [81]
Gymnema sylvestre (Asclepiadaceae) Leaves Inhibit carbohydrate absorption in the gut ANorth Africa [82]
Gynura procumbens (Asteraceae) Leaves Lowers intestinal absorption of glucose;
Increase hepatic insulin sensitivity
A, D North Africa [83,84]
Olea europaea (Oleaceae) Leaves Regulate GLUT4 translocation D North Africa [89]
Opuntia streptacantha L. (Cactaceae) Fruits, stems Stimulatesinsulinreleasefromβ‑cells
of Langerhans
CNorth Africa [90]
Opuntia megacantha (Cactaceae) Fruits, stems Inhibit carbohydrate absorption in the gut ANorth Africa [109]
Panax ginseng (Araliaceae) Leaves Potentiates AMP phosphorylation in liver
and muscle. Improves insulin sensitivity
associated with insulin resistance
A, C Egypt [124]
Urtica dioica (Fabaceae) Leaves Induces hypoglycemic effect; stimulates
insulinreleasefromβ‑cellsofLangerhans
C Algeria, Morocco [125,126]
Zizyphus spina-christi (Rhamnaceae) Leaves Potentiates glucose utilization in the
cells; activates liver phosphorylase and
G6Pase enzymes
A, D Egypt [127]
The herbs have been classied into type A, type B, type C, type D, type E, type F and type G herbs. AMP: Activated protein kinase
Kibiti and Afolayan: Anti‑diabetic plants in Africa
S270 Pharmacognosy Magazine | October-December 2015 | Vol 11 | Issue 44 (Supplement 2)
compounds, hence develop novel drugs for diabetes
management. Considering the rich cultural traditions of
plant use and the high prevalence of diabetes mellitus in
Africa, more investigations should be encouraged in order
to validate the anti‑diabetic activity of the identied plants
as claimed by the traditional healers.
ACKNOWLEDGMENT
This research was supported by grants from Govan Mbeki
Research and Development Centre, University of Fort Hare,
South Africa.
AUTHOR’S CONTRIBUTIONS
CMK carried out the study and wrote the manuscript; AJA
contributed to conception of the review and supervised
the manuscript writing. All authors have read and approved
the nal manuscript.
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Figure 1: Mechanisms underlying plants used in traditional medicine in the management of diabetes mellitus. Some inhibit intestinal absorption
of glucose and alter glucose metabolizing enzymes (type A herbs); have insulin mimetic properties (type B herbs); potentiates glucose‑induced
insulin release (type C herbs); enhances peripheral glucose uptake (type D herbs); promotes regeneration of β‑cell of islets of Langerhans (type
E herbs); and ameliorates oxidative stress (type F herbs)
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Cite this article as: Kibiti CM, Afolayan AJ. Herbal therapy: A review of
emerging pharmacological tools in the management of diabetes mellitus in
Africa. Phcog Mag 2015;11:258-74.
Source of Support: Nil, Conict of Interest: None declared.