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C O M M E N T A R Y Open Access
Δ9-Tetrahydrocannabivarin (THCV): a
commentary on potential therapeutic
benefit for the management of obesity and
diabetes
Amos Abioye
1
, Oladapo Ayodele
2
, Aleksandra Marinkovic
2
, Risha Patidar
2
, Adeola Akinwekomi
2
and
Adekunle Sanyaolu
3*
Abstract
Δ9-Tetrahydrocannabivarin (THCV) is a cannabis-derived compound with unique properties that set it apart
from the more common cannabinoids, such as Δ9-tetrahydrocannabinol (THC). The main advantage of THCV
over THC is the lack of psychoactive effects. In rodent studies, THCV decreases appetite, increases satiety, and
up-regulates energy metabolism, making it a clinically useful remedy for weight loss and management of
obesity and type 2 diabetic patients. The distinctions between THCV and THC in terms of glycemic control,
glucose metabolism, and energy regulation have been demonstrated in previous studies. Also, the effect of
THCV on dyslipidemia and glycemic control in type 2 diabetics showed reduced fasting plasma glucose
concentrationwhencomparedtoaplacebogroup.Incontrast,THCisindicatedinindividualswithcachexia.
However, the uniquely diverse properties of THCV provide neuroprotection, appetite suppression, glycemic
control, and reduced side effects, etc.; therefore, making it a potential priority candidate for the development
of clinically useful therapies in the future. Hopefully, THCV could provide an optional platform for the
treatment of life-threatening diseases.
Keywords: Δ9-Tetrahydrocannabivarin (THCV), Tetrahydrocannabinol (THC), Cannabis sativa (marijuana),
Obesity, Diabetes
Background
The therapeutic benefits of the extracts from the
plant Cannabis sativa L. and its subspecies (hemp,
marijuana) have been extensively studied. Cannabi-
diol (CBD), Δ-9-tetrahydrocannabinol (THC) and Δ-9-
tetrahydrocannabivarin (THCV) are the major components
isolated from Cannabis sativa and have been reported ex-
tensively in modern literature. THC is the primary psycho-
active component of Cannabis sativa and its medicinal
properties are attributed to its specific interaction with the
endocannabinoid system (ECS) (Borgelt et al. 2013;
McPartland et al. 2015; Chakrabarti et al. 2015). ECS con-
sists of two types of endogenous G protein-coupled canna-
binoid receptors (CB
1
and CB
2
) that are located in the
mammalian brain and throughout the central and periph-
eral nervous systems (Pertwee 2008; Solinas et al. 2008).
The EC system represents a major neuromodulatory
system involved in the regulation of emotional re-
sponses, behavioral reactivity, and social interactions.
Pathophysiologic manipulation of the ECS has been
exploited as a key tool in the management of severe
disease conditions of the central nervous system. For
example, in recent years, elements of the ECS and its
pathways have been explored as therapeutic measures
for mitigating some central nervous system diseases
such as Autism Spectrum Disorder (ASD) and epilepsy
(Chakrabarti et al. 2015). The endocannabinoid system
is also responsible for the maintenance of energy
homeostasis and the regulation of lipid and glucose
metabolism (McPartland et al. 2015).Inthesamevein,
molecular markers have been identified in the ECS
© The Author(s). 2020 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
* Correspondence: sanyakunle@hotmail.com
3
Federal Ministry of Health, Abuja, Nigeria
Full list of author information is available at the end of the article
Journal of Cannabi
s
R
esea
r
c
h
Abioye et al. Journal of Cannabis Research (2020) 2:6
https://doi.org/10.1186/s42238-020-0016-7
membrane transporters (AM404) that could trigger aut-
istic behavior when the cannabinoid receptors are acti-
vated (Chakrabarti et al. 2015).
THC produces various psychoactive effects by activa-
tion of the CB
1
cannabinoid receptors in the brain, espe-
cially the basal ganglia, substantia nigra, globus pallidus,
hippocampus, cerebellum, etc. These locations indicate
that THC is involved in the modulation of memory,
emotions, and movement. Activation of the CB
1
recep-
tors leads to inhibition of adenylyl cyclase and blockade
of voltage-operated calcium channels, which in turn sup-
presses neuronal excitability and inhibition of neuro-
transmission of serotonin (Pertwee 2008). Therefore, the
therapeutic benefits of THC include the management of
conditions associated with depression, Parkinson’s dis-
ease, Alzheimer’s disease, resistant childhood seizures,
chronic pain, multiple sclerosis, convulsions, glaucoma,
neuropathic pain and a variety of other conditions (Hill
2015; Grant et al. 2012). It is important to note that
Cannabis sativa is not a miracle plant. Despite the medi-
cinal benefits of marijuana, its chronic use has been
linked with conditions such as psychotic disorders and
cannabis use disorder, while acute consumption is linked
to psychotic symptoms, hyperemesis syndrome and anx-
iety (Bridgeman and Abazia 2017).
Therefore research efforts have been intensified to de-
velop several synthetic high-affinity analogs of CB
1
can-
nabinoid receptor antagonists and inverse agonists as
therapeutic drugs for the management of drug depend-
ence, metabolic syndrome, and diabetes. Literature is
replete with inverse agonists of the CB
1
cannabinoid re-
ceptors that have been developed for the management of
drug dependence, metabolic syndrome, type 2 diabetes
and dyslipidemia (Brown 2007).
Rimonabant, a first-generation synthetic inverse agon-
ist / selective antagonist of the CB
1
receptor, was ap-
proved in Europe in 2006 for the treatment of anorectic
obesity (Bridgeman and Abazia 2017). This drug exerts
its effect on the ECS by selectively blocking the CB
1
re-
ceptors; thus, reducing appetite and inducing hypopha-
gia. In a randomized double-blind, rimonabant-placebo
controlled trial; rimonabant produced a significant re-
duction in body weights of subjects from 2.6 to 6.3 kg
relative to placebo among the groups taking 20 mg of
rimonabant daily. HbA
1C
in obese patients decreased by
0.5–0.6% compared to metformin or sulphonylurea, and
0.8% reduction compared to 0.3% reduction in placebo
group. High-density lipoproptein cholesterol (HDL-C)
also increased significantly by 22.3% compared with
13.4% in the placebo group while the level of triglycer-
ides decreased in all trials by 6.8% compared with an
increase of 8.3% in the placebo group (p< 0.0001). The
levels of adiponectin, a protein hormone regulating
glucose level and fatty acid breakdown in humans,
increased significantly by 23% from the baseline in the
20 mg rimonabant group. It was concluded that rimona-
bant is effective in controlling blood glucose levels and
reducing weight in obese patients; however, it was with-
drawn from the global market in 2008 due to increased
incidences of nausea, upper respiratory tract infections,
and serious psychiatric side effects including depression
and suicide ideation (Buggy et al. 2011; Christopoulou
and Kiortsis 2011; Le Foll et al. 2009). This left a huge
research gap as many pharmaceutical companies aban-
doned the development of inverse CB
1
receptor agonists.
It was opined that the development of novel compounds
that are neutral antagonists of the CB
1
receptor with se-
lectivity for peripheral receptors may be of great value in
obtaining similar metabolic results with little or no psy-
chiatric adverse effects. Therefore, research in this area
is continuous.
THCV is an inverse agonist / selective antagonist of
the CB
1
receptor, similar to rimonabant but it does not
have the identified adverse effects of rimonabant. This
short review discusses the potential therapeutic benefits
of THCV, a naturally occurring analog of THC, in the
management of obesity and type 2 diabetes, its potential
side effects, and the mechanism of action within the
ECS.
Methodology
A narrative electronic literature search was performed
using peer-reviewed articles published from January 1,
1970, until September 30, 2019. An article was selected if it
included keywords such as Δ9-tetrahydrocannabivarin
(THCV), Δ9-tetrahydrocannabinol (THC), Cannabis sativa
(marijuana), obesity, body weight, metabolism, and dia-
betes. Articles were then reviewed and included based on
the applicability to the topic.
Understanding THCV
THCV is a naturally occurring analog of THC. Unlike
THC, which is psychoactive and an agonist at the CB
1
and CB
2
receptors, THCV is a non-psychoactive, neutral
CB
1
antagonist / reverse agonist and may act as agonist
or antagonist at the CB
2
receptors depending on its
dose. It is thought that THCV prevents the psychological
effects of THC however; the mechanism by which
THCV antagonizes the effect of THC is unknown. Also
unlike THC, THCV produces hypophagic effects in both
fasted and non-fasted mice (Riedel et al. 2009). It follows
that THCV has great potential for the management of
obesity.
The effect of THCV in diet-induced obesity (DIO) and
genetic obesity (GO) was evaluated in mice (4 mice per
group) using two orally administered dose ranges of
THCV stock solution. The solution was appropriately di-
luted to the required strength using sesame seed oil, for
Abioye et al. Journal of Cannabis Research (2020) 2:6 Page 2 of 6
the DIO group at 0.3–12.5 mg/kg twice daily for 30 days
and 0.1–12.5 mg/kg once daily for 45 days. One pilot
study of 0.3–3 mg/kg per oral once daily; and one full
dose range of 0.1–12.5 mg/kg once daily for 30 days in
obese mice (Wargent et al. 2013) were also conducted.
The results were compared to a potent CB
1
inverse
agonist (AM251) administered per oral at 10 mg/kg once
daily or 5 mg/kg twice daily as a positive control. Both
doses of AM251 reduced mice’s body weight signifi-
cantly by greater than 8 g (p< 0.001) whereas, THCV did
not have any significant effect on the body weight at any
of the doses used in the study. Similarly, AM251 de-
creased the total food intake over the first 10 days of the
study, but THCV had no significant effect on the mice’s
food intake throughout the study. Neither AM251 nor
THCV affected water intake. However, there was a sig-
nificant reduction in the fat contents by both AM251
(26.4%) and THCV (31.1%) compared to the control
(42.1%). There was generally no statistically significant
effect on these parameters in the genetically obese mice.
It was concluded that similar to AM251, THCV has a
high affinity for CB
1
receptors and high brain penetra-
tion, producing some metabolically beneficial effects
typical of CB
1
receptor inverse agonist in two different
mouse models of obesity. The strongest effect was on
plasma glucose and insulin levels, as well as liver triglyc-
erides. It was opined that THCV may be useful for the
treatment of metabolic syndrome and/or type 2 diabetes,
either alone or as an adjuvant treatment with other
therapeutic options.
Since ECS modulates appetite, food consumption and
feeding behavior in animals and humans (Solinas et al.
2008) the acute use of THC, a partial agonist of the
CB
1
receptors, is classically associated with acute
appetite-enhancing effects, as well as an increase in the
frequency of sucrose ingestion (Jarrett et al. 2005).
When THC was administered to rats before the
intraoral infusion of sucrose solution, it was noted that
THC increased the frequency of sucrose ingestion at 30
and 60 min and particularly, increased palatability at
the 120-min interval (Jarrett et al. 2005). Conversely,
rimonabant, a CB
1
antagonist that is similar to THCV,
resulted in the reversal of the enhanced frequency of
sucrose ingestion and increased palatability (Jarrett
et al. 2005).
In a similar report, THCV, a neutral antagonist of the
CB
1
receptors resulted in decreased food intake and
body weight reduction in mice models; thus, exerting
an anti-obesity effect in mouse models by food aversion
(Wargent et al. 2013; Tudge et al. 2015). The metabolic
effect of THCV can be explained by its interaction with
the transient receptor potential cation channel subfam-
ily V member 1 (TRPV1), also known as the capsaicin
receptor (Riedel et al. 2009). Unlike THC, THCV is
observed to induce a therapeutic metabolic effect by
restoring insulin sensitivity in obese mice models and
interacting with the TRPV1 channels (De Petrocellis
et al. 2011). THCV has been shown to restore insulin
sensitivity in diet-induced obese mice models and redu-
cing obesity by modulating the metabolic processes.
The chemical structures of two of the most abundant
phytocannabinoids in Cannabis sativa L.are
highlighted in Fig. 1: THC (a), THCV (b). These phyto-
cannabinoids share some similar structural features that
includeadibenzopyranringandahydrophobicalkyl
chain, but each interacts with the ECS in a slightly dif-
ferent manner (Gill et al. 1970; Jager and Witkamp
2014). Existing in continuous dynamic equilibrium with
each other, endocannabinoids are a part of a class of
structurally related amides, esters, and ethers of fatty
acids (Gill et al. 1970). Although each of these com-
pounds has a slightly different molecular structure,
biosynthesis, and physicochemical properties, they all
interact with the ECS to maintain homeostasis and
regulate lipid and glucose metabolism (Wargent et al.
2013; Jarrett et al. 2005).
For instance, THC and CBD are biosynthesized as
tetrahydrocannabinolic acid (THC-A) and cannabidiolic
acid (CBD-A) respectively from a common precursor
cannabigerolic acid (CBG). These phytocannabinoids
Fig. 1 Molecular Structures of THC (a), and THCV (b). Data sourced from Jager and colleagues in The Endocannabinoid System and Appetite:
Relevance for Food Reward
19
Abioye et al. Journal of Cannabis Research (2020) 2:6 Page 3 of 6
are inactive in their natural acidic states but are con-
verted to their respective therapeutically active forms
by decarboxylation process when heated. Although they
are from the same precursor, THC acts as an agonist at
the cannabinoid receptors and results in an increased
lipid and glucose intake (McPartland et al. 2015;Jarrett
et al. 2005; Jager and Witkamp 2014), whereas THCV
exhibits antagonistic activities at the cannabinoid recep-
tors (Thomas et al. 2005). Studies using mice models have
indicated dose-dependent therapeutic effects (Jadoon et al.
2016). At low intravenous doses (0.1, 0.3, 1.0 and/or 3 mg/
kg), the plant-derived THCV and its synthetic analogs (O-
4394 and O-4395) show antagonism at the cannabinoid
receptors by reversing some of the effects of THC, such as
THC-induced antinociception and hypothermia (Pertwee
et al. 2007). THC activates both peripheral and central
CB
1
receptors (Muniyappa et al. 2013)whenadministered
alone. At higher doses, both O-4394 and O-4395 exhibit
agonistic effects at the cannabinoid receptors by precipi-
tating hypothermia (above 3 mg/kg) and antinociception
(above 10 mg/kg) (Pertwee et al. 2007). The cannabinoid
receptors and their ligands have been implicated in feed-
ing and metabolic control regulations (Cluny et al. 2015;
Ravinet-Trillou et al. 2004) providing a potential thera-
peutic benefit for the treatment of type 2 diabetes in the
human population.
A significant increase in body weight (24%) and adi-
posity (60%) in CB
1
+/+ mice compared to the CB
1
−/−
mice has been reported when both groups were fed with
standard diet containing 3.5 kcal/g and 14.5% of energy
as fat (Ravinet-Trillou et al. 2004). However, when both
types of mice were fed with a high-fat obesity-prone diet
containing 4.9 kcal/g and 49% of energy as fat, CB
1
−/−
mice did not develop obesity in contrast to the CB
1
+/+
mice in spite of the similar energy intake. This suggests
an improved metabolic regulation in the CB
1
−/−mice
(Ravinet-Trillou et al. 2004). In another study, fasting
plasma glucose levels and oral glucose tolerance test
(OGTT) improved in mice with diet-induced obesity
when plant-derived THCV was administered twice daily
(Wargent et al. 2013). Administration of intraperitoneal
plant-derived THCV in rodents resulted in weight loss,
reduced food intake, reduced body fat content, increased
energy expenditure, rapid insulin response to OGTT
(Wargent et al. 2013), and reduced liver triglycerides
(Ravinet-Trillou et al. 2004; Englund et al. 2015).
Similar to the rimonabant human clinical trials men-
tioned above, the selective CB
1
receptor antagonist
rimonabant, exhibited potent anti-obesity properties in
CB
1
(+/+) obese mice leading to leanness and hypo-
phagia (Wargent et al. 2013; Ravinet-Trillou et al.
2004). In Zucker rats, rimonabant reduced the levels of
plasma triglycerides, free fatty acids, total cholesterol,
and increased the levels of high-density lipoprotein/
low-density lipoprotein (HDL/LDL) ratio (Thomas
et al. 2005). Similar effects on lipid profiles were ob-
served when a high dose of the plant-derived THCV
(12.5 mg/kg) was administered to diet-induced obese
mice once daily (Wargent et al. 2013). There was no
significant change in the glycemic profile until after 3
weeks of administering high dose plant-derived THCV
(12.5 mg/kg), where the once-daily administration of
THCV resulted in a lower fasting glucose and the
twice-daily administrationofTHCVresultedinin-
creased glucose intolerance (Wargent et al. 2013). This
suggests that THCV has a more profound leptin-based
effect on the lipid profile than the glucose profile in
both fasting and non-fasting states. In CB
1
knockout
mice, rimonabant does not display the anti-obesity
properties that were previously observed in diet-induced
obese mice (Ravinet-Trillou et al. 2004). Like THCV,
other synthetic cannabinoid antagonists such as O-4394
and O-4395 (Ravinet-Trillou et al. 2004; Englund et al.
2015), modulate the cannabinoid receptor activity. They
showed similar physiologic activity, displacing the (3)-H-
CP55940 in the mouse brain and antagonizing specific ac-
tivity at the CB
1
receptor sites in the brains of mice and
vas deferens (CP55940 and R-(+)-WIN55212), respectively
(Anavi-Goffer et al. 2012).
In a placebo-controlled, double-blind, cross-over pilot
study involving ten male cannabis users (less than 25
uses/occasion), 10 mg pure THCV or placebo was given
for 5 days followed by 1 mg intravenous THC infusion
on the last day. When a low dose of oral THCV was ad-
ministered before the THC intravenous dose, THCV
blunted the well-known effects of THC including psych-
otic and paranoia effects, and impaired short-term mem-
ory (Englund et al. 2015).
In another randomized, double-blind, placebo-controlled,
parallel-group pilot study, the safety and efficacy of THCV
and CBD were evaluated in patients with type 2 diabetes
using the glycemic and lipid parameters. Sixty-two patient
volunteers with non-insulin treated type 2 diabetes were
randomized to five treatment groups viz.: CBD (100 mg
twice daily), THCV (5 mg twice daily), 1:1 ratio of CBD and
THCV (5 mg/5 mg, twice daily), 20:1 ratio of CBD and
THCV (100 mg/5 mg, twice daily) and matched placebo for
13 weeks. Patients were at least 18 years of age with
hemoglobin A1C (HbA
1C
) levels less than 10% (Jadoon et al.
2016).
THCV significantly decreased fasting plasma glucose
(from 7.4 to 6.7 mmol/L) compared to the placebo group
which increased from 7.6 to 8 mmol/L
21
with an esti-
mated treatment difference (ETD) of −1.2 mmol//L, p<
0.05. It also improved the Homeostasis Model Assessment
(HOMA2) of pancreatic β-cell function from 105.1 to
144.4 points compared to 96.4 to 94.7 points in the pla-
cebo group (ETD = 44.6 ± 16.1, p< 0.01) (Jadoon et al.
Abioye et al. Journal of Cannabis Research (2020) 2:6 Page 4 of 6
2016). Adiponectin is the protein hormone involved in
regulating the plasma glucose levels and fatty acid break-
down (pancreatic function). The pancreatic β-cell function
improved significantly in the THCV treatment group rela-
tive to placebo (ETD = −5.9 × 10
6
pg/mL, p<0.01), aswell
as apolipoprotein A (ETD = −6.02 μmol/L, p<0.05), but
there was no significant effect on the HDL cholesterol.
CBD decreased resistin significantly (−898 pg/mL, p<
0.05) and increased glucose-dependent insulinotropic
peptide (21.9 mL, p < 0.05) compared to the baseline.
It was concluded that THCV and CBD alone and their
combination products were well-tolerated in patient
volunteers with type 2 diabetes. THCV significantly de-
creased the fasting plasma glucose, increased β-cell func-
tion, as well as adiponectin and Apo A concentrations in
type 2 diabetic patients. It was evident that THCV may
provide a template for the development of new thera-
peutic agents for glycemic control, especially for type 2
diabetics.
From the foregoing, it is obvious that the non-
psychoactive effect of THCV provides a therapeutic ad-
vantage over other cannabinoid analogs in addition to its
hypoglycemic and hypolipidemic effects. Hence, further
intensive research is urgently needed to produce clinic-
ally useful medicinal agents from THCV derived from
marijuana (Cannabis sativa). As shown from this short
review, it is important to emphasize that the pure plant-
derived THCV did not elicit the common adverse effects
associated with rimonabant (psychiatric and anxiogenic-
like reaction) and AM251 (nausea) (McPartland et al.
2015) reported in this review. Although the reason for
this difference is not fully understood it was hypothe-
sized that THCV might competitively inhibit one of the
signaling pathways of one or more endogenously pro-
duced endocannabinoids through CB
1
receptor activity
(McPartland et al. 2015). Another explanation for the anti-
obesity feature of THCV can be attributed to its ability to
interact with other receptor sites, including the G-protein-
coupled receptor (GPR55)
27,
the transient receptor poten-
tial vanilloid 1 receptor (TRPV1) (De Petrocellis et al. 2011)
and other endogenous endocannabinoids for the receptor
site (Riedel et al. 2009). A summary of the effects of THCV
on human and mouse/animal: metabolism, glycemic and
lipidemic responses are highlighted in Table 1.
Conclusion
The psychoactive effects of THC in marijuana are the main
reasons for its classification as a Schedule I substance, even
though it is the THC that the U.S. Food and Drug Admin-
istration (FDA) approved for appetite stimulation and
weight gain. In contrast to THC, clinical and therapeutic
advantages of THCV regarding its lack of psychoactive
effects in human studies are of great value in pharmaco-
therapy. On the other hand, the dual pharmacological activ-
ities of THCV on CB
1
/CB
2
receptors, exhibiting agonistic
and antagonistic effects depending on the dosage, indicate
the need for further research. It is envisioned that the
unique and diverse characteristics of THCV could be
explored for further development into clinically useful med-
icines for the treatment of life-threatening diseases.
Table 1 Summarized Metabolic, Glycemic, and Lipidemic Effects of THCV
Metabolic Glycemic Lipidemic
THCV Effects
Human
Studies
Increase FFA suppression
index (FFA auc/Insulin auc)
(Muniyappa et al. 2013)
Induces glucose intolerance in men
(Muniyappa et al. 2013)
Impaired adipose tissue insulin
sensitivity (Muniyappa et al. 2013)
Increase indices of adipose tissue
insulin resistance (Muniyappa et al. 2013)
Normal glucose tolerance due to no
impairments on β-cell glucose sensitivity,
rate sensitivity, or insulin secretion
(Muniyappa et al. 2013)
Decreased fasting plasma glucose
(Jadoon et al. 2016)
Improved pancreatic β-cell function
(Jadoon et al. 2016)
No difference in total cholesterol level
(Muniyappa et al. 2013)
Lower plasma HDL level
(Muniyappa et al. 2013) vs. plasma HDL
unaffected (Jadoon et al. 2016)
No difference in LDL cholesterol
(Muniyappa et al. 2013)
No difference in triglycerides
(Muniyappa et al. 2013)
No difference FFA levels
(Muniyappa et al. 2013)
Animal
Studies
Improved fasting plasma
glucose (Wargent et al.
2013)
Pancreatic CB1R activation leads to β-cell
death and impairs insulin secretion
(Muniyappa et al. 2013)
Improved glucose tolerance
(Wargent et al. 2013)
Increased insulin sensitivity
(Wargent et al. 2013)
Restores insulin sensitivity in cells that are
insulin-resistant (Wargent et al. 2013)
Increase adipocyte hypertrophy - increase
hepatic fat (Muniyappa et al. 2013)
Increase in lipogenesis
(Muniyappa et al. 2013)
No effect on plasma total cholesterol and
triglyceride (Wargent et al. 2013)
No change in HDL cholesterol
concentrations (Wargent et al. 2013)
Note: Data sourced from Muniyappa (Muniyappa et al. 2013) and colleagues, Wargent (Wargent et al. 2013) and colleagues, and Jadoon (Jadoon et al. 2016)
and colleagues
Abioye et al. Journal of Cannabis Research (2020) 2:6 Page 5 of 6
Abbreviations
ASD: Autism Spectrum Disorder; CB: Cannabinoid receptors;
CBD: Cannabidiol; CB1,2: Cannabinoid type 1,2 receptors; CBD-
A: Cannabidiolic acid; CBG: Cannabigerolic acid; DIO: Diet induced obesity;
ECs: Endocannabinoid system; ETD: Estimated Treatment Difference;
FDA: Food and Drug Administration; GPR55: G protein coupled receptor;
GO: Genetic obesity; HbA1C: Hemoglobin A1C; HDL: High density
lipoprotein; HDL-C: High density lipoprotein cholesterol;
HOMA2: Homeostasis Model Assessment; LDL: Low density lipoprotein;
OGTT: Oral glucose tolerance test; THC: Tetrahydrocannabinol; THCV: Δ9
Tetrahydrocannabivarin; TRPV1: Transient receptor potential vanilloid 1
receptor; THC-A: Tetrahydrocannabinolic acid
Acknowledgements
None
Authors’contributions
AmA, AS, AM and OA were involved in the study conception/design; AdA,
AM, OA, and RP were involved in the acquisition, analysis, and interpretation
of data; AS, AM and OA were involved in drafting and revising the
manuscript; AmA and AS approved final version of manuscript for
publication and are responsible for accuracy and integrity of all aspects of
research. All authors read and approved the final manuscript.
Authors’information
Not applicable
Funding
None to declare
Availability of data and materials
Not applicable
Ethics approval and consent to participate
Not applicable
Consent for publication
Not applicable
Competing interests
The authors declare that they have no competing interests.
Author details
1
Lloyd L. Gregory School of Pharmacy, Palm Beach Atlantic University, West
Palm Beach, Florida, USA.
2
Saint James School of Medicine, The Quarter,
Anguilla.
3
Federal Ministry of Health, Abuja, Nigeria.
Received: 26 July 2019 Accepted: 19 January 2020
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