ArticlePDF Available

Abstract and Figures

OBJECTIVE To assess the efficacy of curcumin in delaying development of type 2 diabetes mellitus (T2DM) in the prediabetic population. RESEARCH DESIGN AND METHODS This randomized, double-blinded, placebo- controlled trial included subjects (n = 240) with criteria of prediabetes. All subjects were randomly assigned to receive either curcumin or placebo capsules for 9 months. To assess the T2DM progression after curcumin treatments and to determine the number of subjects progressing to T2DM, changes in β-cell functions (homeostasis model assessment [HOMA]-β, C-peptide, and proinsulin/insulin), insulin resistance (HOMA-IR), anti-inflammatory cytokine (adiponectin), and other parameters were monitored at the baseline and at 3-, 6-, and 9-month visits during the course of intervention. RESULTS After 9 months of treatment, 16.4% of subjects in the placebo group were diagnosed with T2DM, whereas none were diagnosed with T2DM in the curcumin-treated group. In addition, the curcumin-treated group showed a better overall function of β-cells, with higher HOMA-β (61.58 vs. 48.72; P < 0.01) and lower C-peptide (1.7 vs. 2.17; P < 0.05). The curcumin-treated group showed a lower level of HOMA-IR (3.22 vs. 4.04; P < 0.001) and higher adiponectin (22.46 vs. 18.45; P < 0.05) when compared with the placebo group. CONCLUSIONS A 9-month curcumin intervention in a prediabetic population significantly lowered the number of prediabetic individuals who eventually developed T2DM. In addition, the curcumin treatment appeared to improve overall function of β-cells, with very minor adverse effects. Therefore, this study demonstrated that the curcumin intervention in a prediabetic population may be beneficial.
Content may be subject to copyright.
Curcumin Extract for Prevention of
Type 2 Diabetes
OBJECTIVEdTo assess the efcacy of curcumin in delaying development of type 2 diabetes
mellitus (T2DM) in the prediabetic population.
RESEARCH DESIGN AND METHODSdThis randomized, double-blinded, placebo-
controlled trial included subjects (n= 240) with criteria of prediabetes. All subjects were ran-
domly assigned to receive either curcumin or placebo capsules for 9 months. To assess the T2DM
progression after curcumin treatments and to determine the number of subjects progressing to
T2DM, changes in b-cell functions (homeostasis model assessment [HOMA]-b,C-peptide,and
proinsulin/insulin), insulin resistance (HOMA-IR), anti-inammatory cytokine (adiponectin),
and other parameters were monitored at the baseline and at 3-, 6-, and 9-month visits during the
course of intervention.
RESULTSdAfter 9 months of treatment, 16.4% of subjects in the placebo group were di-
agnosed with T2DM, whereas none were diagnosed with T2DM in the curcumin-treated group.
In addition, the curcumin-treated group showed a better overall function of b-cells, with higher
HOMA-b(61.58 vs. 48.72; P,0.01) and lower C-peptide (1.7 vs. 2.17; P,0.05). The
curcumin-treated group showed a lower level of HOMA-IR (3.22 vs. 4.04; P,0.001) and higher
adiponectin (22.46 vs. 18.45; P,0.05) when compared with the placebo group.
CONCLUSIONSdA 9-month curcumin intervention in a prediabetic population signi-
cantly lowered the number of prediabetic individuals who eventually developed T2DM. In
addition, the curcumin treatment appeared to improve overall function of b-cells, with very
minor adverse effects. Therefore, this study demonstrated that the curcumin intervention in a
prediabetic population may be benecial.
Diabetes Care 35:21212127, 2012
The impacts of type 2 diabetes melli-
tus (T2DM) on global health care
and economy are enormous (1). Ac-
cording to the World Health Organiza-
tion, there are ;311 million people
worldwide who live with T2DM. This
number continues to rise, especially in
the newly developing and poorer coun-
tries in Asia and elsewhere. Because
T2DM is currently incurable, a common
treatment approach is to try to control the
disease with lifelong use of antidiabetes
drugs. Limiting the number of newly de-
veloped T2DM cases should be one of the
better key strategies to restrict the global
impacts of T2DM (2). In order to limit the
number of new T2DM cases, the lifestyle
of the prediabetic population has to be
changed. However, this has been shown
to be challenging (3). One of the
alternative approaches to prevent devel-
opment of T2DM is to intervene with the
prediabetic population before disease
progresses into fully developed T2DM
(3). The intervention approach is appeal-
ing. It relies on timely identication of
prediabetic individuals and provision of
preventive treatment before the disease
fully progresses. The intervention rep-
resents a chance for the diabetes-prone
population to halt the disease progression
and maintain a normal and healthy life. In
recent years, several effective T2DM inter-
vention regimens have been developed,
with encouraging results (35). However,
these regimens are not usually economi-
cally accessible, and they are not well-
tolerated because of treatment-related
toxicities (4,5). The focus now is to iden-
tify new effective therapeutic agents,
with relatively low cost and low toxicity,
that can be used regularly to control a
progression of T2DM in the prediabetic
Curcumin is the principal curcumi-
noid found in turmeric (Curcuma longa
Linn.), a popular spice in Asian cuisine.
It is widely consumed and generally be-
lieved to be benecial for human health
(6). Curcumin extract from rhizomes of
turmeric has been shown to contain anti-
inammation and antidiabetic properties
(713). In addition, it could delay devel-
opment of T2DM, improve b-cell func-
tions, prevent b-cell death, and reduce
insulin resistance in animals (816).
This study aimed to determine the effec-
tiveness of curcumin extract as an interven-
tion agent to prevent T2DM development.
We assessed T2DM progression and sev-
eral indicative T2DM parameters in a large
randomized, double-blinded, and pla-
cebo-controlled cohort. We found that
curcumin extract effectively reduced the
number of prediabetic individuals who
progressed toward T2DM as well as im-
proved functions of b-cells.
Study design and participants
This randomized, double-blinded, placebo-
controlled trial was conducted at HRH
Princess Maha Chakri Sirindhorn Medical
From the
Division of Endocrinology and Metabolism, Faculty of Medicine, HRH Princess Maha Chakri
Sirindhorn Medical Center, Srinakharinwirot University, Nakornnayok, Thailand; the
Division of Endo-
crinology, Diabetes and Hypertension, Brigham and Womens Hospital, Boston, Massachusetts; the
partment of Preventive and Social Medicine, Faculty of Medicine, HRH Princess Maha Chakri Sirindhorn
Medical Center, Srinakharinwirot University, Nakornnayok, Thailand; the
Department of Pharmacology
and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand; the
Research and Development Institute, Thai Government Pharmaceutical Organization, Bangkok, Thailand;
Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhon Pratom, Thailand; and the
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Corresponding author: Somlak Chuengsamarn,
Received 18 January 2012 and accepted 9 May 2012.
DOI: 10.2337/dc12-0116. Clinical trial reg. no. NCT01052025,
This article contains Supplementary Data online at
© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly
cited, the use is educa tional and not for prot, and the work is not alte red. See
licenses/by-nc-nd/3.0/ for details. DIABETE S CARE,VOLUME 35, NOVEMB ER 2012 2121
Clinical Care/Education/Nutrition/Psychosocial Research
Center of Srinakharinwirot University (Na-
kornnayok, Thailand). Two hundred forty
patients were selected to participate in this
study by inclusion and exclusion criteria
(for a complete ow chart, see Supple-
mentary Fig. 1). The subjects were en-
rolled in the 12-monthlong study. We
educated all subjects to perform in the
same protocols for diet and exercise
during a 3-month period after the enroll-
ment (before the randomization). Stan-
dard lifestyle recommendations were
provided for all subjects in written form.
All of the subjects took part in a 2030-
min one-on-one workshop that empha-
sized the importance of a healthy lifestyle.
Participants were encouraged to follow the
Medical Nutrition Therapy and physical
activity (17). To avoid any interference
from other medications, during the re-
cruitment process, we excluded all of pa-
tients who were taking any other
medicines, as shown in the exclusion cri-
teria. Only prediabetic subjects aged $35
years were included in this study. Predia-
betes was diagnosed following the Ameri-
can Diabetes Association (ADA) practice
guidelines. Subjects who t into at least
one of these three criteria were included:
subjects with a fasting plasma glucose
(FPG) between 100 and 124 mg/dL (indi-
cating impaired fasting glucose), an oral
glucose tolerance test (OGGT) plasma glu-
cose at 2 h postglucose load (OGTT at 2 h)
between 140 and 199 mg/dL (indicating
impaired glucose tolerance), and a glyca-
ted hemoglobin (HbA
) range from 5.7 to
6.4%. Diagnosis of prediabetes was con-
rmed by a second repeating test of all of
the above-listed criteria on a different day.
Subjects diagnosed with diabetes ac-
cording to the new ADA guidelines
(18,19) were excluded from the study
(subjects who are positive for any one of
these following criteria: FPG level $126
mg/dL, OGTT at 2 h $200 mg/dL, and
$6.5%. The following subjects
were also excluded from the study: sub-
jects receiving oral hypoglycemic agents,
antiplatelet drugs, angiotensin-converting
enzyme inhibitors, angiotensin II receptor
antagonists, fenobrate, atorvastatin, ro-
suvastatin, and uvastatin; subjects with
serum creatinine $2.0 mg/dL or on dial-
ysis; subjects with the liver enzyme alanine
aminotransferase (ALT) $3 folds of upper
limit of normal value range; subjects re-
ceiving other herbal medicines; subjects
with secondary causes of hyperglycemia
(receiving steroids or with pancreatic can-
cer); subjects with acute infections or
chronic inammatory diseases (cancer,
rheumatoid arthritis); and subjects with
gall bladder disease or history of cholecys-
tectomy. This study (clinical trial reg. no.
NCT01052025) was approved by the
Ethic Committee of Faculty of Medicine,
Srinakharinwirot University, Bangkok,
Thailand (serial number SWUEC 9/
2552) in accordance with the Declaration
of Helsinki. Participants were informed
and gave their consent before enrollment.
Randomization procedures
After steps of screening, consenting, and
diet and lifestyle training, all subjects
were randomly assigned to either the
curcumin-treated group (intervention
treatment condition) or placebo-treated
group (control condition) using a xed
randomization scheme with assignment
based on computer-generated random
numbers performed by an independent
researcher. The allocation scheme was
sealed in opaque and consecutively num-
bered envelopes. Envelopes were opened
sequentially by the independent person.
The participants were informed that two
types of interventions were being com-
The intervention
All participants were instructed to take
three capsules with blinded labels of
either curcumin or placebo twice a day
(total of six capsules per day) for 9
months continuously. Each curcumin
capsule has curcuminoid content of 250
mg. Curcumin and identical placebo cap-
sules were manufactured by the Govern-
ment Pharmaceutical Organization of
Thailand. Patients were asked to bring
all capsules back at the follow-up visit at
3, 6, and 9 months for assessing their
compliance. Numbers of capsules taken
by the subjects were recorded (Supple-
mentary Table 3).
Preparation of curcuminoids
Dried rhizomes of turmeric (Curcuma
longa Linn.) grown in Kanchanaburi
province, Thailand, were ground into
powder. The turmeric powder was extrac-
pressure to obtain ethanol extract in the
form of semisolid containing oleoresin
and curcuminoids. The oleoresin was re-
moved to yield curcuminoid extract (total
curcuminoids content between 75 and
85%). The peak ratio of curcumin:deme-
thoxycurcumin and bisdemethoxycurcu-
min in the extract was determined by high-
performance thin-layer chromatography.
The extract (calculated for 250 mg of cur-
cuminoids) was lled into capsules under
the Good Manufacturing Procedures
standard. Fingerprints of the extract
and a detailed analysis of the chemical
composition of the preparation in the ex-
tract are shown in Supplementary Fig. 2.
Study outcomes
The primary outcome was assessed by
numbers of the subjects in the curcumin-
treated or placebo-treated groups diag-
nosed with T2DM according to the ADA
guidelines (18,19). Secondary outcomes
were also measured as follows: changes of
the b-cell functions (homeostasis model
assessment [HOMA]-b, C-peptide, and
proinsulin/insulin ratio), insulin resis-
tance (IR) by HOMA-IR, obesity (body
weight), abdominal obesity (waist cir-
cumference [WC]), and anti-inammatory
cytokine (adiponectin). Adverse effects of
curcumin were determined by elevated
creatinine $1.2 mg/dL and aspartate ami-
notransferase (AST)/ALT $3 times the up-
per limit of normal value range, and any
symptoms of patient complaints were re-
corded (20). Other adverse effects related
to peroxisome proliferatoractivated re-
ceptor-gin curcumin action were as-
sessed, including bone mineral density
(BMD), signs of edema, and coronary
arterial disease (CAD) event.
Data collection and measurement
Measurements were made at baseline (be-
fore treatment) and at 3, 6, and 9 months
after the intervention start. We recorded
demographic data at the baseline; the
researchers administered a questionnaire
on medical history and medication, and
measured body weight, height, and vital
signs. The abdominal obesity/WC were
measured by tape horizontally, midway
between the inferior margin of the wrist
and the superior border of the iliac crest
(21). Histories of CAD and cerebrovascular
disease were tracked from the subjects
medical records. The diagnosis of CAD,
based on the presence of angina symptoms
and abnormalities in resting electrocardio-
gram, was also assessed at baseline and dur-
ing each follow-up visit (at 3, 6, and 9
months). Hypertension was determined
by history of high blood pressure ($130/
85 mmHg). Dyslipidemia was dened by
any of the following: total cholesterol
$200 mg/dL, triglycerides $150 mg/dL,
LDL cholesterol $100 mg/dL, and/or HDL
cholesterol #35 mg/dL or taking lipid-
lowering drugs. BMD, a known fracture
Preventive type 2 diabetes and curcumin extract
risk, was analyzed at the baseline and at 9
months after starting the intervention by
dual X-ray absorptiometry (QDR 4500;
Hologic) at the level of the lumbar spine
region. OGTT at 2 h was performed in all
subjects by taking 75 g oral glucose solu-
tion after overnight fasting; and then 2 h
later, blood glucose level was measured.
Blood was collected at 8:00 AM from the
antecubital vein while the subjects were in
the recumbent position after an overnight
fasting. Plasma samples for insulin, proin-
sulin, C-peptide, and adiponectin assays
were frozen and stored at 2808C until
the analysis of hormones were measured.
, total cholesterol, LDL choles-
terol, HDL cholesterol, and triglyceride
levels were measured according to the
standard procedures. Plasma insulin, pro-
insulin, C-peptide, and adiponectin con-
centrations were determined using the
radioimmunoassay kits from Millipore
(St. Charles, MO) with a gscintillation
counter, which is calibrated for
I mea-
surement. HOMA-b, C-peptide, and the
proinsulin/insulin ratio were measured
for b-cell functions (22,23). HOMA-IR
was calculated to assess change of IR
Sample size
We estimated the size of the sample for
this study based on data from the study by
Nauck et al. (25). Calculations used an SD
of 46.3. We needed to enroll at least 117
subjects in each treatment group to detect a
difference of 17 in HOMA-bwith 80%
power at the 5% level of signicance (26).
Statistical analysis
Demographic data at baseline were ana-
lyzed and presented as mean 6SEM for
continuous variables and number with
percent for categorical variables. Two-tailed
Student ttest and x
test were, respectively,
used for continuous and categorical varia-
bles in comparisons between the two
groups, using P,0.05 for statistically sig-
nicant difference. We used two-sided sig-
nicance tests throughout. For analysis of
outcome variables, values of mean 6SEM
at 3, 6, and 9 months were presented for
both groups. The analyses were performed
on an intention-to-treat basis. Two-tailed
Student ttest was used to assess the statis-
tical signicant differences between means
of the two groups at 3, 6, and 9 months,
separately. Statistical analysis was per-
formed using the Statistical Package for So-
cial Sciences 11.5 software (SPSS Inc.,
Chicago, IL).
RESULTSdAow chart of the trial is
presented (Supplementary Fig. 1). A total
of 240 subjects were initially enrolled in
the study. The baseline characteristics of
237 subjects who were randomly allo-
cated into the two groups are presented
in Table 1. All parameters at the baseline
between placebo-treated group and cur-
cumin-treated group were not statistically
Intervention outcomes
The means of diabetes-related blood
chemistries used to assess the diabetic
progression, such as HbA
OGTT at 2 h were signicantly lower in
the curcumin-treated group when com-
pared with the placebo group (P,0.01)
in all visits at 3, 6, and 9 months (Table 2).
Differences from baselines for these three
variables comparing the two groups are il-
lustrated in the Fig. 1AC.
b-Cell function outcomes
HOMA-b, C-peptide, and proinsulin/in-
sulin ratio were examined as outcomes
related to b-cell functions (Table 2 and
Fig. 1). Figure 1Dshows that HOMA-b
in the curcumin-treated group was increas-
ingly elevated in all follow-up visits (at 3, 6,
and 9 months) and became statistically sig-
nicant at the nal visit (9 months). Blood
levels of C-peptide (Fig. 1E) were found to
be signicantly lower in curcumin-treated
group when compared with those of pla-
cebo group. Although not signicant, pro-
insulin/insulin ratio showed a lower trend
in the curcumin-treated group (Table 2).
Insulin resistance and inammatory
cytokine outcomes
HOMA-IR level is a clinical representative
of insulin resistance (22). HOMA-IR from
both placebo and curcumin-treated
groups was examined. The means of
HOMA-IR of the curcumin-treated group
were lower than those of placebo group at
all follow-up visits (3, 6, and 9 months)
(Fig. 1F). The differences were signicant,
particularly at the 6- and 9-month visits.
Levels of adiponectin, an anti-inamma-
tory cytokine, in the placebo-treated
group were virtually unchanged, whereas
those of the curcumin-treated group were
gradually elevated (at 3 and 6 months)
and became signicantly different from
that of placebo-treated group at the nal
visit (9 months) (Table 2).
Diabetes prevention
At 6, 9, and 12 months after the subjects
were rst identied with prediabetes con-
ditions (at 3-, 6-, and 9-month visits), a
number of subjects in the placebo-treated
Table 1dBaseline characteristics of subjects
Placebo mean
Curcumin mean
(SEM) Pvalue*
Sex (%) (male:female) 35.6:64.4% 35.1:64.9% 0.94
Age (years) 57.93 (1.18) 56.95 (1.10) 0.57
BMI (kg/m
) 26.62 (0.51) 26.66 (0.48) 0.96
Body weight (kg) 67.8 (1.5) 67.7 (1.3) 0.92
WC (cm) 88.9 (1.2) 89.0 (1.0) 0.94
FPG (mg/dL) 103.24 (0.98) 103.65 (0.99) 0.26
OGTT at 2 h (mg/dL) 140.91 (3.24) 143.48 (3.6) 0.36
(%) 5.83 (0.03) 5.86 (0.04) 0.37
Insulin (pmol/L) 109.71 (6.1) 110.25 (6.29) 0.95
Proinsulin (pmol/L) 16.8 (1.42) 15.31 (1.3) 0.44
Proinsulin per insulin 0.18 (0.02) 0.17 (0.01) 0.52
HOMA-IR 3.85 (0.21) 4.03 (0.23) 0.57
HOMA-b(%) 51.08 (3.23) 49.11 (3.12) 0.66
Adiponectin (ng/mL) 18.68 (1.25) 18.18 (1.20) 0.29
C-peptide (ng/mL) 2.14 (0.17) 2.1 (0.13) 0.88
Creatinine (mg/dL) 1.15 (0.06) 1.07 (0.04) 0.27
AST (U/L) 27.21 (1.53) 26.50 (1.65) 0.75
ALT (U/L) 43.42 (1.85) 44.04 (1.94) 0.82
History of cerebrovascular disease 5 (4.3%) 3 (2.5%) 0.46
History of coronary arterial disease 8 (6.8%) 9 (7.0%) 0.96
History of hypertension 78 (67.2%) 83 (70.3%) 0.61
History of dyslipidemia 105 (90.5%) 107 (90.7%) 0.97
*Data were evaluated by independent sample ttest, except sex (%). x
Chuengsamarn and Associates
group developed T2DM: 11 subjects (9.5%)
at 6 months, 18 (15.5%) at 9 months, and
19 (16.4%) at 12 months (Table 3 and Sup-
plementary Table 1). However, none of the
subjects in the curcumin-treated group de-
veloped T2DM (Table 3).
Adverse effects
To monitor possible adverse effects of
curcumin intervention, we determined
kidney and liver functions, BMD, body
weights, and WCs (Supplementary Table
2 and Table 2). We found no signicant
differences in the means of AST, ALT, cre-
atinine, and BMD between the curcumin-
treated and placebo-treated group. In
addition, during the course of our study,
none of the subjects newly developed
shown). A few subjects from the curcu-
min-treated group reported minor symp-
toms such as itching (one subject),
constipation (two subjects), and vertigo
(one subjects). None in the curcumin-
treated group showed hypoglycemia
symptoms. Interestingly, at the last fol-
low-up visit (9 months after interven-
tion), we noticed a slight reduction of
mean body weight and WC from the
group of subjects treated with curcumin.
We did not see such reductions in the
placebo-treated group (Table 2).
Altogether, these results indicated
that curcumin extract can be used for
intervention, at least during a period of 9
months, without serious adverse effect.
At each follow-up visit, we counted
numbers of remaining capsules brought
to us by subjects. Numbers of the capsule
consumed by subjects from both groups
were very comparable (Supplementary
Table 3). Therefore, the effects observed
by us were not a result of different levels of
compliance between two groups.
CONCLUSIONSdIn an attempt to
nd safe, well-tolerated, and easily avail-
able intervention agents for the predia-
betic population, we tested a potential
candidate, ethanol-extracted curcumin,
Table 2dLevels of blood chemistries indicating b-cell functions and obesity parameters
Outcomes Follow-up period
Placebo Curcumin
PvalueMean Minimum maximum Mean Minimum maximum
Body weight (kg) 3 months 67.8 34130 67.7 42118 NS
6 months 68.9 36136 66.0 38114 NS
9 months 70.1 38144 63.8 34110 ,0.05
WC (cm) 3 months 88.9 59134 88.0 68121 NS
6 months 89.8 62130 86.6 64118 NS
9 months 91.6 65144 84.4 60110 ,0.05
FPG (mg/dL) 3 months 106.88 80129 96.11 80122 ,0.01
6 months 108.03 80138 90.76 73122 ,0.01
9 months 108.21 80138 86.47 73122 ,0.01
OGTT at 2 h (mg/dL) 3 months 150.87 90250 135.44 75190 ,0.01
6 months 155.06 90290 127.23 75180 ,0.01
9 months 155.09 90290 123.35 75178 ,0.01
(%) 3 months 5.92 5.27.1 5.77 4.96.3 ,0.01
6 months 5.99 5.27.4 5.68 4.96.2 ,0.01
9 months 6.02 5.27.5 5.60 4.96.8 ,0.01
Proinsulin 3 months 17.77 0.5121 14.58 198.2 NS
6 months 16.83 0.585.6 14.06 0.998 NS
9 months 16.80 0.585.6 13.57 0.897 NS
Proinsulin per insulin 3 months 0.19 01.6 0.16 00.9 NS
6months 0.20 01.2 0.15 00.9 NS
9months 0.21 01.2 0.14 00.9 NS
Insulin (pmol/L) 3 months 109.52 82140 109.49 80136 NS
6 months 109.65 83144 108.73 76132 NS
9 months 109.68 83144 107.62 72128 ,0.05
HOMA-IR 3 months 3.97 0.313.3 3.60 0.411.6 NS
6 months 4.03 0.316.2 3.39 0.411.3 ,0.05
9 months 4.08 0.316.6 3.22 0.411 ,0.001
HOMA-b(%) 6 months 49.32 0.8238.9 54.71 3.1259.7 NS
9 months 48.78 0.8238.0 58.54 3.1266.4 NS
3 months 48.72 0.8237.6 61.58 3.1268.3 ,0.01
Adiponectin (ng/mL) 3 months 18.59 31110.8 18.3 5.560.0 NS
6 months 18.52 31110.8 20.71 6.065.0 NS
9 months 18.45 31110.2 22.46 6.569.5 ,0.05
C-peptide (ng/mL) 3 months 2.15 0.513.8 1.97 0.410.0 NS
6 months 2.16 0.513.8 1.8 0.39.5 NS
9 months 2.17 0.113.8 1.7 0.39.0 ,0.05
Pvalues were calculated by an independent sample ttest (P$0.05).
Preventive type 2 diabetes and curcumin extract
antidiabetes activity (1012,15,16).
In this randomized, double-blinded,
placebo-controlled clinical trial, we found
that curcumin extract was able to sub-
stantially and signicantly prevent
T2DM development in the prediabetic
population (0% of curcumin-treated
subjects developed DM, whereas 16.4%
of placebo-treated subjects developed
DM). In addition, we found that curcu-
min intervention improved b-cell func-
tions, indicated by an increased HOMA-b
and reduced C-peptide. Meanwhile,
although not statistically signicant,
curcumin intervention tended to decrease
proinsulin/insulin ratio. These indicated
that curcumin treatment may result in better
b-cell function in the prediabetic popula-
tion. HOMA-IR clinically represents IR.
We found that in the curcumin-treated
group, HOMA-IR was signicantly lower
Figure 1dMean of parameters with SEM at baseline, 3, 6, and 9 months were compared between placebo- and curcumin-treated group. A:FPG.
*P ,0.01. B: OGTT at 2 h. *P,0. 01. C:HbA
.*P,0.01. D:HOMA-b.*P ,0.01. E: C-peptide. *P ,0.05. F: HOMA-IR. *P ,0.001, #P ,0.05. DIABETE S CARE,VOLUME 35, NOVEMB ER 2012 2125
Chuengsamarn and Associates
when compared with that of the placebo
group. From these results, we believe that
curcumin intervention in the prediabetic
population can prevent T2DM conversion
and lower the IR level by maintaining
healthy b-cell functions.
Adiponectin is an anti-inammatory
cytokine known to play a positive role in
pathogenesis of T2DM (27,28). It has
been shown that a higher adiponectin
level is associated with a lower risk of
T2DM (28). Our study showed that cur-
cumin intervention signicantly increases
adiponectin levels. Curcumin has also
been shown to reduce inammation by
downregulating other inammatory cyto-
kines, such as tumor necrosis factor-a,
leptin, and resistin (7). In an in vivo dia-
betic mouse model, curcumin treatment
signicantly reduced macrophage inltra-
tion of white adipose tissue and reversed
many of the inammatory derangements
(8). Because inammation is one of the
main causes of b-cell degradation, we hy-
pothesize that the anti-inammation activ-
ity of curcumin is a key factor for the
curcumins antidiabetic property.
Of note, we observed from our study
the conversion rate of the placebo-treated
group during a period of 12 months (from
rst screening to the end of study) to be
16.7%, which is signicantly higher than
that in a well-known American study (3).
We reasoned that the high conversion rate
may be specic to the ethnicity of the sub-
jects. However, because of a lack of data
on conversion rate in Thai prediabetes,
we cannot directly verify our data. We
then compared our result to a diabetes
study conducted in a large Thai cohort
by Aekplakorn et al. (29), the Electric
Generating Authority of Thailand (EGAT)
study. In this study, risk scores were devel-
oped from a Thai cohort of 2,677 individ-
uals (29). The EGAT study identied a set
of strong risk factors that accelerate the de-
velopment of T2DM among the Thai pop-
ulation; these are old age, high BMI, high
WC, hypertension, and history of diabetes
in parent or sibling. We found that these
factors also inuenced our study (see the
health parameter of the subject at the base-
line in Table 1). Our subjects are mostly
of old age, with high BMI (according to
with hypertension and a history of diabetes
in parent or sibling.
When we analyzed data based on the
instruction from the EGAT study, we
found that the prediabetic subjects from
our study were assigned with high-risk
scores (Supplementary Tables 46).
When we followed the EGAT calculation,
the estimated overall incidence rate (nor-
malized to a period of 12 months) from
our study would be 21.8% (within 12
months, an estimation of 21.8% of the
prediabetic subjects would develop
T2DM). We observed 16.4%, which is
well within the estimation (not higher
than expected).
Therefore, we believe that the high
conversion rates found in the present
study are a common characteristic of
Thai prediabetes.
Several studies have shown that tra-
ditional Chinese herbs and dietary sup-
plements may have potential antidiabetic
activity (6,3032). Although promising,
most of these studies could not be easily
interpreted, quite often because of inade-
quate study designs, such as lack of ran-
domized control trials (3032), small
sample size (3032), or lack of safety
information (3032). Our study was de-
signed and set up specically to overcome
those previous problems. Our study
showed that the curcumin extract can ef-
fectively prevent the prediabetic popula-
tion from developing T2DM. Although
we found that the results were quite
remarkable, a longer trial may be required
to see if the curcumin-treated prediabetic
population will eventually develop
We found that a 9-month treatment
of curcumin was rather safe. We have not
found any signicant adverse effect
caused by curcumin treatment when
compared to the placebo treatment.
WC, all of the subjects treated with
curcumin appeared to be healthy. Be-
cause of its benets and safety, we
propose that curcumin extract may be
used for an intervention therapy for the
prediabetic population.
AcknowledgmentsdThis study was sup-
ported by a grant from Thai Traditional Medical
Knowledge Fund and the Department for De-
velopment of Thai Traditional and Alternative
Medicine, Ministry of Public Health (to S.C.).
No potential conicts of interest relevant to
this article were reported.
S.C. designed the study, screened and ex-
amined all the recruited subjects, researched
and analyzed data, and wrote and reviewed the
manuscript. S.R. analyzed data and performed
the statistical analysis. R.L. and C.P. provided
trial advice. S.J. designed the study and wrote
and reviewed the manuscript. S.R. is the
guarantor of this work and, as such, had full
access to all the data in the study and takes
responsibility for the integrity of the data and
the accuracy of the data analysis.
The authors thank the Thai Government
Pharmaceutical Organization for the gift of the
curcumin extract and placebo. The authors
also thank all of the subjects for participating
in this study and the team of the outpatient
clinic at HRH Princess Maha Chakri Sirind-
horn Medical Center of Srinakharinwirot
University, Nakornnayok, Thailand.
1. Wild S, Roglic G, Green A, Sicree R, King
H. Global prevalence of diabetes: esti-
mates for the year 2000 and projections
for 2030. Diabetes Care 2004;27:1047
2. Hogan P, Dall T, Nikolov P; American
Diabetes Association. Economic costs of
diabetes in the US in 2002. Diabetes Care
3. Knowler WC, Barrett-Connor E, Fowler
SE, et al.; Diabetes Prevention Program
Research Group. Reduction in the in-
cidence of type 2 diabetes with lifestyle
intervention or metformin. N Engl J Med
4. Rydén L, Standl E, Bartnik M, et al.; Task
Force on Diabetes and Cardiovascular
Diseases of the European Society of Car-
diology (ESC); European Association for
the Study of Diabetes (EASD). Guidelines
on diabetes, pre-diabetes, and cardiovas-
cular diseases: executive summary. Eur
Heart J 2007;28:88136
5. Hanley AJ, Zinman B, Sheridan P, Yusuf S,
Gerstein HC; Diabetes Reduction Assess-
ment With Ramipril and Rosiglitazone
Table 3dNumber and percent of diabetic newly diagnosed subjects during
following period
Months after enrollment
Number (%) in
placebo group
Number (%) in
curcumin group
(N=119) Pvalue
6 months (3-month visit) 11 (9.5) 0 (0) 0.001
9 months (6-month visit) 18 (15.5) 0 (0) ,0.001
12 months (9-month visit) 19 (16.4) 0 (0) ,0.001
Preventive type 2 diabetes and curcumin extract
Medication (DREAM) Investigators. Effect
of Rosiglitazone and Ramipril on beta-cell
function in people with impaired glucose
tolerance or impaired fasting glucose: the
DREAM trial. Diabetes Care 2010;33:
6. Kochhar KP. Dietary spices in health and
diseases (II). Indian J Physiol Pharmacol
7. Aggarwal BB. Targeting inammation-
induced obesity and metabolic diseases by
curcumin and other nutraceuticals. Annu
Rev Nutr 2010;30:173199
8. Weisberg SP, Leibel R, Tortoriello DV.
Dietary curcumin signicantly improves
obesity-associated inammation and di-
abetes in mouse models of diabesity. En-
docrinology 2008;149:35493558
9. Shao W, Yu Z, Chiang Y, et al. Curcumin
prevents high fat diet induced insulin re-
sistance and obesity via attenuating lipo-
genesis in liver and inammatory pathway
in adipocytes. PLoS ONE 2012;7:e28784
10. Kuroda M, Mimaki Y, Nishiyama T, et al.
Hypoglycemic effects of turmeric (Cur-
cuma longa L. rhizomes) on genetically
diabetic KK-Ay mice. Biol Pharm Bull
11. Nishiyama T, Mae T, Kishida H, et al.
Curcuminoids and sesquiterpenoids in
turmeric (Curcuma longa L.) suppress an
increase in blood glucose level in type 2
diabetic KK-Ay mice. J Agric Food Chem
12. Jain SK, Rains J, Croad J, Larson B, Jones
K. Curcumin supplementation lowers
TNF-alpha, IL-6, IL-8, and MCP-1 secre-
tion in high glucose-treated cultured
monocytes and blood levels of TNF-
alpha, IL-6, MCP-1, glucose, and glyco-
sylated hemoglobin in diabetic rats.
Antioxid Redox Signal 2009;11:241249
13. Jacob A, Wu R, Zhou M, Wang P. Mech-
anism of the Anti-inammatory Effect of
Curcumin: PPAR-gamma Activation.
PPAR Res 2007;2007:89369
14. Kanitkar M, Gokhale K, Galande S,
Bhonde RR. Novel role of curcumin in
the prevention of cytokine-induced islet
death in vitro and diabetogenesis in vivo.
Br J Pharmacol 2008;155:702713
15. Seo KI, Choi MS, Jung UJ, et al. Effect of
curcumin supplementation on blood
glucose, plasma insulin, and glucose ho-
meostasis related enzyme activities in di-
abetic db/db mice. Mol Nutr Food Res
16. Jang EM, Choi MS, Jung UJ, et al. Benecial
effects of curcumin on hyperlipidemia and
insulin resistance in high-fat-fed hamsters.
Metabolism 2008;57:15761583
17. American Diabetes Association. Executive
summary: Standards of medical care in
diabetesd2012. Diabetes Care 2012;35
(Suppl. 1):S4S10
18. Report of the Expert Committee on the
Diagnosis and Classication of Diabetes
Mellitus. Report of the Expert Committee
on the Diagnosis and Classication of
Diabetes Mellitus. Diabetes Care 1997;20:
19. International Expert Committee. Interna-
tional Expert Committee report on the role
of the A1C assay in the diagnosis of di-
abetes. Diabetes Care 2009;32:13271334
20. Chainani-Wu N. Safety and anti-in-
ammatory activity of curcumin: a com-
ponent of tumeric (Curcuma longa).
J Altern Complement Med2003;9:161168
21. Alberti KG, Zimmet P, Shaw J; IDF Epi-
demiology Task Force Consensus Group.
The metabolic syndromeda new world-
wide denition. Lancet 2005;366:1059
22. Matthews DR, Hosker JP, Rudenski AS,
Naylor BA, Treacher DF, Turner RC. Ho-
meostasis model assessment: insulin re-
sistance and beta-cell function from
fasting plasma glucose and insulin con-
centrations in man. Dia betologia 1985;28:
23. Tura A, Pacini G, Kautzky-Willer A,
Ludvik B, Prager R, Thomaseth K. Basal
and dynamic proinsulin-insulin relation-
ship to assess beta-cell function during
OGTT in metabolic disorders. Am J
Physiol Endocrinol Metab 2003;285:
24. Katz A, Nambi SS, Mather K, et al.
Quantitative insulin sensitivity check in-
dex: a simple, accurate method for as-
sessing insulin sensitivity in humans.
J Clin Endocrinol Metab 2000;85:2402
25. Nauck MA, Meininger G, Sheng D,
Terranella L, Stein PP; Sitagliptin Study
024 Group. Efcacy and safety of the di-
peptidyl peptidase-4 inhibitor, sitagliptin,
compared with the sulfonylurea, glipi-
zide, in patients with type 2 diabetes in-
adequately controlled on metformin
alone: a randomized, double-blind, non-
inferiority trial. Diabetes Obes Metab
26. Dupont WD, Plummer WD Jr. Power and
sample size calculations for studies involving
linear regression. Control Clin Trials 1998;
27. Yokoyama H, Emoto M, Mori K, et al.
Plasma adiponectin level is associated
with insulin-stimulated nonoxidative
glucose disposal. J Clin Endocrinol Metab
28. Li S, Shin HJ, Ding EL, van Dam RM.
Adiponectin levels and risk of type 2 di-
abetes: a systematic review and meta-
analysis. JAMA 2009;302:179188
29. Aekplakorn W, Bunnag P, Woodward M,
et al. A risk score for predicting incident
diabetes in the Thai population. Diabetes
Care 2006;29:18721877
30. Hsu CH, Cheng AL. Clinical studies with
curcumin. Adv Exp Med Biol 2007;595:
31. Collins M, McFarlane JR. An exploratory
study into the effectiveness of a combi-
nation of traditional Chinese herbs in the
management of type 2 diabetes. Diabetes
Care 2006;29:945946
32. Yeh GY, Eisenberg DM, Kaptchuk TJ,
Phillips RS. Systematic review of herbs
and dietary supplements for glycemic
control in diabetes. Diabetes Care 2003;
26:12771294 DIABETE S CARE,VOLUME 35, NOVEMB ER 2012 2127
Chuengsamarn and Associates
... Many clinical trials using curcumin showed a significantly reduced T2DM incidence among people with prediabetes. In addition, curcumin treatment in a diabetic mouse model improved β-cell function with higher homeostasis model assessment of β-cell function (HOMA-β) and lower homeostasis model assessment of insulin resistance (HOMA-IR) compared to the placebo group [93]. It has been reported that diabetes-induced pathological changes in the aorta are protected by curcumin, mainly through inhibition of JNK2, accompanied by upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) expression and function [94]. ...
Cellular senescence is accelerated by hyperglycemia through multiple pathways. Therefore, senescence is an important cellular mechanism to consider in the pathophysiology of type 2 diabetes mellitus (T2DM) and an additional therapeutic target. The use of drugs that remove senescent cells has led to improvements in blood glucose levels and diabetic complications in animal studies. Although the removal of senescent cells is a promising approach for the treatment of T2DM, two main challenges limit its clinical application: the molecular basis of cellular senescence in each organ is yet to be understood, and the specific effect of removing senescent cells in each organ has to be determined. This review aims to discuss future applications of targeting senescence as a therapeutic option in T2DM and elucidate the characteristics of cellular senescence and senescence-associated secretory phenotype in the tissues important for regulating glucose levels: pancreas, liver, adipocytes, and skeletal muscle.
... This therapeutic effect was observed in its significant effect on pain, joint swelling, reducing inflammatory markers, and improving disease activity score [150][151][152] . In patients confirmed to be suffering from type II diabetes mellitus, curcumin treatment improved endothelial function observed through a regulation of malondialdehyde (MDA), ET-1, IL-6 and TNF-levels and ameliorating macroscopic proteinuria [155][156] . An oral or systemic application of Curcuma longa has been observed to improve several eye disorders, such as conjunctivitis, conjunctival xerosis and the degenerative conditions associated with cataracts [ 157 , 158 ]. ...
Full-text available
Introduction: Curcuma longa, popularly known as Turmeric, is a rhizomatous herbaceous perennial plant used in folk medicine for the treatment, prevention, and management of various illnesses such as cancer, diabetes, Arthritis, diarrhoea, inflammation, psoriasis, hepatobiliary diseases, gastric and peptic ulcers. Results: This study reviewed the ethnomedicinal potentials, phytochemicals, and pharmacological activities of C. longa. In vitro and in vivo studies reported that C. longa and its major bioactive constituent (curcumin) possess various pharmacological properties. These include; anticancer, antidiabetic, anti-osteoarthritis, antidiarrheal, cardioprotective, anti-oxidative, neuroprotective, hepatoprotective, anti-microbial, renoprotective and anti-inflammatory activities. This review demonstrated that the various pharmacological activities of C. longa might be attributed to the presence of numerous bioactive compounds. However, these varying potentials have not been effectively analysed for optimal application in developing new therapies. Also, the applicability and mode of action of the different bioactive compounds found in C. longa have not been fully exploited. Conclusion: This study showed that C. longa could be exploited by pharmaceutical industries to develop pharmaceutical products. However, there is a need for human clinical trials and quality control studies to establish effective and safe doses of C. longa and its major bioactive constituent-curcumin suitable for treating several diseases.
... As previously mentioned, the selection criteria for herbs are also dependent on the comorbidities in the patients and numerous other factors. Some instances include the usage of curcumin in pre-diabetic therapy to prevent T2DM (Chuengsamarn et al. 2012). Similarly, cinnamon is used among patients with hypertension and diabetes (Howard and White 2013). ...
Diabetes is a metabolic disorder owing to the insulin faulty production or the resistance to the action mechanism where the accumulation of glucose is the major side effect in the body in the case of diabetes. Numerous herbs with the potential of reducing glucose production along with combating the secondary ailments associated with it but >1% out of 250,000 have been pharmacologically validated. Affordability and historical usage of these herbal remedies often result in patients' preference as primary or as adjunctive to conventional therapies. Clinical trials conducted with herbs are necessary for determining the efficacy of the herbs against diabetes. Additional benefits of herbal employment include the treatment of secondary ailments in patients along with diabetes including triglyceride reduction, cholesterol level management, body mass index, and cardiovascular disease control.
Background: Curcumin supplementation may promote weight loss and ameliorate obesity-related complications through its anti-oxidative and anti-inflammatory properties. Objective: An umbrella review and updated meta-analysis of randomized controlled trials (RCTs) was conducted to evaluate the effect of curcumin supplementation on anthropometric indices. Methods: Systematic reviews and meta-analyses (SRMAs) of RCTs were identified from electronic databases (Medline, Scopus, Cochrane and Google Scholar) up to 31st March 2022 without language restriction. SRMAs were included if they assessed curcumin supplementation on any of body mass index (BMI), body weight (BW), or waist circumference (WC). Subgroup analyses were performed, stratifying by patient types, severity of obesity and curcumin formula. The study protocol was a priori registered (PROSPERO; CRD42022321112) RESULTS: From an umbrella review, fourteen SRMAs with 39 individual RCTs were included with a high degree of overlap. Additionally, searching was updated from the last search of included SRMAs in April, 2021 up to 31st March 2022, and we found 11 additional RCTs, bringing the total up to 50 RCTs included in the updated MA. Of these, 21 RCTs were classified as high risk of bias. Curcumin supplementation significantly reduced BMI, BW, and WC with mean differences (MD) of -0.24 kg/m2 (95% CI: -0.32, -0.16), -0.59 kg (95% CI: -0.81, -0.36) and -1.32 cm (95% CI: -1.95, -0.69), respectively. The bioavailability-enhanced form reduced BMI, BW and WC more with MD of -0.26 kg/m2 (95% CI: -0.38, -0.13), -0.80 kg (95% CI: -1.38, -0.23) and -1.41cm (95% CI: -2.24, -0.58), respectively. Significant effects were also seen in subgroups of patients, especially in adults with obesity and diabetes. Conclusions: Curcumin supplementation significantly reduces anthropometric indices and bioavailability-enhanced formulas are preferred. Augmenting curcumin supplement with lifestyle modification should be an option for weight reduction.
In the present study, we explored the effect of curcumin/turmeric supplementation on anthropometric indices of obesity, leptin, and adiponectin. We searched PubMed, Scopus, Web of Science, Cochrane Library, and Google Scholar up to August 2022. Randomized clinical trials (RCTs) investigating the impact of curcumin/turmeric on obesity indices and adipokines were included. We applied the Cochrane quality assessment tool to evaluate the risk of bias. The registration number is CRD42022350946. Sixty eligible RCTs, with a total sample size of 3691 individuals were included for quantitative analysis. We found that supplementation with curcumin/turmeric significantly reduced body weight (WMD: −0.82 kg, 95% CI: −1.30, −0.35; p = 0.001), body mass index (WMD: −0.30 kg/m2, 95% CI: −0.53, −0.06, p = 0.013), waist circumference (WMD: −1.31 cm, 95% CI: −1.94, −0.69, p < 0.001), body fat percentage (WMD: −0.88%, 95% CI: −1.51, −0.25, p = 0.007), leptin (WMD = −4.46 ng/mL; 95% CI: −6.70, −2.21, p < 0.001), and increased adiponectin (WMD = 2.48 μg/mL; 95% CI: 1.34, 3.62, p < 0.001). Overall, our study shows that supplementation with curcumin/turmeric significantly improves anthropometric indices of obesity and adiposity‐related adipokines (leptin and adiponectin). However, due to high between‐studies heterogeneity, we should interpret the results with caution.
Full-text available
Medicinal properties of turmeric (Curcuma longa L.), a plant used for centuries as an anti-inflammatory, are attributed to its polyphenolic curcuminoids, where curcumin predominates. Although “curcumin” supplements are a top-selling botanical with promising pre-clinical effects, questions remain regarding biological activity in humans. To address this, a scoping review was conducted to assess human clinical trials reporting oral curcumin effects on disease outcomes. Eight databases were searched using established guidelines, yielding 389 citations (from 9528 initial) that met inclusion criteria. Half focused on obesity-associated metabolic disorders (29%) or musculoskeletal disorders (17%), where inflammation is a key driver, and beneficial effects on clinical outcomes and/or biomarkers were reported for most citations (75%) in studies that were primarily double-blind, randomized, and placebo-controlled trials (77%, D-RCT). Citations for the next most studied disease categories (neurocognitive [11%] or gastrointestinal disorders [10%], or cancer [9%]), were far fewer in number and yielded mixed results depending on study quality and condition studied. Although additional research is needed, including systematic evaluation of diverse curcumin formulations and doses in larger D-RCT studies, the preponderance of current evidence for several highly studied diseases (e.g., metabolic syndrome, osteoarthritis), which are also clinically common, are suggestive of clinical benefits.
Full-text available
Bioactive compounds (BCs) are known to exhibit antioxidant, anti-inflammatory, and anti-cancer properties by regulating the cellular redox balance and histone acetylation state. BCs can control chronic oxidative states caused by dietary stress, i.e., alcohol, high-fat, or high-glycemic diet, and adjust the redox balance to recover physiological conditions. Unique functions of BCs to scavenge reactive oxygen species (ROS) can resolve the redox imbalance due to the excessive generation of ROS. The ability of BCs to regulate the histone acetylation state contributes to the activation of transcription factors involved in immunity and metabolism against dietary stress. The protective properties of BCs are mainly ascribed to the roles of sirtuin 1 (SIRT1) and nuclear factor erythroid 2–related factor 2 (NRF2). As a histone deacetylase (HDAC), SIRT1 modulates the cellular redox balance and histone acetylation state by mediating ROS generation, regulating nicotinamide adenine dinucleotide (NAD+)/NADH ratio, and activating NRF2 in metabolic progression. In this study, the unique functions of BCs against diet-induced inflammation, oxidative stress, and metabolic dysfunction have been considered by focusing on the cellular redox balance and histone acetylation state. This work may provide evidence for the development of effective therapeutic agents from BCs.
Full-text available
Metabolic diseases have become a serious threat to human health worldwide. It is crucial to look for effective drugs from natural products to treat metabolic diseases. Curcumin, a natural polyphenolic compound, is mainly obtained from the rhizomes of the genus Curcuma. In recent years, clinical trials using curcumin for the treatment of metabolic diseases have been increasing. In this review, we provide a timely and comprehensive summary of the clinical progress of curcumin in the treatment of three metabolic diseases, namely type 2 diabetes mellitus (T2DM), obesity and non-alcoholic fatty liver disease (NAFLD). The therapeutic effects and underlying mechanisms of curcumin on these three diseases are presented categorically. Accumulating clinical evidence demonstrates that curcumin has good therapeutic potential and a low number of side effects for the three metabolic diseases. It can lower blood glucose and lipid levels, improve insulin resistance and reduce inflammation and oxidative stress. Overall, curcumin may be an effective drug for the treatment of T2DM, obesity and NAFLD. However, more high-quality clinical trials are still required in the future to verify its efficacy and determine its molecular mechanisms and targets.
Full-text available
An International Expert Committee with members appointed by the American Diabetes Association, the European Association for the Study of Diabetes, and the International Diabetes Federation was convened in 2008 to consider the current and future means of diagnosing diabetes in non pregnant individuals. The report of the International Expert Committee represents the consensus view of its members and not necessarily the view of the organizations that appointed them. The International Expert Committee hopes that its report will serve as a stimulus to the international community and professional organizations to consider the use of the A1C assay for the diagnosis of diabetes.
Full-text available
Mechanisms underlying the attenuation of body weight gain and insulin resistance in response to high fat diet (HFD) by the curry compound curcumin need to be further explored. Although the attenuation of the inflammatory pathway is an accepted mechanism, a recent study suggested that curcumin stimulates Wnt signaling pathway and hence suppresses adipogenic differentiation. This is in contrast with the known repressive effect of curcumin on Wnt signaling in other cell lineages. We conducted the examination on low fat diet, or HFD fed C57BL/6J mice with or without curcumin intervention for 28 weeks. Curcumin significantly attenuated the effect of HFD on glucose disposal, body weight/fat gain, as well as the development of insulin resistance. No stimulatory effect on Wnt activation was observed in the mature fat tissue. In addition, curcumin did not stimulate Wnt signaling in vitro in primary rat adipocytes. Furthermore, curcumin inhibited lipogenic gene expression in the liver and blocked the effects of HFD on macrophage infiltration and the inflammatory pathway in the adipose tissue. We conclude that the beneficial effect of curcumin during HFD consumption is mediated by attenuating lipogenic gene expression in the liver and the inflammatory response in the adipose tissue, in the absence of stimulation of Wnt signaling in mature adipocytes.