Association of the leptin-to-adiponectin ratio with metabolic syndrome in a sub-Saharan African population
Ayina et al. Diabetol Metab Syndr
Association of the leptin-to-adiponectin ratio with metabolic syndrome in a sub-Saharan African population
Clarisse Noël A. Ayina 3
Francky Teddy A. Endomba 0 2
Samuel Honoré Mandengue 3
Jean Jacques N. Noubiap 1
Laurent Serge Etoundi Ngoa 7
Philippe Boudou 6
Jean‑François Gautier 4 5
Jean Claude Mbanya 0 2 8 9
Eugene Sobngwi 0 2 8 9
0 Department of Internal Medicine and Specialties, Faculty of Medicine and Biomedical Science, University of Yaoundé I , Yaoundé , Cameroon
1 Department of Medicine, Groote Schuur Hospital, University of Cape Town , Cape Town , South Africa
2 Department of Internal Medicine and Specialties, Faculty of Medicine and Biomedical Science, University of Yaoundé I , Yaoundé, Cam‐ eroon
3 Department of Animal Science, Faculty of Science, University of Douala , Douala , Cameroon
4 INSERM UMRS 1138, Cordeliers Research Centre, University Pierre et Marie Curie‐Paris 6 , Paris , France
5 Department of Diabetes and Endocrinology, Lariboisiere Hospital, Public Assistance - Paris Hospitals, University Paris‐Diderot Paris‐7 , Paris , France
6 Department of Hormonal Biology, Saint‐Louis Hospital, Public Assistance ‐Paris Hospitals, University Paris‐Diderot Paris‐7 , Paris , France
7 Department of Animal Science, Higher Teacher's Training College, University of Yaoundé I , Yaounde , Cameroon
8 National Obesity Center, Yaoundé Central Hospital , Yaoundé , Cameroon
9 Laboratory for Molecular Medicine and Metabolism, Biotechnology Center, University of Yaoundé I , Yaoundé , Cameroon
Background: Worldwide there is an increased prevalence of metabolic syndrome mainly due to life‑ style modifications, and Africans are not saved of this situation. Many markers have been studied to predict the risk of this syndrome but the most used are leptin and adiponectin. Data on these metabolic markers are scare in Africa and this study aimed to assess the association between the leptin‑ to‑ adiponectin ratio (LAR) with metabolic syndrome in a Cameroonian population. Methods: This was a cross‑ sectional study that included 476 adults among a general population of Cameroon. Data collected concerned the body mass index, waist circumference, systolic blood pressure, diastolic blood pressure, fasting blood glucose, plasma lipids, adiponectin, leptin, insulin and homeostasis model for assessment of insulin resistance (HOMA‑ IR). To assess correlations we used Spearman's analyses and association of the studied variables with metabolic syndrome were done using binary logistic regression analysis. Results: The leptin to adiponectin ratio was significantly and positively correlated with the body mass index (r = 0.669, p < 0.0001), waist circumference (r = 0.595, p < 0.0001), triglycerides (r = 0.190, p = 0.001), insulin levels (r = 0.333, p < 0.0001) and HOMA‑ IR (r = 0.306, p < 0.0001). Binary logistic regression analysis revealed that leptin, adiponectin and LAR were significantly associated with metabolic syndrome with respective unadjusted OR of 1.429, 0.468 and 1.502. After adjustment, for age and sex, the associations remained significative; LAR was also found to be significantly associated with metabolic syndrome (OR = 1.573, p value =0.000) as well as lower levels of adiponectin (OR = 0.359, p value =0.000) and higher levels of leptin (OR = 1.469, p value =0.001). Conclusion: This study revealed that LAR is significantly associated with metabolic syndrome in sub‑ Saharan African population, independently to age and sex.
Adiponectin; Leptin; Leptin‑ to‑ adiponectin ratio; Metabolic syndrome
There is a surge in the global prevalence of metabolic
syndrome and its components including obesity, insulin
resistance, diabetes mellitus, dyslipidemia and
hypertension, as a result of reduced physical activity and
unhealthy diet [
].The burden of metabolic syndrome
has been rising over the past decade in African
populations, driven by urbanization, sedentarity and nutritional
]. To assess people at risk for the
development of metabolic syndrome, several markers have
been studied, with the large majority of them related to
the adipose tissue [
]. Two markers are of particular
interest, adiponectin and leptin, which are strongly
associated to cardiometabolic health or disease [
1, 3, 7, 8
For instance, in obese patients who are at risk of insulin
resistance and thus metabolic syndrome, secretion of
adiponectin by hypertrophic adipocytes is reduced, while
that of leptin is increased [
]. Indeed, leptin and
adiponectin levels have been found to be respectively
positively and negatively correlated with obesity, diabetes
mellitus, hypertension and metabolic syndrome [
Leptin and adiponectin also have opposite’s effects on
inflammatory markers and thus subclinical inflammation
]. Leptin is considered as a proinflammatory cytokine
since it up regulates pro-inflammatory cytokines such
as TNF-α and IL-6 [
]. On the contrary, adiponectin
displays anti-inflammatory properties by down
regulation of the expression and release of proinflammatory
Recent studies have demonstrated in the potential of
the leptin-to-adiponectin ratio (LAR) as a novel
predictor of cardio-metabolic outcomes including metabolic
]. LAR has been shown to be
associated with insulin resistance, metabolic syndrome,
carotid intima-media thickness, “at-risk phenotype” in
young severely obese patients, and chronic kidney
disease, among others [
]. Some others studies found
this marker to be a better tool for the diagnosis of
metabolic syndrome and risk stratification of subjects, than
adiponectin or leptin alone [
15, 16, 21
]. In a recent study
we demonstrated that leptin and adiponectin correlate to
surrogates of obesity, blood lipids and insulin resistance
in sub-Saharan Africans . The current study aimed
investigates the association of LAR with metabolic
syndrome in a group of Cameroonians.
This is a cross-sectional study conducted in May 2010 in
Douala and Edéa, two urban cities of the Littoral region
of Cameroon. The study population consisted of
individuals of both sex aged ≥18 years from the general
population, who accepted to participate in the study after an
invitation through radio announcements. Pregnant and
breast-feeding women, as well as subjects with serious
chronic illness, or ongoing or recent (<10 days) acute
illness, or those taking any current medication were
excluded from the study. After applying the exclusion
criteria, 476 participants were included in the study.
For each subject, weight was measured in light clothes
with a seca scale balance to the nearest 0.1 kg, height
with a calibrated stadiometer, waist circumference (WC)
at midway between the lowest rib and the iliac crest and
hip circumference at the outermost points of the greater
trochanters to the nearest 0.5 cm and waist-to-hip ratio
(WHR) as waist circumference divided by hip
circumference. Body mass index (BMI) was calculated using the
Quetelet’s formula as weight (in kg) divided by height
(in m2). We measured resting blood pressures twice
using standardized procedures with the participant in a
seated position, and after at least 10 min rest with a
validated automated blood pressure measuring device, the
Omron HEM-757 (Omron Corporation, Tokyo, Japan).
The mean of two measures performed at least 3 min
apart was used for all analyses. Percentage body fat (%BF)
was measured by bioelectric impedance analysis using
the OMRON BF 302 (OMRON Matsusaka Co., Tokyo,
Japan). After 8–12 h overnight fast, blood glucose was
measured between 7 and 10 a.m. using the Accu-Chek®
compact plus glucometer (F. Hoffmann-La Roche AG,
Basel, Switzerland) on total fresh capillary blood
samples, and venous blood samples were obtained from an
antecubital vein. Serum was then separated and stored at
−20 °C for lipid measurements and at −80 °C for further
biochemical analysis. Serum lipids were analyzed within
1 week after the collection. Serum cholesterol (TC)
(cholesterol oxidase phenol 4-amino antipyrine peroxidase
method), serum triglycerides (TG) (glycerol phosphatase
oxidase–phenol4-amino antipyrine peroxidase method),
and high-density lipoprotein-cholesterol (HDL-c)
(cholesterol oxidase phenol4-amino antipyrine peroxidase
method) were measured on a spectrophotometer (UV
mini 1240) using Chronolab kits (Chronolab Systems,
Barcelona, Spain). Low-density lipoprotein-cholesterol
(LDL-c) was calculated using the Friedwald’s formula.
Insulin levels were measured using an
electrochemiluminescence immunoassay (Roche Diagnostics, Indianapolis,
USA), while serum leptin and adiponectin were
measured by radio immuno assay (RIA) using Linco Research
kits (Linco Research Inc., St Charles, Missouri, USA) with
the following characteristics: Adiponectin assay
coefficient of variation (CV) ≤10%; detection limit of 2 ng/
mL for 100 µl sample size; a linearity range of 500 ng/mL
for 100 µL sample size. Leptin assay’s coefficient of
variation ≤10% (intra-assay’s CV ≤8.3% and inter assay’s CV
≤6.2%); a detection limit of 0.5 ng/mL for 100 µL
sample size; a linearity range of 100 ng/mL for 100 µL sample
size. Anthropometrical and biochemical measurements
was made once on each participant.
Homeostasis model assessment of insulin resistance
HOMA − IR =
Fasting insulin μ
× Fasting blood glucose
Definition of anthropomorphic indices of obesity
According to the World Health Organization guidelines,
obesity was defined as BMI ≥30 kg/m2 [
], WC >94 cm
in men and >80 cm in women, WHR ≥0.90 in men and
≥0.85 in women [
]. The BF% cutoffs chosen to define
obesity were the values most frequently cited by
international scientific literature: BF% ≥25 for men and ≥35 for
Definition of metabolic syndrome
The metabolic syndrome was defined using, the IDF/
AHA/NHLBI consensus harmonized definition
published by Alberti et al. in 2009 [
], that recommends
three or more of any of the following criteria: WC
≥80 cm (women) ≥94 cm (men), SBP ≥130 mmHg and/
or DBP ≥85 mmHg, or blood pressure lowering
treatment, fasting plasma glucose ≥5.6 mmol/L [101 mg/
dL], or anti diabetic treatment, fasting triglycerides
>1.70 mmol/L [154.5 mg/dL] or triglyceride
lowering drugs and HDL-c <1 mmol/L [40 mg/dL] (women)
<1.3 mmol/L [52 mg/dL] (men).
Data were coded, entered and analyzed using the
statistical package for social science (SPSS) version 20.0 for
Windows (IBM Corp. Released 2011. IBM SPSS statistics
for windows, version 20.0. Armonk, NY: IBM Corp.). The
distribution pattern of the variables was checked.
Normally distributed variables are expressed as mean with
standard deviation (SD). Skewed variables are reported
as median (interquartile range). Skewed variables were
log transformed. The L/A ratios are expressed as the
absolute value of plasma leptin (ng/mL) divided by the
absolute value of plasma adiponectin (μg/mL). The
independent sample t test was used to compare clinical and
biological parameters between men and women.
Spearman’s correlations were used to determine correlates of
leptin and adiponectin serum levels, as well as LAR’s.
Binary logistic regression analysis included adiponectin,
leptin and LAR as dependent variables, and were used
to identify independent factors able to predict metabolic
syndrome after adjustment for age, sex and BMI.
Statistical tests are two tailed. A p value <0.05 was considered
This study was performed in accordance with the
guidelines of the Helsinki declaration and was approved
by the national ethics committee for human health
research and by the ministry of public health of
Cameroon. Written informed consent was obtained from all
Clinical and metabolic characteristics of the study population
A total of 476 subjects (167 men and 309 women) were
enrolled in the study. The median age (interquartile) was
55.0 (23.6) for men and 50.0 (20.0) for women (p < 0.05).
WHR, SBP and DBP were significantly higher in men
(p < 0.05 respectively). Triglycerides, LDL-c, insulin,
adiponectin, leptin, and HOMA-IR were significantly higher
in women (p < 0.05 respectively) (Table 1).
Correlations between leptin‑to‑adiponectin ratio and anthropometric indexes of obesity, blood pressure, blood lipids and insulin resistance
As represented in Table 2, leptin-to-adiponectin ratio
was significantly and positively correlated with body
mass index (r = 0.669, p < 0.0001), waist
circumference (r = 0.595, p < 0.0001), triglycerides (r = 0.190,
p = 0.001), insulin levels (r = 0.333, p < 0.0001) and
HOMA-IR (r = 0.306, p < 0.0001). There was no
significant correlation within LAR and systolic or diastolic
blood pressure, glycaemia and HDL cholesterol.
Association between leptin‑to‑adiponectin ratio and metabolic syndrome
Binary logistic regression analysis (see Table 3) metabolic
syndrome was significantly associated with higher
levels of leptin (OR = 1.42, p value =0.003) as well as with
lower levels of adiponectin (OR = 0.46, p value =0.001)
and LAR (OR = 1.5, p value <0.0001). After adjustment
for age and sex, the LAR was also found to be
significantly associated with metabolic syndrome (OR = 1.573,
p value =0.000) as well as lower levels of adiponectin
(OR = 0.359, p value =0.000) and higher levels of leptin
(OR = 1.469, p value =0.001).
It’s nowadays accepted that adipokines mostly leptin
and adiponectin, play an important role in many
physiological pathways including glucose metabolism through
insulin regulation [
]. It has been demonstrated that
these molecules can be predictive of metabolic
syndrome. Indeed lower adiponectin levels have been found
to be significantly associated with metabolic syndrome
1, 3, 7, 8
]. In the other hand, metabolic syndrome is
found to be associated with higher levels of leptin. Even
though these markers are well described in literature,
some recent findings revealed the possible role of
leptinto-adiponectin ratio in the prediction of cardiometabolic
diseases including metabolic syndrome [
study was conducted to so assess the relationship of LAR
with some anthropometric indexes, blood lipids, blood
WC waist circumference, BMI body mass index, SBP systolic blood pressure, DBP diastolic blood pressure, TG triglycerides, HDL-c high density lipoprotein-cholesterol,
HOMA-IR homeostasis model assessment of insulin resistance, * Significant correlation
pressure and insulin resistance among a sub-Saharan
Our study revealed a positive correlation of LAR to
body mass index, waist circumference, triglycerides and
insulin resistance. These findings are similar to those of
Kotani et al. [
] in a study that involved 678
non-smoking Japanese subjects. The authors found that the LAR
was significantly and positively associated with
components of metabolic syndrome including BMI and
triglycerides, especially in men. Nevertheless, contrary to them,
no significant correlation was found between glucose
levels and LAR. Zyl et al. [
] found similar results in their
study on South African urban women, although LAR was
significantly higher in women with elevated blood
glucose. This finding seems to be specific to Africans. In the
literature, it has been proved that LAR is associated with
increased waist circumference and also decreased
vascular response to acetylcholine [
]. Also, the LAR has
been found to be associated with an increased
vasoconstrictive response to angiotensin II .
With and without adjustment for age and sex,
metabolic syndrome was significantly associated with LAR,
leptin and adiponectin. Thus the LAR levels were
significantly higher in metabolic syndrome subjects than in
non metabolic syndrome, as well as the levels of leptin.
Meanwhile, adiponectin levels were significantly lower
in subjects with metabolic syndrome. These results look
like those of Kotani et al. [
] who found that LAR was
significantly higher in peoples with metabolic syndrome,
even when adjusted for sex. Zhuo et al. [
] in a study
that involved 950 males and 1096 females aged between
60 and 96 years; found that LAR, as well as leptin, may
be better markers than adiponectin for the diagnosis of
metabolic syndrome. Also, the authors found that LAR
has better capacity in the classification of subjects with
and without metabolic syndrome than adiponectin or
leptin alone. Many others studies have noticed the
function of LAR as a good marker of obesity, diabetes
mellitus, insulin resistance and metabolic syndrome compared
to adiponectin or leptin alone [
6, 19, 21
]. LAR has also
been found to be related to low grade inflammation and
insulin resistance independently of obesity, with a more
powerful association with CRP and HOMA-IR than
leptin or adiponectin alone [
]. Our study has a principal
strength that this population was not receiving
potentially confounding medications during the investigation.
Nevertheless, this study has two main limitations. First,
its cross-sectional design prevented us from identifying
cause-and-effect associations LAR and MS. Secondly, we
used HOMA-IR to evaluate insulin sensitivity rather than
gold-standard methods such as the hyperinsulinemic
euglycemic clamp and the frequently sampled
intravenous glucose tolerance test which, however, would have
been significantly very difficult to perform in such a
population-based study in a resource-limited setting. Despite
these limitations, our study appears to be the first of this
type among a sub-Saharan African population, and noted
the possible role of LAR as a diagnostic marker of MS in
black Africans peoples.
In this study higher levels of LAR have been found to be
significantly associated with metabolic syndrome as well
as higher levels of leptin and lowered ones of
adiponectin. Thus, studies with appropriate design must be carried
out to really assess whether LAR can be a predictive
factor of metabolic syndrome or not, independently of
BF%: percent body fat; BMI: body mass index; CRP: C‑reactive protein; HDL ‑ c:
high‑ density lipoprotein cholesterol; HOMA‑IR: homeostasis model for assess‑
ment of insulin resistance; IL: interleukin; LAR: leptin‑to ‑adiponectin ratio;
LDL‑ c: low‑ density lipoprotein cholesterol; TC: total cholesterol; TG: triglyc‑
erides; TNF‑α: tumor necrosis factor alpha; WC: waist circumference; WHR:
waist‑to ‑hip ratio.
Study conception and design: CNAA, PB, LSEN, SHM, JFG, JCM, ES. Data col‑
lection: CNAA, PB, ES. Statistical analysis and interpretation: CNAA, JJNN, FTAE.
Drafting: JJNN, CNAA, FTAE. Critical discussion and manuscript revision: CNAA,
FTAE, SHM, JJNN,ES, PB, LSEN, JCM, JFG. All authors read and approved the
We are grateful to all the volunteers who participated in the study.
The authors declare that they have no competing interests.
Ethics approval and consent to participate
The authors attest that the present study was approved by the National Ethics
Committee for Human Health Research and by the Ministry of Public Health of
Cameroon. Written informed consent was obtained from all participants.
This study was funded by the Service of Action and Cooperation of the French
embassy in Cameroon.
Springer Nature remains neutral with regard to jurisdictional claims in pub‑
lished maps and institutional affiliations.
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