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Table of Contents
ORIGINAL ARTICLE
Year : 2016  |  Volume : 15  |  Issue : 1  |  Page : 14-19  

Relationship between serum leptin and insulin resistance among obese Nigerian women


1 Department of Chemical Pathology, University of Nigeria Teaching Hospital, Enugu, Nigeria
2 Department of Chemical Pathology, University of Calabar Teaching Hospital, Calabar, Nigeria
3 Department of Clinical Pathology, Lagos University Teaching Hospital, Idi-araba, Lagos, Nigeria

Date of Web Publication8-Feb-2016

Correspondence Address:
Ifeyinwa Osegbe
Department of Chemical Pathology, University of Nigeria Teaching Hospital, Ituku.Ozalla, Enugu
Nigeria
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Source of Support: None, Conflict of Interest: None


PMID: 26857932

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   Abstract 


Background: Leptin is a hormone produced directly from adipocytes and has been associated with type 2 diabetes mellitus (T2DM) which is characterized by insulin resistance (IR). Due to the increasing prevalence of obesity in sub-Saharan Africa, serum leptin can be explored as a predictive risk factor for T2DM. Therefore, the aim of this study was to determine the relationship between serum leptin and IR among obese women.
Methods: This was a cross-sectional study of obese, adult Nigerian females. Participants with body mass index (BMI) ≥30 kg/m2 and nondiabetic were recruited as subjects. Fasting serum leptin, insulin, and plasma glucose were determined. IR was calculated using the formula: Homeostatic model assessment-IR (HOMA-IR) = (glucose × insulin)/22.5. Statistical analyses were performed using SPSS and P < 0.05 was considered to be significant.
Results: Eighty obese females with mean ± standard deviation BMI 39.1 ± 7.2 kg/m2 and serum leptin level 48.4 ± 24.4 ng/ml participated in study. Prevalence of hyperleptinemia was 92.5% (confidence interval: 87.3–97.7%). The relationship between leptin and HOMA-IR among the subjects was: BMI 30–34.9 kg/m2: n = 27, r = 0.18, P = 0.42; BMI 35–39.9 kg/m2: n = 24, r = 0.36, P = 0.11; BMI ≥ 40 kg/m2: n = 29, r = 0.52, P = 0.004*; and after controlling for BMI (n = 29, r = 0.46, P = 0.014*). Multiple linear regression showed that leptin did not predict for IR (P = 0.837).
Conclusion: Serum leptin levels were positively correlated with IR, which was significant among the Class III (morbid) obesity class. However, leptin was not a predictive factor for IR in obese Nigerian women.

   Abstract in French 

Résumé
Contexte: la leptine est une hormone produite directement des adipocytes et a été associé avec le diabète sucré de type 2 (T2DM) qui se caractérise par une résistance à l'insuline (IR). En raison de l'augmentation de la prévalence de l'obésité dans l'Afrique subsaharienne, vous pourrez explorer la leptine sérique comme un facteur de risque pour T prédictive2DM. Par conséquent, le but de cette étude était de déterminer la relation entre les taux sériques de la leptine et IR chez les femmes obèses.
Méthodes: Il s'agissait d'une étude transversale des personnes obèses, adultes femelles nigériane. Les participants avec l'indice de masse corporelle (IMC) ≥30 kg/m2 et non diabétiques ont été recrutés en tant que sujets. La leptine, l'insuline sérique à jeun, les concentrations plasmatiques de glucose ont été déterminées. IR a été calculé en utilisant la formule: modèle d'évaluation homéostatique (HOMA-IR-IR) = (glucose × l'insuline)/22,5. Les analyses statistiques ont été effectuées à l'aide de SPSS et P < 0,05 a été considérée comme importante.
Résultats: 80 femelles obèses avec moyenne ± écart type IMC 39,1 ± 7,2 kg/m2 et le taux de leptine sérique 48,4 ± 24,4 ng/ml ont participé à l'étude. Prévalence de hyperleptinemia était de 92,5% (intervalle de confiance : 87,3-97,7%). La relation entre la leptine et HOMA-IR parmi les sujets était: IMC de 30 à 34,9 kg/m2: n = 27, r = 0,18, P = 0,42; IMC de 35 à 39,9 kg/m2: n = 24, r = 0,36, P = 0,11; IMC ≥ 40 kg/m2: n = 29, r = 0,52, P = 0,004*; et après un contrôle de l'IMC (n = 29, r = 0,46, P = 0,014*). Une régression linéaire multiple ont révélé que la leptine ne permet pas de prédire pour l'IR (P = 0,837).
Conclusion: Concentrations de leptine sérique étaient positivement corrélés avec IR, qui était significative parmi la classe III) l'obésité morbide (classe. Toutefois, la leptine n'était pas un facteur prédictif pour IR dans obèses femmes nigérianes.
Mots-clιs: Rιsistance ΰ l'insuline, leptine, l'obιsitι, le diabθte sucrι de type 2

Keywords: Insulin resistance, leptin, obesity, type 2 diabetes mellitus


How to cite this article:
Osegbe I, Okpara H, Azinge E. Relationship between serum leptin and insulin resistance among obese Nigerian women. Ann Afr Med 2016;15:14-9

How to cite this URL:
Osegbe I, Okpara H, Azinge E. Relationship between serum leptin and insulin resistance among obese Nigerian women. Ann Afr Med [serial online] 2016 [cited 2019 Dec 13];15:14-9. Available from: http://www.annalsafrmed.org/text.asp?2016/15/1/14/158524




   Introduction Top


Obesity, an increase in body fat mass, is one of the leading preventable causes of death worldwide.[1] It is well-documented in the developed world with increasing prevalence in developing countries. In Nigeria, adult obesity prevalence rates of 12.5%, 13.1%, and 22.2% have been reported.[2],[3],[4]

Obesity has been associated with insulin resistance (IR) which precedes type 2 diabetes mellitus (T2DM).[5] Although the mechanism how this occurs is not fully understood, many cellular and molecular factors interplay, including inflammatory processes.[6] Some studies have demonstrated the prevalence of IR/T2DM as a complication of obesity,[7] while others have shown an increased prevalence of obesity in T2DM patients.[8],[9]

A direct product of adipose cells is leptin, a satiety hormone, which regulates food intake and energy utilization.[10],[11] Leptin was identified and cloned from the obesity gene discovered in ob/ob obese mice, and has also been observed in humans.[12] It has been independently associated with T2DM, hypercholesterolemia and metabolic syndrome in both men and women in developed countries.[13] Both leptin and insulin act at the same key hypothalamic areas to decrease food intake and increase energy expenditure thereby regulating long-term energy. Insulin stimulates production of leptin when adipocytes are exposed to glucose to encourage satiety; while leptin, via a negative feedback, decreases the secretion of insulin and enhances tissue sensitivity to it, leading to glucose uptake for energy utilization or storage.[14],[15],[16]

Contrary to the leptin deficiency observed in obese ob/ob mice, high serum leptin levels probably reflecting leptin resistance are seen in obese humans,[17] which can predict an increased risk for T2DM.[18] This may be because deregulation of the adipocyte-insulin axis in pancreatic beta cells in a state of hyperleptinemia results in hyperinsulinemia; of which the anabolic action of insulin stimulates adipogenesis thereby leading to a further increase in insulin secretion, and consequently, IR with the development of T2DM.[19],[20]

Although anthropometric measurements such as; body mass index (BMI) and waist circumference (WC), are well-known variables used to describe general and central obesity, respectively,[21] a biomarker like human serum leptin concentration, which is closely linked with BMI and fat mass, and increases steadily with adiposity [22] may be proposed to designate obesity levels. Consequently, the aim of this study was to determine the relationship between leptin and IR among obese Nigerian women.


   Methods Top


This was a cross-sectional study of obese, adult Nigerian females attending the medical outpatient clinic of the Lagos University Teaching Hospital (LUTH), which is an 800-bed tertiary health institution located in Lagos, South-West Nigeria. This study was reviewed and approved by the Research and Ethics Committee of LUTH as being in compliance with the Declaration of Helsinki (HREC number: ADM/DCST/HREC/433). Informed consent was obtained from each participant.

Females aged 21–60 years were examined to obtain their anthropometric measurements. WC was measured with a tape rule to the nearest 0.1 cm at the end of a normal expiration at the midpoint between the subcostal plane and the iliac crest of an exposed abdomen. Hip circumference (HC) was also measured at the largest standing horizontal circumference of the buttock to determine the waist-to-hip ratio (WHR = WC/HC). Body weight in kilogram (kg), was measured in the upright position using a portable, digital weighing scale that had been validated with calibrated weighing masses; and their height in meters (m), for the calculation of BMI = weight in kg/(height in m 2). Those with BMI ≥ 30 kg/m 2 were voluntarily recruited as subjects while those with BMI 18.5–24.9 kg/m 2 were recruited as normal weight controls. Adequately tested questionnaires were administered, and patients being managed for T2DM, polycystic ovarian syndrome, hypothyroidism, and Cushing's syndrome were excluded.

The subjects were instructed to return on an agreed morning within the week after an overnight 10–12 h fast. After antiseptic preparation of the antecubital vein was effected with methylated spirit swabs, venous blood was collected into a plain specimen tube (5 ml) for serum leptin and insulin; and fluoride oxalate tube (3 ml) for fasting plasma glucose determination.

The specimens were taken to the laboratory for processing, where the samples in the plain tube were allowed to clot and retract for 30 min, and then all samples were centrifuged at 4000 rpm for 10 min at room temperature. Plasma specimens were analyzed for glucose daily, but the serum was aliquoted into two cryogenic storage tubes (one for serum leptin and insulin each) and stored at − 20°C in a well-monitored freezer (NuAire, USA), for 1-month until the analyses were performed. Hemolyzed, icteric, and lipemic samples were excluded.

Glucose oxidase method was used to estimate fasting plasma glucose concentration on a Roche Hitachi 902 analyzer (Roche diagnostics, Germany). A sandwich, solid-phase enzyme-linked immunosorbent assay (ELISA) was used to measure serum leptin (Diagnostic Automation Inc., USA); and serum insulin (Diagnostic Automation Inc., USA), both with intra- and inter-assay coefficients of variation of <10%; which were read using a BioRad microwell reader (BioRad, USA).

Insulin resistance was calculated with the homeostatic model assessment (HOMA) method which reflects the degree of IR as: HOMA-IR = (glucose × insulin)/22.5 for glucose in mmol/L.[23] Quality control was performed for plasma glucose using bovine precision multi-sera (levels 2 and 3) (RANDOX laboratories, UK); while the ELISA kit quality control material (low and high) (Diagnostic Automation Inc., USA) with reference intervals of leptin: 1.7–4.5 ng/ml, 22.1–40.9 ng/ml and insulin: 8.7–17.3 µIU/ml, 27.1–53.7 µIU/ml, respectively, were used.

Statistical analysis of the data was performed using SPSS software version 20 (IBM Corp., Armonk, New York) statistical package. The data were tested for normality using Kolmogorov–Smirnov test and data that were not normally distributed were log-transformed. Student's t-test was used to compare the means of leptin, insulin, glucose, and HOMA-IR between the subjects and controls. Pearson's correlation coefficient was performed to determine relationships while multiple linear regression was performed to determine prediction using HOMA-IR as the outcome, and age, BMI, WC, WHR, leptin, glucose as predictors. A P < 0.05 was considered to be statistically significant.


   Results Top


Eighty female subjects with mean ± standard deviation (SD) age 44.9 ± 9.8 years; and BMI 39.1 ± 7.2 kg/m 2 were recruited for this study and grouped into Class I, Class II, and Class III obesity (morbid obesity) using BMI groups of 30.0–34.9, 35.0–35.9, ≥ 40 kg/m 2, respectively, while 76 age-matched, normal weight (BMI = 18.5–24.9 kg/m 2) females were recruited as controls.

The mean ± SD serum leptin in the subjects was 48.5 ± 24.7 ng/ml, which was significantly higher than that of the controls 19.8 ± 17.2 ng/ml (P < 0.001); but not the fasting serum insulin, plasma glucose, and HOMA-IR (P > 0.05) [Table 1].
Table 1: Mean (SD) values in obese subjects versus normal weight controls

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The prevalence of hyperleptinemia observed among the obese subjects was 74 (92.5%, confidence interval: 87.3–97.7%), using a cut-off value of >5.5 ng/ml for females.[13]

The correlation between serum leptin and insulin levels among all the obese subjects showed a positive relationship (r = 0.31, P = 0.008*), as well as with glucose (r = 0.25, P = 0.036*) and HOMA-IR (r = 0.422, P < 0.001*). On subdivision into obesity classes, the positive correlation with HOMA-IR was replicated in the morbid obesity group only (r = 0.52, P = 0.004*) even after controlling for BMI (r = 0.46, P = 0.014*) [Table 2].
Table 2: Relationship between serum leptin, BMI, and insulin resistance

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Multiple linear regression of data obtained from all obese subjects (BMI ≥ 30 kg/m 2) showed only WC (P = 0.026*) was a significant predictor of HOMA-IR; but when subdivided, the morbid obesity group (BMI ≥ 40 kg/m 2) showed both WC (P = 0.005*) and WHR (P = 0.017*) were significant predictors of HOMA-IR. Leptin did not show significant prediction for HOMA-IR (all subjects with BMI ≥ 30 kg/m 2 P = 0.837; BMI ≥ 40 kg/m 2 P = 0.840).


   Discussion Top


A high prevalence of hyperleptinemia (92.5%) was observed in this study which deliberately comprised of only females, because serum leptin concentration has been described to exhibit significant sexual dimorphism, with females having higher concentrations at every level of relative and absolute adiposity than males.[22],[24] This is because hyperleptinemia is more closely associated with adipose cell hypertrophy, which is seen more in females, than adipose tissue hyperplasia which is seen more in males.[25]

As expected, serum leptin levels were higher among the subjects than controls in this study because they have increased adiposity which directly produces leptin. However, the controls still had a mean level of 19.8 ng/ml which well above the reference interval of 0.07–0.13 ng/ml for healthy, normal weight females given in a Caucasian population study;[26] as well as >5.51 ng/ml defined as hyperleptinemia among Taiwanese adults.[13] This supports the findings of a study in South Africa that observed that lean and overweight black females had higher serum leptin concentrations than their age and obesity-matched white females.[27]

The positive, linear relationship shown between leptin and BMI in our study is consistent with other studies [24],[28] suggesting that obese females may be insensitive to endogenous leptin production, and therefore try to compensate by producing more; supporting the theory of leptin resistance and hyperleptinemia seen in humans which differs from animal models where leptin deficiency predominates in obesity.[29]

A study demonstrated higher leptin levels in normal weight diabetics than nondiabetic controls.[30] This corroborates the findings of Fischer et al. that subjects with T2DM have higher serum leptin levels independent of body fat mass,[31] but differs from an Iranian study which discovered that serum leptin levels were reduced in nonobese subjects with T2DM.[32] Based on these conflicting reports, known diabetics were excluded from this study.

Despite the similar HOMA-IR observed between the subjects and controls, serum leptin levels showed a linear relationship with insulin levels as well as HOMA-IR, corroborating a study which described a significant positive correlation between serum leptin levels and parameters of IR in a nondiabetic, healthy population,[33] and another which showed a strong relationship between fasting insulin level and leptin concentration.[34] Karatela and Sainani reported an association between leptin and IR/T2DM in obese patients,[35] which may be explained by the close interaction of the adipocyte-insulin axis and leptin regulatory pathways.

After obesity class subdivision, the significant positive relationship between serum leptin and HOMA-IR initially seen among all the subjects was attributed to the Class III obese (morbid obesity) group, even after correcting for BMI. This may suggest that Nigerian women may need to attain very high BMI percentiles, and consequently high leptin levels before frank IR or T2DM develops, but more research will be needed to confirm this. The findings can be welcoming in African societies where obesity is socially acceptable.[36]

Our study could not demonstrate leptin as a predictive factor for IR as similarly reported by Ezenwaka et al.[37] This may be due the limited sample size both studies used. They sampled 43 nondiabetics while we sampled 80 nondiabetics. But the popular anthropometric WC measurement is still useful in predicting IR,[30],[38] which our study corroborates.

Further studies can be done to determine the obesity level at which IR commences. The cross-sectional design of this study limits our ability to determine this, and it is beyond the scope of this research work.


   Conclusion Top


We demonstrated a positive relationship between leptin and IR, which was particularly significant at the morbid obesity level. Further molecular studies may be needed to explain this. Furthermore, we did not observe leptin as a predictor for IR. Given the high prevalence of obesity in developing countries, as well as its associated risk for T2DM, large population cohort studies on serum leptin levels can be performed to predict risk for this condition.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. JAMA 2004;291:1238-45.  Back to cited text no. 1
    
2.
Adedoyin RA, Mbada CE, Balogun MO, Adebayo RA, Martins T, Ismail S. Obesity prevalence in adult residents of Ile-Ife, Nigeria. Nig Q J Hosp Med 2009;19:63-8.  Back to cited text no. 2
    
3.
Bakari AG, Onyemelukwe GC, Sani BG, Aliyu IS, Hassan SS, Aliyu TM. Obesity, overweight and underweight in sub-Saharan Africa. Int J Diabetes Metab 2007;15:68-9.  Back to cited text no. 3
    
4.
Amira CO, Sokunbi DO, Sokunbi A. The prevalence of obesity and its relationship with hypertension in an urban community: Data from world kidney day screening programme. Int J Med Bio Res 2012;1:104-10.  Back to cited text no. 4
    
5.
Carey VJ, Walters EE, Cloditz GA. Body fat distribution and risk of NIDD in women: The nurses' health study. Am J Epidemiol 1997;145:614-9.  Back to cited text no. 5
    
6.
Osborn O, Olefsky JM. The cellular and signaling networks linking the immune system and metabolism in disease. Nat Med 2012;18:363-74.  Back to cited text no. 6
    
7.
Asfaw A. The effects of obesity on doctor-diagnosed chronic diseases in Africa: Empirical results from Senegal and South Africa. J Public Health Policy 2006;27:250-64.  Back to cited text no. 7
    
8.
Alebiosu CO, Odusan BO. Metabolic syndrome in subjects with type-2 diabetes mellitus. J Natl Med Assoc 2004;96:817-21.  Back to cited text no. 8
    
9.
Fasanmade OA, Okubadejo NU. Magnitude and gender distribution of obesity and abdominal adiposity in Nigerians with type 2 diabetes mellitus. Niger J Clin Pract 2007;10:52-7.  Back to cited text no. 9
[PUBMED]  Medknow Journal  
10.
Halaas JL, Gajiwala KS, Maffei M, Cohen SL, Chait BT, Rabinowitz D, et al. Weight-reducing effects of the plasma protein encoded by the obese gene. Science 1995;269:543-6.  Back to cited text no. 10
    
11.
Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature 1998;395:763-70.  Back to cited text no. 11
    
12.
Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature 1994;372:425-32.  Back to cited text no. 12
    
13.
Chiu FH, Chuang CH, Li WC, Weng YM, Fann WC, Lo HY, et al. The association of leptin and C-reactive protein with the cardiovascular risk factors and metabolic syndrome score in Taiwanese adults. Cardiovasc Diabetol 2012;11:40.  Back to cited text no. 13
    
14.
Grundy SM. Obesity, metabolic syndrome, and cardiovascular disease. J Clin Endocrinol Metab 2004;89:2595-600.  Back to cited text no. 14
    
15.
Turpeinen AK, Haffner SM, Louheranta AM, Niskanen LK, Miettinen H, Uusitupa MI. Serum leptin in subjects with impaired glucose tolerance in relation to insulin sensitivity and first-phase insulin response. Int J Obes Relat Metab Disord 1997;21:284-7.  Back to cited text no. 15
    
16.
Barzilai N, Wang J, Massilon D, Vuguin P, Hawkins M, Rossetti L. Leptin selectively decreases visceral adiposity and enhances insulin action. J Clin Invest 1997;100:3105-10.  Back to cited text no. 16
    
17.
Maffei M, Stoffel M, Barone M, Moon B, Dammerman M, Ravussin E, et al. Absence of mutations in the human OB gene in obese/diabetic subjects. Diabetes 1996;45:679-82.  Back to cited text no. 17
    
18.
Schmidt MI, Duncan BB, Vigo A, Pankow JS, Couper D, Ballantyne CM, et al. Leptin and incident type 2 diabetes: Risk or protection? Diabetologia 2006;49:2086-96.  Back to cited text no. 18
    
19.
Frühbeck G, Salvador J. Relation between leptin and the regulation of glucose metabolism. Diabetologia 2000;43:3-12.  Back to cited text no. 19
    
20.
Wang J, Obici S, Morgan K, Barzilai N, Feng Z, Rossetti L. Overfeeding rapidly induces leptin and insulin resistance. Diabetes 2001;50:2786-91.  Back to cited text no. 20
    
21.
Report of a WHO Expert Committee. Physical Status: The Use and Interpretation of Anthropometry. WHO Technical Report Series 854. Geneva: World Health Organization; 1995. p. 51-6.  Back to cited text no. 21
    
22.
Luke AH, Rotimi CN, Cooper RS, Long AE, Forrester TE, Wilks R, et al. Leptin and body composition of Nigerians, Jamaicans, and US blacks. Am J Clin Nutr 1998;67:391-6.  Back to cited text no. 22
    
23.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9.  Back to cited text no. 23
    
24.
Oshodi T, Ebuehi OA, Ojewunmi O, Udenze I, Soriyan T. Circulating adipokine levels in type 2 diabetes mellitus in Lagos, Nigeria. Nig Q J Hosp Med 2012;22:25-8.  Back to cited text no. 24
    
25.
Couillard C, Mauriège P, Imbeault P, Prud'homme D, Nadeau A, Tremblay A, et al. Hyperleptinemia is more closely associated with adipose cell hypertrophy than with adipose tissue hyperplasia. Int J Obes Relat Metab Disord 2000;24:782-8.  Back to cited text no. 25
    
26.
Pilon B. Leptin and inflammation. Inflammation theory. Available from: http://www. Press75.com. [Last retrieved on 2011 Apr 19].  Back to cited text no. 26
    
27.
Schutte AE, van Vuuren D, van Rooyen JM, Huisman HW, Schutte R, Malan L, et al. Inflammation, obesity and cardiovascular function in African and Caucasian women from South Africa: The POWIRS study. J Hum Hypertens 2006;20:850-9.  Back to cited text no. 27
    
28.
Ntyintyane L, Panz V, Raal FJ, Gill G. Leptin, adiponectin, and high-sensitivity C-reactive protein in relation to the metabolic syndrome in urban South African blacks with and without coronary artery disease. Metab Syndr Relat Disord 2009;7:243-8.  Back to cited text no. 28
    
29.
Kennedy A, Gettys TW, Watson P, Wallace P, Ganaway E, Pan Q, et al. The metabolic significance of leptin in humans: Gender-based differences in relationship to adiposity, insulin sensitivity, and energy expenditure. J Clin Endocrinol Metab 1997;82:1293-300.  Back to cited text no. 29
    
30.
Oli JM, Adeyemo AA, Okafor GO, Ofoegbu EN, Onyenekwe B, Chukwuka CJ, et al. Basal insulin resistance and secretion in Nigerians with type 2 diabetes mellitus. Metab Syndr Relat Disord 2009;7:595-9.  Back to cited text no. 30
    
31.
Fischer S, Hanefeld M, Haffner SM, Fusch C, Schwanebeck U, Köhler C, et al. Insulin-resistant patients with type 2 diabetes mellitus have higher serum leptin levels independently of body fat mass. Acta Diabetol 2002;39:105-10.  Back to cited text no. 31
    
32.
Mohammadzadeh G, Zarghami N. Serum leptin level is reduced in non-obese subjects with type 2 diabetes. Int J Endocrinol Metab 2013;11:3-10.  Back to cited text no. 32
    
33.
Yadav A, Jyoti P, Jain SK, Bhattacharjee J. Correlation of adiponectin and leptin with insulin resistance: A pilot study in healthy North Indian population. Indian J Clin Biochem 2011;26:193-6.  Back to cited text no. 33
    
34.
Wallace AM, McMahon AD, Packard CJ, Kelly A, Shepherd J, Gaw A, et al. Plasma leptin and the risk of cardiovascular disease in the West of Scotland coronary prevention study (WOSCOPS). Circulation 2001;104:3052-6.  Back to cited text no. 34
    
35.
Karatela RA, Sainani GS. Interrelationships of Factor VII activity and plasma leptin with insulin resistance in coronary heart disease. Atherosclerosis 2010;209:235-40.  Back to cited text no. 35
    
36.
BeLue R, Okoror TA, Iwelunmor J, Taylor KD, Degboe AN, Agyemang C, et al. An overview of cardiovascular risk factor burden in sub-Saharan African countries: A socio-cultural perspective. Global Health 2009;5:10.  Back to cited text no. 36
    
37.
Ezenwaka CE, Nwagbara E, Seales D, Okali F, Sell H, Eckel J. Insulin resistance, leptin and monocyte chemotactic protein-1 levels in diabetic and non-diabetic Afro-Caribbean subjects. Arch Physiol Biochem 2009;115:22-7.  Back to cited text no. 37
    
38.
Tulloch-Reid MK, Ferguson TS, Younger NO, Van den Broeck J, Boyne MS, Knight-Madden JM, et al. Appropriate waist circumference cut points for identifying insulin resistance in black youth: A cross sectional analysis of the 1986 Jamaica birth cohort. Diabetol Metab Syndr 2010;2:68.  Back to cited text no. 38
    



 
 
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