Résumé
Background: Obese people, especially females, are known to have high circulating levels of leptin, a hormone that increases energy expenditure and also regulates glucose metabolism. However, the link between obesity and type 2 diabetes (T2DM) through leptin is yet to be clearly defined.
Objectives: This study determined and compared the levels of serum leptin and HOMA-IR scores in obese and non-obese females with or without T2DM. We also determined the relationship between their serum leptin levels and glycaemic control.
Methodology:This was a cross sectional study involving 60 obese T2DM females, 60 non-obese T2DM females and 60 obese nondiabetic female adults who met selection criteria. Their demographic data and anthropometric parameters were obtained using standard methods. Fasting blood samples were collected aseptically from participants for determination of plasma glucose, serum leptin, HbAlcand HOMA-IR.
Results: Serum leptin levels in obese T2DM, obese non-diabetic and non-obese T2DM femaless were (15.61 +10.63), (11.33+14.22) and (5.92+3.68) ng/ml respectively. There were significantly much higher serum leptin levels in obese T2DM than in obese non-diabetic females (p = 0.035S). In the obese T2DM participants, serum leptin levels had strong negative correlation with HOMA-IR (r = -0.293, p = 0.023) and HbAIC ( r = -0.255, p = 0.049).
Conclusion: Serum leptin levels were much higher in obese females with diabetes than in those without diabetes. However, the strong negative correlation of serum leptin levels with improving glycaemic control may suggest a therapeutic potential of leptin for diabetes which needs to be further explored.
Keywords: Obesity, Type 2 diabetes mellitus, Serum leptin, Insulin resistance, HOMA-IR, HbA1C
Résumé
Contexte : Les personnes obèses, en particulier les femmes, sont connues pour leurs taux élevés de leptine en circulation, une hormone qui augmente la dépense énergétique et régule également le métabolisme du glucose. Cependant, le lien entre l’obésité et le diabète de type 2 (DT2) par le biais de la leptine n’est pas encore clairement défini.
Objectifs: Cette étude a déterminé et comparé les taux de leptine sérique et de scores HOMA-IR chez les femmes obèses et non obèses avec ou sans DT2. Nous avons également déterminé la relation entre leurs taux sériques de leptine et le contrôle glycémique .
Méthodologie:Il s’agissait d’une étude transversale portant sur 60 femelles DT2 obèses, 60 femelles DT2 non obèses et 60 femelles obèses non diabétiques qui répondaient aux critères de sélection.Leurs données démographiques et paramètres anthropométriques ont été obtenus en utilisant des méthodes standard.Des échantillons de sang à jeun ont été prélevés de manière aseptique chez les participants pour la détermination du glucose plasmatique, de laleptine sérique, de l’HbA1Cet de l’HOMA-IR.
Résultats: Les tauxde leptinesériquedes femelles DT2 obèses, obèses non diabétiques et non obèses DT2étaient(15,61+10,63), (11,33+14,22) et (5,92+3,68)ng/ml,respectivement.Les taux deleptine sérique étaient significativement plus élevés chez les femelles DT2 obèses que chez les femelles obèses non diabétiques (p = 0,035S).Chez les participantes DT2 obèses, lesniveaux de leptine sériqueavaient une forte corrélation négative avec l’HOMA-IR (r = -0,293, p = 0,023) etHbA1C(r= -0,255, p = 0,049).
Conclusion:Les taux de leptine sériqueétaient beaucoup plus élevés chez les femelles obèses diabétiques que chez celles non diabétiques. Cependant, la forte corrélation négative desniveauxsériques de leptine avec l’amélioration ducontrôleglycémiquepeut suggérer un potentiel thérapeutique de la leptinepour le diabète qui doit être davantage exploré.
Mots clés: Obésité, diabète sucré de type 2, leptine sérique, résistance à l’insuline, HOMA-IR, HbA1C
Correspondence: Dr. G.O.D. Ajani, Department of Medicine, Endocrinology, Federal Teaching Hospital, Ido Ekiti, Ekiti State, Nigeria, E-mail: gbadebo11@yahoo.com
Références
Zamboni M, Mazzali G, Zoico E, et al. Health consequences of obesity in the elderly: a review of four unresolved questions. Int J Obes (Lond) 2005; 29(9):1011-1029.
Enriori PJ, Evans AE, Sinnayah P and Cowley MA. Leptin resistance and obesity. Obesity (Silver Spring) 2006; 14 Suppl 5:254S-258S. 3. Dyson PA. The therapeutics of lifestyle management on obesity. Diabetes Obes Metab 2010;12(11):941-946.
Goldstein BJ. Insulin resistance: from benign to type 2 diabetes mellitus. Rev Cardiovasc Med 2003; 4 Suppl 6:S3-10.
Wild S, Roglic G, Green A, Sicree R and King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004; 27(5):1047-1053.
Yach D, Stuckler D and Brownell KD. Epidemiologic and economic consequences of the global epidemics of obesity and diabetes. Nat Med 2006; 12(1):62-66.
World Health Organization. Global health risks: mortality and burden of disease attributable to selected major risks. Geneva, Switzerland: World Health Organization; 2009.
Djiane J and Attig L. Role of leptin during perinatal metabolic programming and obesity. J Physiol Pharmacol 2008; 59 Suppl 1:55-63. 9. Olatunbosun ST, Kaufman JS and Bella AF. Prevalence of obesity and overweight in urban adult Nigerians. Obes Rev 2011; 12:233-241.
Akintomide AO, Adedoyin RA, Adebayo RA, et al. Relationship between adiposity and blood pressure among semi-urban adult of Odo-Ogbe community in Ile-lfe, Nigeria. Nig Journal of Health Sc 2009; 9 (2):11-18.
Dong F and Ren J. Fitness or fatness—the debate continues for the role of leptin in obesity- associated heart dysfunction. Curr Diabetes Rev 2007;3(3):159-164.
de Luis DA, Perez Castrillon JL and Duenas A. Leptin and obesity. Minerva Med 2009; 100(3):229- 236.
Girard J. Is leptin the link between obesity and insulin resistance? Diabetes Metab 1997; 23 Suppl 3:16-24.
Esteghamati A, Khalilzadeh O, Anvari M, et al. Association of serum leptin levels with homeostasis model assessment-estimated insulin resistance and metabolic syndrome: the key role of centra~obesity. Metab Syndr Relat Disord 2009; 7(5):447- 452.
Guier S, Cakir B, Demirbas B, et al. Leptin concentrations are related to glycaemic control, but do not change with short-term oral antidiabetic therapy in female patients with type 2 diabetes mellitus. Diabetes Obes Metab 2000;2(5):313-316.
Liuzzi A, Savia G, Tagliaferri M, et al. Serum leptin concentration in moderate and severe obesity: relationship with clinical, anthropometric and metabolic factors. lnt J Obes Relat Metab Disord 1999;23(10):1066-1073.
Perez F, Santos JL, Albala C, Calvillan M and Carrasco E. Obesity and leptin association in three Chilean aboriginal populations. Rev Med ChiI 2000; 128(1):45-52.
Luke AH, Rotimi CN, Cooper RS, et al. Leptin and body composition of Nigerians, Jamaicans and US blacks. Am J Clin Nutr 1998; 67:391-396.
Ajala MO, Ogunro PS, Idogun SE and Osundeko O. Relationship between plasma antioxidant status and leptin in controlled and non-controlled type 2 diabetic non-obese women. Int J Endocrinol Metab 2009; 4:214-221.
Alberti KG and Zimmet Pl. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med 1998; 15(7):539-553.
International Diabetes Federation. IDF diabetes atlas: diabetes and Impaired glucose tolerance 4th ed. Sicree R, Shaw J, Zimmet P, Baker IDI Heart and Diabetes Institute, editors. Belgium: International Diabetes Federation; 2011.
Mathews DR, HoskerJP, Rudenski AS, et al. Homeostasis model assessment: insulin. resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28(7):412-419.
Esteghamati A, Ashraf H, Khalilzadeh O, et al. Optimal cut-off of homeostasis model assessment of insulin resistance (HOMA-IR) for the diagnosis of metabolic syndrome: third national surveillance of risk factors of non-communicable diseases in Iran (SuRFNCD-2007). Nutr Metab (Lond) 2010; 7:26.
Trinder P. Determination of blood glucose using 4-aminohenzone as oxygen acceptor. Ann Clin Biochem.1969; 22:26.
Oli JM, Adeyemo AA, Okafor GO, et al. Basal insulin resistance and secretion in Nigerians with type 2 diabetes mellitus. Metab Syndr Relat Disord 2009;7(6):595-599.
World Health Organization. Obesity: preventing and managing the global epidemic: report of a WHO consultation. Geneva: World Health Organization; 2000.
Alberti KG, Zimmet P and Shaw J. Metabolic syndrome—a new world-wide definition. A consensus statement from the International Diabetes Federation. Diabet Med 2006; 23(5):469-480.
Santos JL, Martinez JA, Perez F and Albala C. Genetic epidemiology of obesity: family studies. Rev Med ChiI 2005; 133(3):349-361.
Fasanmade OA and Okubadejo NU. Magnitude and gender distribution of obesity and abdominal adiposity in Nigerians with type 2 diabetes mellitus. Niger J Clin Pract 2007; 10(1):52-57.
Wilborn C, Beckham J, Campbell B, et al. Obesity: prevalence, theories, medical consequences, management, and research directions. J Int Soc Sports Nutr 2005; 2:4-31.
Oshodi T, Ebuehi OA, Ojewunmi O, Udenze I and Soriyan T. Circulating adipokine levels in type 2 diabetes mellitus in Lagos, Nigeria. Nig QJ Hosp Med 2012; 22(1):25-28.
Friedman JM. Leptin and the regulation of body weight. Harvey Lect 1999; 95:107-136.
Buyukbese MA, Cetinkaya A, Kocabas R, Guven A and Tarakcioglu M. Leptin levels in obese women with and without type 2 diabetes mellitus. Mediators Inflamm [Research Support! Non-U.S. Gov’t]. 2004; 13(5-6):321-325.
Wabitsch. M, Jensen PJ, Blum WF, et al. Insulin and cortisol promote leptin Production in cultured human fat cell. Diabetes 1996; 45(10):1435-1438.
Considine RV, Sinha MK, Heiman; Mark. L, et al. Serum. immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med 1996; 334(5):292-295.
Suzuki K, Ito V, Ochiai J, et al. Relationship between obesity and serum markers of oxidative stress and inflammation in Japanese. Asian Pac J Cancer Prevent 2003; 4(3):259-266.