The Determinants of Leptin Levels in Diabetic and Nondiabetic Saudi Males

Hindawi International Journal of Endocrinology Volume 2017, Article ID 3506871, 7 pages https://doi.org/10.1155/2017/3506871 Research Article The Determinants of Leptin Levels in Diabetic and Nondiabetic Saudi Males Mona Hmoud Al Sheikh Department of Physiology, College of Medicine, University of Dammam, Dammam, Saudi Arabia Correspondence should be addressed to Mona Hmoud Al Sheikh; Received 19 September 2016; Revised 28 November 2016; Accepted 20 December 2016; Published 1 March 2017 Academic Editor: Małgorzata Kotula-Balak Copyright © 2017 Mona Hmoud Al Sheikh. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. This study aimed to identify the main determinants of serum leptin levels. Methods. A sample of 113 Saudi adult males (55 diabetic and 58 nondiabetic) was selected according to the inclusion and exclusion criteria identified below. Blood samples were taken from participants after fasting for 12 hours. For diabetic patients, the insulin dose was given 12 hours before. In general, the study instrument consisted of blood biochemical tests. Metabolic parameters, glycosylated hemoglobin (HbA1c), low-density lipoprotein (LDL), high-density lipoprotein (HDL), cholesterol, and triglyceride (TG), and adipokines, leptin, adiponectin, visfatin, and resistin, were measured. Multivariate model was utilized to identify the relationship between leptin levels and the independent variables. Results. When adjusted for resistin in the diabetic group, the results demonstrated a significant relationship between visfatin, LDL and TG, and leptin levels (p 0 05). However, when controlled for resistin, the effect of LDL and TG disappeared while that of visfatin stayed in the model. For the nondiabetic group, the results indicated a significant relationship between insulin, BMI, and leptin levels when adjusted for resistin (p 0 05). However, the effect of insulin disappeared when the model was controlled for resistin. The study results found no relationship between leptin and adiponectin levels in either the diabetic or nondiabetic group and whether adjusted or controlled for resistin. Conclusion. This study provided better understanding of the metabolism of leptin and unveiled the major determinants of leptin levels in diabetic and nondiabetic males. In conclusion, these results show that the association between leptin and metabolic parameters decreases with the progress of disease. 1. Introduction The prevalence of obesity has dramatically increased in the past ten years among the world’s population [1]. According to Blüher and Mantzoros [2], obesity has increased the incidence of diet-related diseases such as type 2 diabetes, hypertension, and cardiovascular diseases. The common features of these diseases are eating and overfeeding which consequently lead to obesity and disease [3–7]. Biologically, researchers have attributed that to adipose tissue which is regarded not only as an energy-storing organ but also as an endocrine organ [8]. It releases a number of humoral factors known as adipokines [9]. It is a group of endocrine organs and can be divided into white adipose tissue and brown adipose tissue [10]. Visceral and subcutaneous adipose tissues are known to be the most abundant sites of adipose tissues in the body. Such tissues produce adipokines [11]. It plays an important role in insulin resistance through production of adipose-derived proteins. The adipokine molecules belong to numerous functional categories including endocrine function that are related to leptin, adiponectin, and visfatin. Furthermore, adipokines play a major role in a number of metabolic functions as well as in the control of energy metabolism [12]. Leptin is produced from the ob gene [13] that contributes to body weight regulation. Leptin plays a critical role in human pathophysiology of a group of diseases because it elicits considerable interest in its potential in treating obesity 2 and insulin resistance [14]. In other words, evidence suggests that leptin is a protein involved in the pathology of obesity [15]. Empirical studies suggest that serum leptin is critical in regulating blood sugar through two different brain passage ways. The first one is responsible for controlling appetite and fat while the second one is responsible for telling the liver what to do with its stored glucose [16]. According to Tuominen et al. [17], there is a positive interaction between insulin and leptin. Additionally, leptin is linked with body fat percentage, BMI, and insulin concentration. Leptin resistance entails different interpretations since its complexity gives a range of definitions. Resistance may occur due to inability of serum leptin to reach or influence target sites within the brain [18]. Adiponectin is another adipokine released by adipose tissue. According to a number of studies, adiponectin concentration decreases in obese people and patients with type two diabetes and hypertension [19]. Furthermore, adiponectin decreases plasma triglycerides by decreasing cholesterol levels in the blood. According to Jurimae et al. [20], adiponectin plays a major role in glucose and lipid metabolism. Therefore, it is thought to enhance insulin resistance as well as reduce very-low-density lipoprotein (VLDL) cholesterol which decreases the incidence of dyslipidaemia [21]. Visfatin is another insulin-resistance-enhancing factor which is determined by obesity and type 2 diabetes. It was basically defined by Samal et al. [22] as “a novel human pre-B-cell colony-enhancing factor (PBEF).” Visfatin consists of ten introns and eleven exons that are spanned over 34.4 Kb of genomic DNA. Visfatin is a unique adipokine that is mainly secreted by visceral adipose tissue [23]. According to a number of studies, visfatin levels are increased in type two diabetes patients and it is associated with insulin resistance [23–26]. Although visfatin is related to insulin secretion, no studies have shown an association between visfatin and insulin sensitivity. Resistin is another adipokine which is regarded as a derived signalling cysteine-rich molecule and made of 144 amino acids. It is involved in different processes of inflammation. Additionally, human resistin has been detected in various tissues such as the stomach, thymus, placenta, thyroid gland, and skeletal muscle [27]. Clearly from its name, resistin resists the action of insulin and predominantly increases in obese people. This leads to a proinflammatory molecule that plays a critical role in the pathogenesis of diabetes and its complications [28]. Furthermore, researchers suggested that the hormone resistin links between diabetes and obesity [29]. On the basis of this brief description of adipose tissues and their role in insulin resistance, this study aims to determine the main factors that contribute to change in the (...truncated)