E n d o c r i n o l o g y & M e t a b o li c S y n d r o m e ISSN: 2161-1017 Endocrinology & Metabolic Syndrome Mohamed and Ashour, Endocrinol Metab Syndr 2016, 5:1 DOI: 10.4172/2161-1017.1000226 Research Article Open Access Endocrinol Metab Syndr ISSN: 2161-1017 EMS, an open access journal Volume 5 • Issue 1 • 1000226 Effect of Obesity on Albino Rat Kidney Waleed S. Mohamed 1,2* and Ahamed S. Ashour 3t 1 Internal Medicine Department, Tanta Faculty of Medicine, Tanta University, Egypt 2 Internal Medicine Department, Taif College of Medicine, Taif University, KSA 3 Anatomy and Embryology Department, Tanta Faculty of Medicine, Tanta University, Egypt Abstract Background and study aim: Obesity and concomitant co-morbidities have emerged as public health problems of the frst order. Obese individuals have an increased risk for Chronic Kidney Disease (CKD). The aim of this study is to study the metabolic and early renal histopathologic changes that are associated with obesity in experimental animals. Materials and Methods: This study was conducted on sixty adult male albino rats; thirty with body weight ranging between 180-200 gm (control) beside thirty rates with body weight more than 250 gm. Control animals were fed a standard rat chow while obese rats were fed a semisynthetic diet enriched in sucrose. After 4 weeks, blood samples were collected to assess: Fasting Blood Glucose (FBG), Serum Insulin (SI), serum Total Lipid (TL), serum Triglyceride (TG), Total Cholesterol (TC), serum High Density Lipoprotein (HDL) and serum Low Density Lipoprotein (LDL). Kidney tissue samples were stained with Hematoxylin and Eosin, Anti-Collagen IV antibody then examined by light and electron Microscope. Results: There was a signifcant increased Body Weight (BW) and kidneys weight of obese group. There was a signifcant increased of FBS (p 0.0001), SI (p 0.0001), TL (p 0.0001), TC (p 0.0001), TG (p 0.0001), and LDL (p 0.0043) with signifcant decreased of HDL (p 0.0133) in obese group. Serum creatinine was signifcantly increased in obese group with a signifcant positive correlation between it and BW, FBS, SI, and TG. Histological examination revealed moderately expanded Bowman’s capsule, wide renal tubules, a positive reaction for collagen IV, increased thickness of glomerular basement membrane, foot processes fusion and many vacuolation in the cells lining of proximal convoluted tubules of obese rats kidneys. Conclusions: Obesity is associated with many metabolic abnormalities like insulin resistance, impaired glucose tolerance, dyslipidemia, morphological and structural renal changes which may proceed to Glomerulosclrosis (GS) and CKD. *Corresponding author: Waleed S. Mohamed, Internal Medicine Department, Tanta Faculty of Medicine, Tanta University, Egypt, Internal Medicine Department, Taif College of Medicine, Taif University, KSA, Tel: +966/0553420886; Fax: +966/27256900; E-mail: wsmohamed1@yahoo.com Received December 16, 2015; Accepted January 04, 2016; Published January 18, 2016 Citation: Mohamed WS, Ashour AS (2016) Effect of Obesity on Albino Rat Kidney . Endocrinol Metab Syndr 5: 226. doi:10.4172/2161-1017.1000226 Copyright: © 2016 Mohamed WS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Keywords: Chronic kidney disease; Metabolic abnormalities; Obesity; Renal histological changes Introduction Obesity has become a serious global health issue afecting both adults and children. Te prevalence of overweight and obesity is approximately 66% in the United States [1]. Over the last two decades, a worldwide rise in obesity has resulted in 1.46 billion overweight (Body Mass Index (BMI] >25) and 502 million obese (BMI >30) adults [2]. Obesity potentially leads to a decrease in overall life expectancy [3]. Te metabolic syndrome a major consequence of obesity [4]. Te prevalence of the metabolic syndrome in the United States is 23% in those who are 20 year or older and 40% in those who are 60 year or older [5]. Te metabolic syndrome is defned as the presence of at least three of the following criteria, with or without diabetes: central obesity (waist circumference in men 102 cm and in women 88 cm), hypertriglyceridemia (150 mg/dl), low HDL cholesterol (men 40 mg/dl, women 50 mg/dl), elevated fasting glucose (110 mg/dl), and hypertension (130/85 mmHg) [6]. A central feature of the metabolic syndrome is insulin resistance, which results in hyperglycemia and hyper-insulinemia, and eventually leads to the development of diabetes [7]. Chronic infammation is another feature of the metabolic syndrome, which, together with insulin resistance, results in complex metabolic derangements [8]. Obesity has deleterious efects on metabolic homeostasis, and afects numerous body organs. Co-morbidities for obesity include type 2 diabetes mellitus, cardiovascular diseases, hepatic steatosis, Alzheimer’s disease, CKD and certain cancers [9,10]. Obesity was shown to afect independently the progression of preexisting renal diseases, such as IgA nephropathy, [11] patients with unilateral renal agenesis, [12] or afer unilateral nephrectomy [13]. Kidneys obtained from obese donors were more likely to exhibit a lower Glomerular Filtration Rate (GFR] and a higher rate of allograf dysfunction over several years than kidneys obtained from lean individuals [14]. Tese data suggest that obesity contributes to and perhaps even initiates CKD. Published data quantifying the real impact of obesity on renal function are defcient. Some studies revealed a link between variable degrees of proteinuria and obesity [15]. Clinically, patients may present with nephrotic syndrome [13]. Praga et al. [16] reported the absence of features of nephrotic syndrome despite heavy proteinuria in 15 obese patients. Te histopathologic changes founded in a proteinuric obese patient consist of glomerulomegaly with or without Focal Segmental Glomerulosclerosis (FSGS). Tese patients tend to have less podocyte injury and a more indolent progression than patients with idiopathic FSGS [15]. Te changes are thought to be related to altered renal hemodynamics, namely increased renal blood fow, hyper-fltration, and increased fltration fraction [17]. However, it is likely that these observations are somewhat biased as renal biopsies are usually obtained only in patients with proteinuria. Terefore, obesity-related glomerulopathy may not be the only histopathologic feature of obesity-related renal disease, particularly in non-proteinuric obese patients. Hence, the aim of this