Fructose-rich diet-induced abdominal adipose tissue endocrine dysfunction in normal male rats

• Published in: Endocrine Vol. 35; no. 2; pp. 227 - 232
• Main Authors: Alzamendi, Ana, Giovambattista, Andrés, Raschia, Agustina, Madrid, Viviana, Gaillard, Rolf C., Rebolledo, Oscar, Gagliardino, Juan J., Spinedi, Eduardo
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.04.2009
• Subjects: Abdominal Fat - cytology; Abdominal Fat - drug effects; Abdominal Fat - metabolism; Adipocytes - chemistry; Adipocytes - drug effects; Adipocytes - secretion; Animals; Biomarkers - blood; Dexamethasone - pharmacology; Diabetes; Diet; Endocrinology; Fructose - administration & dosage; Gene Expression; Glucose Intolerance - etiology; Humanities and Social Sciences; Insulin - pharmacology; Insulin Receptor Substrate Proteins - genetics; Internal Medicine; Leptin - genetics; Leptin - secretion; Male; Medicine; Medicine & Public Health; multidisciplinary; Original Paper; Oxidative Stress - drug effects; Rats; Rats, Wistar; RNA, Messenger - analysis; Science; Lipids; Dexamethasone; Insulin signalling; Adipokines; Metabolic syndrome
• ISSN: 1355-008X; 1559-0100
• DOI: 10.1007/s12020-008-9143-1

We have currently studied the changes induced by administration of a fructose-rich diet (FRD) to normal rats in the mass and the endocrine function of abdominal (omental) adipose tissue (AAT). Rats were fed ad libitum a standard commercial chow and tap water, either alone (control diet, CD) or containing fructose (10%, w/vol) (FRD). Three weeks after treatment, circulating metabolic markers and leptin release from adipocytes of AAT were measured. Plasma free fatty acids (FFAs), leptin, adiponectin, and plasminogen activator inhibitor-1 (PAI-1) levels were significantly higher in FRD than in CD rats. AAT mass was greater in FRD than in CD rats and their adipocytes were larger, they secreted more leptin and showed impaired insulin sensitivity. While leptin mRNA expression increased in AAT from FRD rats, gene expression of insulin receptor substrate, IRS1 and IRS2 was significantly reduced. Our study demonstrates that administration of a FRD significantly affects insulin sensitivity and several AAT endocrine/metabolic functions. These alterations could be part of a network of interacting abnormalities triggered by FRD-induced oxidative stress at the AAT level. In view of the impaired glucose tolerance observed in FRD rats, these alterations could play a key role in both the development of metabolic syndrome (MS) and β-cell failure.