title: Fructose-rich diet-induced abdominal adipose tissue endocrine dysfunction in normal male rats.
abstract: 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 beta-cell failure.
authors.affiliation: Neuroendocrine Unit, IMBICE (CONICET-CICPBA), 1900 La Plata, Argentina.
authors.forename: Ana
authors.initials: A
authors.lastname: Alzamendi
authors.forename: Andrés
authors.initials: A
authors.lastname: Giovambattista
authors.forename: Agustina
authors.initials: A
authors.lastname: Raschia
authors.forename: Viviana
authors.initials: V
authors.lastname: Madrid
authors.forename: Rolf C
authors.initials: RC
authors.lastname: Gaillard
authors.forename: Oscar
authors.initials: O
authors.lastname: Rebolledo
authors.forename: Juan J
authors.initials: JJ
authors.lastname: Gagliardino
authors.forename: Eduardo
authors.initials: E
authors.lastname: Spinedi
mesh_terms: D050153:Abdominal Fat / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D017667:Adipocytes / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D004032:Diet; D005632:Fructose / Q000008:administration & dosage*; D015870:Gene Expression; D018149:Glucose Intolerance / Q000209:etiology; D007328:Insulin / Q000494:pharmacology; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar
chemical_list: D015415:Biomarkers; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; C526296:Irs1 protein, rat; C526299:Irs2 protein, rat; D020738:Leptin; D012333:RNA, Messenger; D005632:Fructose; D003907:Dexamethasone