Article: article from journal or magazin.
Parametrial adipose tissue and metabolic dysfunctions induced by fructose-rich diet in normal and neonatal-androgenized adult female rats.
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Hyperandrogenemia predisposes an organism toward developing impaired insulin sensitivity. The aim of our study was to evaluate endocrine and metabolic effects during early allostasis induced by a fructose-rich diet (FRD) in normal (control; CT) and neonatal-androgenized (testosterone propionate; TP) female adult rats. CT and TP rats were fed either a normal diet (ND) or an FRD for 3 weeks immediately before the day of study, which was at age 100 days. Energy intake, body weight (BW), parametrial (PM) fat characteristics, and endocrine/metabolic biomarkers were then evaluated. Daily energy intake was similar in CT and TP rats regardless of the differences in diet. When compared with CT-ND rats, the TP-ND rats were heavier, had larger PM fat, and were characterized by basal hypoadiponectinemia and enhanced plasma levels of non-esterified fatty acid (NEFA), plasminogen activator inhibitor-1 (PAI-1), and leptin. FRD-fed CT rats, when compared with CT-ND rats, had high plasma levels of NEFA, triglyceride (TG), PAI-1, leptin, and adiponectin. The TP-FRD rats, when compared with TP-ND rats, displayed enhanced leptinemia and triglyceridemia, and were hyperinsulinemic, with glucose intolerance. The PM fat taken from TP rats displayed increase in the size of adipocytes, decrease in adiponectin (protein/gene), and a greater abundance of the leptin gene. PM adipocyte response to insulin was impaired in CT-FRD, TP-ND, and TP-FRD rats. A very short duration of isocaloric FRD intake in TP rats induced severe metabolic dysfunction at the reproductive age. Our study supports the hypothesis that the early-androgenized female rat phenotype is highly susceptible to developing endocrine/metabolic dysfunction. In turn, these abnormalities enhance the risk of metabolic syndrome, obesity, type 2 diabetes, and cardiovascular disease.
Adipocytes/pathology, Adipokines/metabolism, Adiponectin/metabolism, Adipose Tissue/metabolism, Adiposity, Androgens/metabolism, Animals, Body Weight, Dietary Sucrose/administration & dosage, Dietary Sucrose/pharmacology, Disease Models, Animal, Energy Intake, Fatty Acids, Nonesterified/blood, Female, Fructose/pharmacology, Genitalia, Female, Glucose Metabolism Disorders/blood, Glucose Metabolism Disorders/etiology, Glucose Metabolism Disorders/metabolism, Hyperandrogenism/blood, Hyperandrogenism/complications, Insulin/metabolism, Leptin/blood, Leptin/genetics, Obesity/blood, Obesity/etiology, Plasminogen Activator Inhibitor 1/blood, Rats, Rats, Sprague-Dawley, Risk Factors, Testosterone Propionate/metabolism, Triglycerides/blood
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