title: Parametrial adipose tissue and metabolic dysfunctions induced by fructose-rich diet in normal and neonatal-androgenized adult female rats.
abstract: 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.
authors.affiliation: Neuroendocrine Unit, IMBICE (CONICET-CICPBA), La Plata, Argentina.
authors.forename: Ana
authors.initials: A
authors.lastname: Alzamendi
authors.forename: Daniel
authors.initials: D
authors.lastname: Castrogiovanni
authors.forename: Hugo H
authors.initials: HH
authors.lastname: Ortega
authors.forename: Rolf C
authors.initials: RC
authors.lastname: Gaillard
authors.forename: Andres
authors.initials: A
authors.lastname: Giovambattista
authors.forename: Eduardo
authors.initials: E
authors.lastname: Spinedi
mesh_terms: D017667:Adipocytes / Q000473:pathology; D054392:Adipokines / Q000378:metabolism; D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D050154:Adiposity; D000728:Androgens / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D019422:Dietary Sucrose / Q000008:administration & dosage / Q000494:pharmacology; D004195:Disease Models, Animal; D002149:Energy Intake; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005632:Fructose / Q000494:pharmacology*; D005836:Genitalia, Female; D044882:Glucose Metabolism Disorders / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D017588:Hyperandrogenism / Q000097:blood / Q000150:complications*; D007328:Insulin / Q000378:metabolism; D020738:Leptin / Q000097:blood / Q000235:genetics; D009765:Obesity / Q000097:blood / Q000209:etiology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D043343:Testosterone Propionate / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: D054392:Adipokines; D052242:Adiponectin; D000728:Androgens; D019422:Dietary Sucrose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D020738:Leptin; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D005632:Fructose; D043343:Testosterone Propionate