Fructose rich diet-induced high plasminogen activator inhibitor-1 (PAI-1) production in the adult female rat: protective effect of progesterone

• Published in: Nutrients Vol. 4; no. 8; pp. 1137 - 1150
• Main Authors: Castrogiovanni, Daniel, Alzamendi, Ana, Ongaro, Luisina, Giovambattista, Andrés, Gaillard, Rolf C, Spinedi, Eduardo
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.08.2012; MDPI
• Subjects: Adipocytes; adipokines; Age; allostasis; Animals; Blood Glucose; Body fat; Cholesterol - blood; Corticosterone - blood; Diet - adverse effects; Fatty Acids, Nonesterified - blood; Female; Fructose - chemistry; Fructose - pharmacology; Gene Expression Regulation - drug effects; Gene Expression Regulation - physiology; Glucose; glucose tolerance; Glucose Tolerance Test; high carbohydrate diet; Insulin; Insulin - blood; Laboratories; Leptin - blood; Metabolism; Metabolites; Plasma; Plasminogen Activator Inhibitor 1 - genetics; Plasminogen Activator Inhibitor 1 - metabolism; Progesterone - metabolism; Rats; Rats, Sprague-Dawley; Steroids; Testosterone; Testosterone - blood; Triglycerides - blood; Argentina; allostasis; adipokines; insulin; glucose tolerance; high carbohydrate diet
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu4081137

The effect of progesterone (P4) on fructose rich diet (FRD) intake-induced metabolic, endocrine and parametrial adipose tissue (PMAT) dysfunctions was studied in the adult female rat. Sixty day-old rats were i.m. treated with oil alone (control, CT) or containing P4 (12 mg/kg). Rats ate Purina chow-diet ad libitum throughout the entire experiment and, between 100 and 120 days of age drank ad libitum tap water alone (normal diet; CT-ND and P4-ND) or containing fructose (10% w/v; CT-FRD and P4-FRD). At age 120 days, animals were subjected to a glucose tolerance test or decapitated. Plasma concentrations of various biomarkers and PMAT gene abundance were monitored. P4-ND (vs. CT-ND) rats showed elevated circulating levels of lipids. CT-FRD rats displayed high (vs. CT-ND) plasma concentrations of lipids, leptin, adiponectin and plasminogen activator inhibitor-1 (PAI-1). Lipidemia and adiponectinemia were high (vs. P4-ND) in P4-FRD rats. Although P4 failed to prevent FRD-induced hyperleptinemia, it was fully protective on FRD-enhanced plasma PAI-1 levels. PMAT leptin and adiponectin mRNAs were high in CT-FRD and P4-FRD rats. While FRD enhanced PMAT PAI-1 mRNA abundance in CT rats, this effect was absent in P4 rats. Our study supports that a preceding P4-enriched milieu prevented the enhanced prothrombotic risk induced by FRD-elicited high PAI-1 production.