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This study investigates the effect of the ergogenic supplement β-hydroxy-β-methylbutyrate (HMB) on insulin resistance induced by high-fructose diet (HFD) in rats. Male Sprague Dawley rats were fed 60% HFD for 12 weeks and HMB (320 mg x [kg.sup.-1] x [day.sup.-1], orally) for 4 weeks. HFD significantly increased fasting insulin, fasting glucose, glycosylated hemoglobin ([HB.sub.A1C]), liver glycogen content, and homeostasis model assessment of insulin resistance (HOMA-IR) index, while it decreased glucose and insulin tolerance. Furthermore, HFD significantly increased serum triglycerides (TG), low density lipoprotein cholesterol (LDL-C), and very low density lipoprotein cholesterol (VLDL-C) levels, while it significantly decreased high density lipoprotein cholesterol (HDL-C). Moreover, HFD significantly increased mRNA expression of glucose transporter type-2 (GLUT-2), the mammalian target of rapamycin (mTOR), and sterol regulatory element-binding protein-1c (SREBP-1c) but decreased peroxisome proliferator-activated receptor-alpha (PPAR-α) in liver. Aortic relaxation to acetylcholine (ACh) was impaired and histopathology showed severe hepatic steatosis. HMB significantly increased insulin tolerance and decreased fasting insulin, HOMA-IR, [HB.sub.A1C], hepatic glycogen content, serum TG, LDL-C, and VLDL-C. Additionally, HMB enhanced ACh-induced relaxation, ameliorated hepatic steatosis, and decreased mRNA expression of GLUT-2. In conclusion, HMB may attenuate insulin resistance and hepatic steatosis through inhibiting GLUT-2 in liver. Key words: insulin resistance, β-hydroxy-β-methylbutyrate, high fructose diet, glucose transporter type-2, hepatic steatosis. Cette etude porte sur l'effet du β-hydroxy-β-methylbutyrate (HMB), un supplement ergogenique, sur la resistance a l'insuline induite par l'administration d'un regime a haute teneur en fructose chez le rat. Nous avons administre un regime a haute teneur (60%) en fructose a des rats Sprague Dawley males pendant 12 semaines et du HMB (a 320 mg x [kg.sup.-1] x [jour.sup.-1]) par voie orale pendant 4 semaines. L'administration du regime a haute teneur en fructose a permis d'obtenir une augmentation des taux d'insuline a jeun, de la glycemie a jeun, des taux d'hemoglobine glyquee ([HB.sub.A1C]), de la teneur en glycogene hepatique et de l'indice de l'HOMA-IR (pour << Homeostasis Model Assessment of Insulin Resistance >>) ainsi qu'une diminution de la tolerance au glucose et a l'insuline. En outre, l'administration du regime a haute teneur en fructose a entraine une nette augmentation des taux seriques de triglycerides (TG) et des taux de cholesterol lie a des lipoproteines de basse et de tres basse densite (C-LDL et C-VLDL) ainsi qu'une diminution marquee des taux de cholesterol lie a des lipoproteines de haute densite (C-HDL). De plus, l'administration du regime a haute teneur en fructose a entraine une augmentation marquee de l'expression de l'ARNm des genes GLUT-2 (transporteur du glucose de type-2), mTOR (mammalian target of rapamycin) et SREBP-1c (proteine-1 se liant a l'element regulateur du sterol) et une diminution de l'activation du recepteur PPAR-α (recepteur active par les proliferateurs de peroxysomes-alpha) dans le foie. En outre, nous avons mesure une inhibition de la relaxation aortique induite par l'acetylcholine (ACh) et l'examen histopathologique du foie a revele la presence d'une steatose importante. Nos resultats ont montre que l'administration de HMB permettait d'augmenter nettement la tolerance a l'insuline et de diminuer les taux d'insuline a jeun, l'indice de l'HOMA-IR, les taux [d'HB.sub.A1C], la teneur en glycogene hepatique ainsi que les taux seriques de TG, de C-LDL et de C-VLDL. De plus, la relaxation induite par l'ACh etait amplifiee en presence de HMB, lequel permettait d'attenuer la steatose hepatique et de diminuer l'expression de l'ARNm du gene GLUT-2. Conclusion : L'administration de HMB pourrait permettre d'attenuer la resistance a l'insuline et la steatose hepatique en inhibant l'expression du gene GLUT-2 au niveau du foie. [Traduit par la Redaction] Mots-cles : resistance a l'insuline, β-hydroxy-β-methylbutyrate, regime a haute teneur en fructose, transporteur du glucose de type 2, steatose hepatique., Introduction Body builders and athletes use ergogenic supplements extensively to maintain their strength and increase their muscle mass and exercise performance. Many of these supplements have hazardous effects on health [...]

Abstract: Non-alcoholic fatty liver (NAFL) disease (NAFLD) affects 30% of overweight adolescents and increases the risk of type 2 diabetes mellitus (T2D). Resveratrol is a naturally occurring compound with potential [...]

The systemic expression of the bile acid (BA) sensor farnesoid X receptor (FXR) has led to promising new therapies targeting cholesterol metabolism, triglyceride production, hepatic steatosis and biliary cholestasis. In contrast to systemic therapy, bile acid release during a meal selectively activates intestinal FXR. By mimicking this tissue-selective effect, the gut-restricted FXR agonist fexaramine (Fex) robustly induces enteric fibroblast growth factor 15 (FGF15), leading to alterations in BA composition, but does so without activating FXR target genes in the liver. However, unlike systemic agonism, we find that Fex reduces diet-induced weight gain, body-wide inflammation and hepatic glucose production, while enhancing thermogenesis and browning of white adipose tissue (WAT). These pronounced metabolic improvements suggest tissue-restricted FXR activation as a new approach in the treatment of obesity and metabolic syndrome., FXR (encoded by Nr1h4) is a ligand-activated transcriptional factor expressed in diverse tissues including the adrenal gland, kidney, stomach, duodenum, jejunum, ileum, colon, gall bladder, liver and macrophages, as well [...]