Nutrition and Obesity Group, Department of Nutrition and Food Science, Faculty of Pharmacy and Lucio Lascaray Research Centre, University of the Basque Country (UPV/EHU), 01006 Vitoria-Gasteiz, Spain.
CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, 28222 Madrid, Spain.
Food Funct. 2023 Oct 2;14(19):8865-8875. doi: 10.1039/d3fo01307c.
Insulin resistance and type 2 diabetes are obesity-related health alterations, featuring an ever-increasing prevalence. Besides inadequate feeding patterns, gut microbiota alterations stand out as potential contributors to these metabolic disturbances. The aim of this study was to investigate whether the administration of a probiotic ( GG) effectively prevents diet-induced insulin resistance in rats and to compare these potential effects with those exerted by its heat-inactivated parabiotic. For this purpose, 34 male Wistar rats were fed a standard or a high-fat high-fructose diet, alone or supplemented with viable or heat-inactivated GG. The body and white adipose tissue weight increases, induced by the obesogenic diet, were prevented by probiotic and parabiotic administration. The trend towards higher basal glucose levels and significantly higher serum insulin concentration observed in the non-treated animals fed with the obesogenic diet were effectively reverted by both treatments. Similar results were also found for serum adiponectin and leptin, whose levels were brought back by the probiotic and parabiotic administration to values similar to those of the control animals. Noteworthily, parabiotic administration significantly reduced skeletal muscle triglyceride content and activated CPT-1b compared to the non-treated animals. Finally, both treatments enhanced Akt and AS160 phosphorylation in the skeletal muscle compared to the non-treated animals; however, only parabiotic administration increased GLUT-4 protein expression in this tissue. These results suggest that heat-inactivated GG seem to be more effective than its probiotic of origin in preventing high-fat high-fructose diet-induced insulin resistance in rats.
胰岛素抵抗和 2 型糖尿病是肥胖相关的健康改变，其患病率呈不断上升趋势。除了不良的喂养模式外，肠道微生物群的改变也可能是这些代谢紊乱的潜在原因。本研究旨在探讨益生菌（ GG）的给药是否能有效预防大鼠饮食诱导的胰岛素抵抗，并将这些潜在的影响与它的灭活共生菌的影响进行比较。为此，34 只雄性 Wistar 大鼠分别喂食标准或高脂肪高果糖饮食，或补充活菌或灭活 GG。益生菌和共生菌给药可预防肥胖饮食引起的体重和白色脂肪组织重量增加。未治疗的肥胖饮食喂养动物的基础血糖水平升高和血清胰岛素浓度显著升高的趋势被两种治疗方法有效逆转。在血清脂联素和瘦素方面也发现了类似的结果，其水平通过益生菌和共生菌给药恢复到与对照动物相似的水平。值得注意的是，共生菌给药可显著降低骨骼肌甘油三酯含量并激活 CPT-1b，与未治疗动物相比。最后，与未治疗动物相比，两种治疗方法均可增强骨骼肌中 Akt 和 AS160 的磷酸化；然而，只有共生菌给药可增加该组织中的 GLUT-4 蛋白表达。这些结果表明，与原始益生菌相比，灭活 GG 似乎更能有效预防大鼠高脂肪高果糖饮食诱导的胰岛素抵抗。
