Hauffe Robert, Rath Michaela, Agyapong Wilson, Jonas Wenke, Vogel Heike, Schulz Tim J, Schwarz Maria, Kipp Anna P, Blüher Matthias, Kleinridders André
Department of Molecular and Experimental Nutritional Medicine, Institute of Nutritional Science, University of Potsdam, D-14558 Nuthetal, Germany.
German Institute of Human Nutrition (DIfE), D-14558 Nuthetal, Germany.
Antioxidants (Basel). 2022 Apr 28;11(5):862. doi: 10.3390/antiox11050862.
The intake of high-fat diets (HFDs) containing large amounts of saturated long-chain fatty acids leads to obesity, oxidative stress, inflammation, and insulin resistance. The trace element selenium, as a crucial part of antioxidative selenoproteins, can protect against the development of diet-induced insulin resistance in white adipose tissue (WAT) by increasing glutathione peroxidase 3 (GPx3) and insulin receptor (IR) expression. Whether selenite (Se) can attenuate insulin resistance in established lipotoxic and obese conditions is unclear. We confirm that mRNA expression in adipose tissue correlates with BMI in humans. Cultivating 3T3-L1 pre-adipocytes in palmitate-containing medium followed by Se treatment attenuates insulin resistance with enhanced GPx3 and IR expression and adipocyte differentiation. However, feeding obese mice a selenium-enriched high-fat diet (SRHFD) only resulted in a modest increase in overall selenoprotein gene expression in WAT in mice with unaltered body weight development, glucose tolerance, and insulin resistance. While Se supplementation improved adipocyte morphology, it did not alter WAT insulin sensitivity. However, mice fed a SRHFD exhibited increased insulin content in the pancreas. Overall, while selenite protects against palmitate-induced insulin resistance in vitro, obesity impedes the effect of selenite on insulin action and adipose tissue metabolism in vivo.
摄入含有大量饱和长链脂肪酸的高脂饮食（HFD）会导致肥胖、氧化应激、炎症和胰岛素抵抗。微量元素硒作为抗氧化硒蛋白的关键组成部分，可通过增加谷胱甘肽过氧化物酶3（GPx3）和胰岛素受体（IR）的表达，预防白色脂肪组织（WAT）中饮食诱导的胰岛素抵抗的发展。亚硒酸盐（Se）是否能在已建立的脂毒性和肥胖条件下减轻胰岛素抵抗尚不清楚。我们证实，人体脂肪组织中的mRNA表达与体重指数相关。在含棕榈酸的培养基中培养3T3-L1前脂肪细胞，随后进行硒处理，可通过增强GPx3和IR的表达以及脂肪细胞分化来减轻胰岛素抵抗。然而，给肥胖小鼠喂食富含硒的高脂饮食（SRHFD），仅导致体重未改变、糖耐量和胰岛素抵抗的小鼠WAT中总体硒蛋白基因表达适度增加。虽然补充硒改善了脂肪细胞形态，但并未改变WAT胰岛素敏感性。然而，喂食SRHFD的小鼠胰腺中胰岛素含量增加。总体而言，虽然亚硒酸盐在体外可预防棕榈酸诱导的胰岛素抵抗，但肥胖会阻碍亚硒酸盐对体内胰岛素作用和脂肪组织代谢的影响。
