College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Department of Animal Science and Technology, Jiangsu Agri-Animal Husbandry Vocational College, Taizhou, China.
Anim Sci J. 2021 Jan-Dec;92(1):e13674. doi: 10.1111/asj.13674.
Glucose oversupply promotes formation of fatty liver, and fatty liver is usually accompanied with hyperglycemia. However, the mechanism by which glucose promotes formation of fatty liver is not very clear. In this study, fatty liver was successfully induced in Landes goose by 19 days of overfeeding with corn-based feed, the overfed geese had a significantly higher level of blood glucose than the normally fed geese (control group). In goose primary liver cells, high level of glucose promoted fat deposition and induced the expression of SREBF2(or SREBP2), a key regulator of lipid metabolism, and its intronic gene, miR-33. Moreover, overexpression of miRNA-33(miR-33) promotes lipid accumulation in goose primary liver cells. Consistently, miR-33 inhibitor suppressed glucose induced lipid accumulation in liver cells. Interestingly, the relative abundance of miR-33 in goose fatty liver was significantly higher than that in normal liver, while the relative mRNA and protein abundances of CROT, the target gene of miR-33, in goose fatty liver were significantly lower than those in goose normal liver. Taken together, these findings suggest that miR-33 mediates glucose promotion of lipid accumulation in goose primary liver cells, and that glucose participates in formation of goose fatty liver by regulating the expression of miR-33/CROT.
葡萄糖供应过剩会促进脂肪肝的形成，而脂肪肝通常伴随着高血糖。然而，葡萄糖促进脂肪肝形成的机制尚不清楚。在这项研究中，通过 19 天过量喂食玉米基饲料成功诱导朗德鹅脂肪肝，过度喂养的鹅的血糖水平明显高于正常喂养的鹅（对照组）。在鹅原代肝细胞中，高浓度的葡萄糖促进脂肪沉积，并诱导脂质代谢关键调节因子 SREBF2（或 SREBP2）及其内含子基因 miR-33 的表达。此外，miR-33 的过表达促进鹅原代肝细胞中的脂质积累。一致地，miR-33 抑制剂抑制葡萄糖诱导的肝细胞脂质积累。有趣的是，miR-33 在鹅脂肪肝中的相对丰度明显高于正常肝，而 miR-33 的靶基因 CROT 的相对 mRNA 和蛋白丰度在鹅脂肪肝中明显低于正常肝。总之，这些发现表明 miR-33 介导葡萄糖促进鹅原代肝细胞中的脂质积累，葡萄糖通过调节 miR-33/CROT 的表达参与鹅脂肪肝的形成。
