Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture of P.R.C, Fishery College, Huazhong Agricultural University, Wuhan 430070, China.
Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture of P.R.C, Fishery College, Huazhong Agricultural University, Wuhan 430070, China; Collaborative Innovation Center for Efficient and Health Production of Fisheries, Hunan University of Arts and Science, Changde 415000, China.
Food Chem. 2018 Dec 15;269:595-602. doi: 10.1016/j.foodchem.2018.07.048. Epub 2018 Jul 9.
Cu could act as a modifier and influence lipid metabolism, but the potential mechanism was not explored. Juvenile yellow catfish were fed diet containing 0.71 (low Cu), 3.93 (intermediate Cu) and 88.81 (high Cu) mg Cu kg, for 8 weeks to explore the modulation of intestinal lipid metabolism following dietary Cu addition. Using specific pathway inhibitors (Fatostatin for SREBP1, T0070907 for PPARG and Compound C for AMPK), primary enterocytes of yellow catfish were used to explore the molecular mechanisms of Cu reducing intestinal lipid deposition. Dietary Cu addition triggered Cu accumulation but suppressed lipid deposition in the fore- and mid-intestine. The reduced lipid deposition was attributable to the suppressed lipogenesis and lipid absorption, and accelerated lipid transport. The PPARG, SREBP1 and AMPK signaling pathways mediated the Cu-induced changes in lipogenesis, lipid uptake and lipid transport in the intestine of yellow catfish.
铜可以作为一种调节剂影响脂质代谢,但潜在的机制尚未被探索。研究人员用含有 0.71(低铜)、3.93(中铜)和 88.81(高铜)mg Cu/kg 的饲料喂养幼年黄颡鱼 8 周,以探讨膳食铜添加后肠道脂质代谢的调节作用。使用特定的途径抑制剂(Fatostatin 用于 SREBP1、T0070907 用于 PPARG 和 Compound C 用于 AMPK),研究人员还利用黄颡鱼的原代肠细胞来探索铜减少肠道脂质沉积的分子机制。膳食铜的添加会触发铜的积累,但会抑制前肠和中肠的脂质沉积。脂质沉积的减少归因于脂肪生成和脂质吸收的抑制以及脂质转运的加速。PPARG、SREBP1 和 AMPK 信号通路介导了铜诱导的黄颡鱼肠道脂肪生成、脂质摄取和脂质转运的变化。