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Effects of dietary starch and metformin levels on the growth performance, body composition, hepatic glycolipid metabolism, and liver histology of juvenile largemouth bass Micropterus salmoides

生物 糖原 糖原发生 内科学 内分泌学 葡萄糖稳态 蛋白质效率比 饲料转化率 脂肪生成 二甲双胍 淀粉 糖耐量受损 糖异生 糖原合酶 胰岛素 生物化学 新陈代谢 胰岛素抵抗 医学 体重
作者
Qinqin Liu,Ru Xia,Xin Deng,Huijun Yang,Li Luo,Shi‐Mei Lin,Qin Chuan-Jie,Yongjun Chen
出处
期刊:Aquaculture [Elsevier BV]
卷期号:573: 739582-739582 被引量:18
标识
DOI:10.1016/j.aquaculture.2023.739582
摘要

In this study, an 8-week feeding trial was performed to evaluate the effects of dietary metformin inclusion on the growth performance, body composition, glucose homeostasis and liver histology of juvenile largemouth bass Micropterus salmoides (LMB) fed high starch diets. Using a 2 × 2 factorial design, four isoproteinic (50%) and isolipidic (13%) diets were formulated with two starch levels (9% and 14%) with or without 0.25% metformin inclusion at each starch level. Each diet was assigned to triplicate tanks of LMB with an initial body weight of 10.8 g. The results showed that an increase of dietary starch from 9% to 14% retarded the growth performance (weight gain ratio and specific growth rate) of LMB through impairing feed utilization (feed efficiency ratio, protein efficiency ratio and protein productive value). Though feed consumption increased, the growth performance of LMB did not benefit from dietary metformin administration as a result of the impaired feed utilization. Both the glucose homeostasis (fasting blood glucose) and glucose tolerance of LMB were impaired with increasing dietary starch from 9% to 14%. However, LMB metabolically adapted well to high starch diets through stimulating glycolysis and glycogen synthesis while inhibiting gluconeogenesis in the liver at the molecular level. Moreover, an increase of dietary starch from 9% to 14% upregulated hepatic lipogenic capacities while down-regulated fatty acid oxidation thereby promoting lipid deposition in the liver and whole fish. Dietary metformin improved the glucose homeostasis and glucose tolerance of LMB through promoting glycolysis and de novo lipogenesis rather than glycogen deposition in the liver. However, dietary metformin did not mitigate the liver injuries (the activities of alanine aminotransferase and aspartate aminotransferase in the plasma along with histological appearance) in LMB fed high starch diets. In conclusion, our results demonstrated that dietary metformin inclusion did not mitigate the growth retardation and liver injury of LMB fed high starch diets, but improved the glucose homeostasis and glucose tolerance through promoting the glycolytic and lipogenic pathways in the liver.
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