4.6 Article

Time-Restricted Feeding Could Not Reduce Rainbow Trout Lipid Deposition Induced by Artificial Night Light

期刊

METABOLITES
卷 12, 期 10, 页码 -

出版社

MDPI
DOI: 10.3390/metabo12100904

关键词

artificial night light; feeding regime; lipid metabolism; serum metabolites; rainbow trout

资金

  1. National Key Research and Development Program of China [2019YFD0901000]
  2. K.C. Wong Magna Fund in Ningbo University

向作者/读者索取更多资源

Artificial night light can disrupt circadian rhythm and lipid metabolism, while time-restricted feeding helps maintain metabolic homeostasis. This study found that continuous light exposure led to lipid accumulation and decreased levels of long-chain polyunsaturated fatty acids in juvenile rainbow trout. However, time-restricted feeding failed to alleviate these negative effects.
Artificial night light (ALAN) could lead to circadian rhythm disorders and disrupt normal lipid metabolism, while time-restricted feeding (TRF) could maintain metabolic homeostasis. In mammals, TRF has been demonstrated to have extraordinary effects on the metabolic regulation caused by circadian rhythm disorders, but studies in lower vertebrates such as fish are still scarce. In this study, the impacts of ALAN on the body composition and lipid metabolism of juvenile rainbow trout were investigated by continuous light (LL) exposure as well as whether TRF could alleviate the negative effects of LL. The results showed that LL upregulated the expression of lipid synthesis (fas and srebp-1c) genes and suppressed the expression of lipid lipolysis (ppar beta, cpt-1a, and lpl) genes in the liver, finally promoting lipid accumulation in juvenile rainbow trout. However, LL downregulated the expression of genes (Delta 6-fad, Delta 9-fad, elovl2, and elovl5) related to long-chain polyunsaturated fatty acid (LC-PUFA) synthesis, resulting in a significant decrease in the proportion of LC-PUFA in the dorsal muscle. In serum, LL led to a decrease in glucose (Glu) levels and an increase in triglyceride (TG) and high-density lipoprotein cholesterol (H-DLC) levels. On the other hand, TRF (mid-dark stage feeding (D)) and mid-light stage feeding (L)) upregulated the expression of both the lipid synthesis (srebp-1c and ppar gamma), lipolysis (ppar alpha, ppar beta, and cpt-1a), and lipid transport (cd36/fat and fatp-1) genes, finally increasing the whole-body lipid, liver protein, and lipid content. Meanwhile, TRF (D and L groups) increased the proportion of polyunsaturated fatty acid (PUFA) and LC-PUFA in serum. In contrast, random feeding (R group) increased the serum Glu levels and decreased TG, total cholesterol (T-CHO), and H-DLC levels, suggesting stress and poor nutritional status. In conclusion, ALAN led to lipid accumulation and a significant decrease in muscle LC-PUFA proportion, and TRF failed to rescue these negative effects.

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