Open AccessMitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish
Author(s) -
Lingyu Li,
Jiamin Li,
Lijun Ning,
Dongliang Lu,
Yuan Luo,
Qiang Ma,
Samwel Mchele Limbu,
Dongliang Li,
Liqiao Chen,
Irfan J. Lodhi,
Pascal Degrace,
MeiLing Zhang,
ZhenYu Du
Publication year - 2020
Publication title -
journal of nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.463
H-Index - 265
eISSN - 1541-6100
pISSN - 0022-3166
DOI - 10.1093/jn/nxaa187
Subject(s) - homeostasis , energy homeostasis , mitochondrion , beta oxidation , chemistry , glucose homeostasis , biochemistry , metabolism , fish <actinopterygii> , fatty acid , microbiology and biotechnology , biology , endocrinology , fishery , insulin resistance , insulin , receptor
Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied.
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