Effects of short-term carbohydrate deprivation on glycolipid metabolism and hepatic lipid accumulation in mice

To investigate the effect of dietary carbohydrate levels on liver glycolipid metabolism, this study used C57BL/6J male mice receiving standard diet (CON), no-carbohydrate high-fat diet (NCD), and high-carbohydrate no-fat diet (HCD). One week after intervention, mice in the NCD group showed lower blood glucose, HbA1c and LDL-C as well as liver weight and liver index compared with the CON group. Further research found that the liver fat synthesis genes of mice in the NCD group were significantly down-regulated at the gene level, and histopathological sections showed that the livers of mice in the NCD group had less lipid accumulation. Furthermore, liver metabolomic analysis showed that primary bile acid levels and acylcarnitine levels in the liver of mice in the NCD group were significantly increased, and conversely, lysophosphatidylcholine and fatty acyl metabolites were significantly decreased. KEGG metabolic pathway analysis showed that metabolic pathways such as biosynthesis of unsaturated fatty acids and starch and sucrose metabolism were significantly inhibited in mice in the NCD group, while metabolic pathways such as primary bile acid biosynthesis, linoleic acid metabolism and glycerophospholipid metabolism were enhanced. Taken together, these results indicate that short-term carbohydrate deprivation improves blood glucose and lipid metabolism levels in mice; the molecular mechanism of action may involve inhibition of de novo lipogenesis and enhancement of bile acid metabolism. To investigate the effects of dietary carbohydrate levels on hepatic glycolipid metabolism, this study characterized the effects of short-term carbohydrate deprivation on glycolipid metabolism in mice through various methods including biochemical detection and metabolomics.