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.

Broad beans, natural sources of L-DOPA and bioactive phenolics show promise for Parkinson’s disease intervention. This study investigated broad bean extracts’ protective mechanisms against PD pathogenesis. Among screened varieties, QC25 extract exhibited optimal protection in MPP⁺-injured PC12 cells, improving viability, reducing LDH release, and mitigating cell cycle arrest. QC25 extract rescued mitochondrial dysfunction by suppressing ROS, restoring membrane potential, normalizing Ca²⁺ homeostasis, and recovering ATP synthesis. Metabolomics identified glycerophospholipid metabolism as the core protective pathway, mediating mitochondrial membrane stabilization. QC25 extract further activated PINK1/Parkin-mediated mitophagy, upregulating PINK1 and Parkin expression. Crucially, 6-gingerol—uniquely detected in QC25 extract—synergized with L-DOPA, enhancing cell viability and amplifying mitophagy through complementary mitochondrial repair mechanisms. These findings demonstrate QC25 broad bean variety exerts’ protective effects on PD model cells by regulating mitochondrial function and mitophagy, and its unique component 6-gingerol synergizes with L-DOPA to strengthen these effects. This study provides a theoretical basis for the development of QC25 as a functional food ingredient for neurological health maintenance.