Camel whey protein improves diabetic liver injury by targeting ACMSD and promoting de novo NAD+ synthesis
[Display omitted] •ACMSD levels are elevated in the liver of T2DM rat and HG/PA-induced L-O2 cells.•Inhibition of ACMSD ameliorate mitochondrial function in the liver of T2DM rats and HG/PA-induced L-O2 cells.•Camel whey protein (CWP) improves diabetic liver injury by inhibiting ACMSD and enhancing...
Gespeichert in:
Veröffentlicht in: | Journal of functional foods 2023-11, Vol.110, p.105835, Article 105835 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | [Display omitted]
•ACMSD levels are elevated in the liver of T2DM rat and HG/PA-induced L-O2 cells.•Inhibition of ACMSD ameliorate mitochondrial function in the liver of T2DM rats and HG/PA-induced L-O2 cells.•Camel whey protein (CWP) improves diabetic liver injury by inhibiting ACMSD and enhancing mitochondrial function.
Diabetic liver injury is a complication of diabetes without any specific medicine approved for its effective treatment or prevention. In this research, the effect of camel whey protein (CWP) on diabetic liver injury in T2DM rats (T2DM induced by a high-fat diet) and streptozotocin along with its possible mechanism were investigated by means of transcriptome and proteomics. The results demonstrated that CWP lowered fasting blood glucose and improved abnormal blood lipid profiles in T2DM rats. CWP reduced lipid accumulation, diminished oxidative stress, and effectively improved the pathological changes in the liver of T2DM rats. Further experiments indicated that CWP intake had adjusted mitochondrial dysfunction in the livers of T2DM rats and L-O2 cells induced by high glucose (HG)/palmitic acid (PA) by inhibiting α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) expression. In conclusion, CWP can ameliorate diabetic liver injury in T2DM rats by inhibiting the expression of ACMSD, promote de novo NAD+ synthesis and enhance mitochondrial function. |
---|---|
ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2023.105835 |