4.7 Article

Diosgenin Ameliorated Type II Diabetes-Associated Nonalcoholic Fatty Liver Disease through Inhibiting De Novo Lipogenesis and Improving Fatty Acid Oxidation and Mitochondrial Function in Rats

Journal

NUTRIENTS
Volume 14, Issue 23, Pages -

Publisher

MDPI
DOI: 10.3390/nu14234994

Keywords

Diosgenin; non-alcoholic fatty liver disease; de novo lipogenesis; fatty acid beta-oxidation; mitochondrial fission and apoptosis

Funding

  1. Student's Platform for Innovation and Entrepre-neurship Training Program
  2. Science and Technology Plan Project of Shaanxi Province
  3. [S202110712619]
  4. [X2021107122054]
  5. [2020NY-106]

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The present study suggests that Diosgenin (DIO) protects against type II diabetes-associated nonalcoholic fatty liver disease (D-NAFLD) by inhibiting hepatic de novo lipogenesis, improving dyslipidemia, and enhancing mitochondrial function.
Diosgenin (DIO) is a dietary and phytochemical steroidal saponin representing multiple activities. The present study investigated the protective effect of DIO on type II diabetes-associated nonalcoholic fatty liver disease (D-NAFLD). The rat model was established by high-fat diet and streptozotocin injection and then administered DIO for 8 weeks. The results showed that DIO reduced insulin resistance index, improved dyslipidemia, and relieved pancreatic damage. DIO decreased hepatic injury markers, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT). H & E staining showed that DIO relieved hepatic lipid deposition. Mechanistically, DIO inhibited hepatic de novo lipogenesis (DNL) and increased fatty acid beta-oxidation (FAO) through regulation of the AMPK-ACC/SREBP1 pathway. Endoplasmic reticulum (ER) stress was inhibited by DIO through regulation of PERK and IRE1 arms, which may then inhibit DNL. DIO also decreased reactive oxygen species (ROS) and enhanced the antioxidant capacity via an increase in Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx) activities. The mitochondria are the site for FAO, and ROS can damage mitochondrial function. DIO relieved mitochondrial fission and fusion disorder by inhibiting DRP1 and increasing MFN1/MFN2 expressions. Mitochondrial apoptosis was then inhibited by DIO. In conclusion, the present study suggests that DIO protects against D-NAFLD by inhibiting DNL and improving FAO and mitochondrial function.

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