Effects of high-fat diet-induced diabetes on autophagy in the murine liver: A systematic review and meta-analysis

Life Sci. 2022 Nov 15:309:121012. doi: 10.1016/j.lfs.2022.121012. Epub 2022 Sep 28.

Abstract

Aims: We conducted a meta-analysis to investigate whether diabetes induced by a high-fat diet (HFD) has the potential to alter the process of autophagy in the murine liver.

Methods: A systematic literature search was performed with electronic databases (PubMed, EMBASE, Web of Science). Study design, population, intervention, outcome, and risk of bias were analyzed. Given the availability of studies, a quantitative meta-analysis including 23 studies was performed.

Key findings: The search found 5754 articles, with 48 matching the eligibility criteria, comprising of 1033 animals. The meta-analysis showed that diabetic murines fed with HFD presented an absence of p62 degradation (SMD 4.63, 95 % CI 2.02 to 7.24, p = 0.0005; I2 = 77 %), higher expression of p-mTOR/mTOR (SMD 5.20, 95 % CI 1.00 to 9.39, p = 0.01; I2 = 78 %), and a decreased p-AMPK/AMPK ratio (SMD -2.02, 95 % CI -3.96 to -0.09, p = 0.04; I2 = 85 %) when compared to nondiabetic murines. When associated with streptozotocin, the animals presented decreased ATG-7 and LC3-II. The meta-regression results showed a decrease in autophagy responses due to increased glycemic levels, fat content, and long-term exposure to HFD, and advanced animal age. The common and species-specific protein responses were also consistent with the inhibition of autophagy.

Significance: The normal process of autophagy mechanisms in the liver is less competent after HFD consumption. The destabilization of (auto)phagolysosomes contributes to the perpetuation of diabetes, metabolic dysfunction-associated fatty liver disease, and cell death.

Keywords: Animal models; Hepatocyte; High-fat diet; Hyperglycemia; Macroautophagy.

Publication types

  • Meta-Analysis
  • Systematic Review
  • Review

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Autophagy
  • Diabetes Mellitus* / etiology
  • Diabetes Mellitus* / metabolism
  • Diet, High-Fat* / adverse effects
  • Liver / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Streptozocin / pharmacology
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • AMP-Activated Protein Kinases
  • Streptozocin
  • TOR Serine-Threonine Kinases