Effects of Metabolites Derived from Guava (Psidium guajava L.) Leaf Extract Fermented by Limosilactobacillus fermentum on Hepatic Energy Metabolism via SIRT1-PGC1α Signaling in Diabetic Mice

Nutrients. 2024 Dec 24;17(1):7. doi: 10.3390/nu17010007.

Abstract

Background/objectives: Type 2 diabetes mellitus (T2DM) is considered a serious risk to public health since its prevalence is rapidly increasing worldwide despite numerous therapeutics. Insulin resistance in T2DM contributes to chronic inflammation and other metabolic abnormalities that generate fat accumulation in the liver, eventually leading to the progression of metabolic dysfunction-associated fatty liver disease (MAFLD). Recently, the possibility that microbial-derived metabolites may alleviate MAFLD through enterohepatic circulation has emerged, but the underlying mechanism remains unclear. In this research, we utilized metabolites obtained from the fermentation of guava leaf extract, which is well-known for its antidiabetic activity, to investigate their effects and mechanisms on MAFLD.

Methods: Diabetes was induced by a high-fat diet and streptozotocin injection (80 mg/kg body weight) twice in mice. Subsequently, mice whose fasting blood glucose levels were measured higher than 300 mg/dL were administered with metabolites of Limosilactobacillus fermentum (LF) (50 mg/kg/day) or guava leaf extract fermented by L. fermentum (GFL) (50 mg/kg/day) by gavage for 15 weeks.

Results: GFL supplementation mitigated hyperglycemia and hepatic insulin resistance. Moreover, GFL regulated abnormal hepatic histological changes and lipid profiles in diabetic mice. Furthermore, GFL enhanced energy metabolism by activating the sirtuin1 (SIRT1)/proliferator-activated receptor γ coactivator 1α (PGC1α)/peroxisome proliferator-activated receptor (PPAR)-α pathway in diabetic mice. Meanwhile, GFL supplementation suppressed hepatic inflammation in diabetic mice.

Conclusions: Taken together, the current study elucidated that GFL could be a potential therapeutic to ameliorate hyperglycemia and hepatic steatosis by improving SIRT1/PGC-1α/ PPAR-α-related energy metabolism in T2DM.

Keywords: energy metabolism; metabolic dysfunction-associated fatty liver disease; metabolites; probiotic fermentation; type 2 diabetes mellitus.

MeSH terms

  • Animals
  • Blood Glucose / drug effects
  • Blood Glucose / metabolism
  • Diabetes Mellitus, Experimental* / drug therapy
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / metabolism
  • Diet, High-Fat / adverse effects
  • Energy Metabolism* / drug effects
  • Fermentation*
  • Hypoglycemic Agents / pharmacology
  • Insulin Resistance
  • Liver* / drug effects
  • Liver* / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha* / metabolism
  • Plant Extracts* / pharmacology
  • Plant Leaves* / chemistry
  • Psidium* / chemistry
  • Signal Transduction* / drug effects
  • Sirtuin 1* / metabolism

Substances

  • Sirtuin 1
  • Plant Extracts
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Sirt1 protein, mouse
  • Ppargc1a protein, mouse
  • Hypoglycemic Agents
  • Blood Glucose