Tier 3 — preclinical

Fisetin Alleviates Hepatic and Adipocyte Fibrosis and Insulin Resistance in Diet-Induced Obese Mice

Myung-Sook Choi, Ji-Young Choi, Eun-Young Kwon
Journal of Medicinal Food 2020 23(10):1019–1032

Bibliography

PubMed
PMID 32856978
DOI
10.1089/jmf.2019.4619
Funding
Supported by the BK21 Plus Program at Kyungpook National University and National Research Foundation of Korea grants NRF-2020R1I1A3074694 and NRF-2019R1C1C1009530.
Competing interests
The authors reported no competing financial interests.

Study snapshot

DesignControlled 16-week dietary intervention in diet-induced obese mice.
ModelMale C57BL/6J mice assigned to normal-fat diet, high-fat diet, or high-fat diet plus fisetin.
Sample39 mice total; n=13 per group.
InterventionHigh-fat diet containing 0.02% (w/w) fisetin versus high-fat diet alone and normal-fat control.
Duration16 weeks.
EndpointsBody weight and adiposity; Hepatic steatosis and fibrosis; Adipose fibrosis; Insulin resistance and glucose regulation; Inflammatory cytokines and oxidative stress; Brown adipose and skeletal-muscle metabolic gene expression

What the study showed, in plain terms

Researchers fed mice a high-fat diet for 16 weeks, with or without a small amount of fisetin mixed into the diet. Fisetin-treated mice gained less body fat and showed improvements across liver fat, tissue fibrosis, inflammation and insulin-resistance markers.

The study provides a broad preclinical metabolic rationale for fisetin, but it is a mouse experiment. It cannot establish that fisetin causes weight loss, reverses fatty liver, or treats insulin resistance in humans.

Key findings

  • Fisetin reduced body weight, white-adipose mass and adipocyte size despite increased food intake relative to high-fat-diet controls.
  • Hepatic steatosis, inflammatory signaling and extracellular-matrix accumulation were reduced.
  • Insulin resistance improved alongside changes in pancreatic islet function, hepatic gluconeogenesis and adipokine signaling.

What this study can and cannot tell us

  • Mouse model only; human bioavailability, dose equivalence and clinical efficacy are unknown.
  • Male mice only, limiting assessment of sex-specific effects.
  • The dietary fisetin exposure and controlled high-fat-diet model do not directly reproduce human supplementation or obesity.

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology