Guo · Chinese journal of integrative medicine 2026 · controlled animal and in vitro laboratory experiment · n=16 db/db mice (plus unspecified number of db/m controls) and HepG2 cell culture

Berberine Regulates Hepatic Fatty Acid Metabolism via AMPK/SIRT1/PGC-1α Pathway.

Cited 1 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal and in vitro cell culture study with no human participants

PubMed 42126802 · doi:10.1007/s11655-026-3846-0 · record verified 2026-08-26

What was done

Researchers evaluated the therapeutic effects and mechanisms of berberine on hepatic fatty acid metabolism in models of non-alcoholic fatty liver disease with type 2 diabetes mellitus. In vivo, 16 db/db mice were randomized (n=8 per group) to receive either berberine [100 mg/(kg·d)] or distilled water via gavage for 4 weeks, with db/m mice as controls. In vitro, palmitic acid- and high glucose-induced HepG2 cells were treated for 24 hours with berberine (5 µmol/L), the AMPK agonist AICAR (0.8 mmol/L), the AMPK inhibitor compound C (10 µmol/L), or a combination of berberine and compound C. Biochemical assays, pathological staining, qPCR, and Western blot were performed to assess lipid/glucose metabolism and AMPK/SIRT1/PGC-1α signaling pathway targets.

What was found

The abstract reports directions of effect and significance levels without raw numerical values or baseline figures. In vivo, berberine-treated mice showed lower TG, TC, LDL-C, fasting blood glucose, and liver lipid accumulation, with improved insulin sensitivity (P<0.05 or P<0.01). In liver tissues, berberine decreased FASN protein expression and fatp5 and CD36 mRNA expressions, while increasing ACSL1 and CPT1A protein levels and CPT1A, CPT2, SCAD, LCAD, and VLCAD mRNA levels (P<0.05). Hepatic AMPK/SIRT1/PGC-1α pathway activation was increased (P<0.05 or P<0.01). In vitro, berberine reduced lipid accumulation and activated the AMPK/SIRT1/PGC-1α pathway, effects that were reversed by compound C (P<0.05 or P<0.01).

Why it matters

The findings identify activation of the AMPK/SIRT1/PGC-1α pathway as a mechanism through which berberine modulates hepatic fatty acid synthesis, transport, and β-oxidation in diabetic fatty liver models.

Limits

This is purely preclinical animal and in vitro research, precluding direct clinical conclusions for humans. The abstract omits exact numerical values, effect sizes, variance estimates, and the exact sample size for the db/m control group. Cellular findings were restricted to an immortalized cell line (HepG2).

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