Tier 3 — preclinical

Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I: a mechanism for the action of berberine to activate AMP-activated protein kinase and improve insulin action

Turner N, Li JY, Gosby A, To SW, Cheng Z, Miyoshi H, Taketo MM, Cooney GJ, Kraegen EW, James DE, Hu LH, Li J, Ye JM
Diabetes 2008 57(5):1414-1418

Bibliography

PubMed
PMID 18285556
Funding
Funding was not established from the accessible source; this is not a declaration of no funding.
Competing interests
A complete competing-interest declaration was not available in the accessible source; no absence of conflicts is inferred.

Study snapshot

DesignAnimal and/or cellular experimental study
ModelMuscle-cell models, isolated mitochondria and high-fat-fed rodents
SampleMyotube/mitochondrial experiments and high-fat-fed rodents
InterventionBerberine and dihydroberberine with respiratory-chain measurements
DurationExperimental periods vary by assay
EndpointsCellular or animal mechanisms; Model-specific outcomes; Route and exposure

What the study showed, in plain terms

The paper links complex-I inhibition with AMPK activation and improved insulin action in experimental models.

Key findings

  • The paper links complex-I inhibition with AMPK activation and improved insulin action in experimental models.

What this study can and cannot tell us

Rodent and cellular pathways do not validate a human dose or demonstrate that dihydroberberine improves clinical outcomes.

Source detail: indexed abstract and bibliographic record; unavailable methods or disclosures are identified rather than assumed.

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