β‑hydroxybutyric acid as a potential therapeutic metabolite for type 2 diabetes mellitus (Review).
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and clinical observations without systematic review methodology.
PubMed 41201041 · doi:10.3892/ijmm.2025.5683
What was done
This narrative review summarizes preclinical and clinical literature examining the physiological roles, metabolic mechanisms, and therapeutic potential of beta-hydroxybutyric acid in type 2 diabetes mellitus models and patients.
What was found
The abstract reports no numerical data, effect sizes, or statistical metrics. It describes qualitative findings that beta-hydroxybutyrate modulates glucose and lipid metabolism, preserves pancreatic beta-cell integrity, mitigates insulin resistance, reduces oxidative stress and inflammation, and regulates autophagy and apoptosis, with reported impacts on body weight, fasting glucose, and memory in clinical settings.
Why it matters
Synthesizes mechanistic arguments for how ketone bodies may serve as signaling molecules rather than just alternative fuel sources in metabolic disease.
Limits
The abstract provides no quantitative data, sample sizes, or systematic search criteria. It does not evaluate potential risks such as ketoacidosis or distinguish between preclinical models and human clinical evidence.
Cited by
- supports Ketones act as signaling molecules that prompt mitochondria to repair themselves and undergo mitogenesis.