Summary
This narrative review examines the emerging evidence that dysfunctional branched-chain amino acid catabolism contributes to metabolic disturbances in obesity and type 2 diabetes. The authors synthesise findings from in vitro and animal studies demonstrating that modulation of BCAA catabolic pathways alters glucose homeostasis, whilst acknowledging that integrated understanding of tissue-specific BCAA catabolism in humans remains limited. The review considers whether enhancing BCAA catabolism represents a viable therapeutic approach to improve metabolic health in insulin resistance and type 2 diabetes.
Regional applicability
The review examines mechanistic pathways applicable across populations with obesity and type 2 diabetes. Findings would be relevant to United Kingdom dietary and clinical practice, though most evidence cited is from animal models and proof-of-concept human studies; translation to practical dietary or pharmacological interventions in UK populations would require additional evidence.
Key measures
Plasma BCAA levels, glucose homeostasis, insulin resistance, BCAA catabolic pathway modulation, tissue-specific BCAA catabolism
Outcomes reported
The review examines the role of branched-chain amino acid (BCAA) catabolism in metabolic disturbances associated with obesity and type 2 diabetes, and evaluates whether enhancing BCAA catabolism could serve as a therapeutic strategy. It synthesises evidence from in vitro, animal, and human studies on tissue-specific BCAA metabolism and its relationship to insulin resistance and glucose homeostasis.
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