Branched chain amino acids—friend or foe in the control of energy substrate turnover and insulin sensitivity?

Abstract

Branched chain amino acids (BCAA) and their derivatives are bioactive molecules with pleiotropic functions in the human body. elevated fasting blood BCAA concentrations are considered as a metabolic hallmark of obesity, insulin resistance, dyslipidaemia, nonalcoholic fatty liver disease, type 2 diabetes and cardiovascular disease. However, since increased BCAA amount is observed both in metabolically healthy and obese subjects, a question whether BCAA are mechanistic drivers of insulin resistance and its morbidities or only markers of metabolic dysregulation, still remains open. The beneficial effects of BCAA on body weight and composition, aerobic capacity, insulin secretion and sensitivity demand high catabolic potential toward amino acids and/or adequate BCAA intake. On the opposite, BCAA-related inhibition of lipogenesis and lipolysis enhancement may preclude impairment in insulin sensitivity. Thereby, the following review addresses various strategies pertaining to the modulation of BCAA catabolism and the possible roles of BCAA in energy homeostasis. we also aim to elucidate mechanisms behind the heterogeneity of ramifications associated with BCAA modulation.

The Role of Branched-Chain Amino Acids and Branched-Chain α-Keto Acid Dehydrogenase Kinase in Metabolic Disorders

“…In the end, the carbons from BCAA catabolism are either released as CO 2 or enter the tricarboxylic acid (TCA) cycle ( 1 ). Except for complete oxidation, the BCAA intermediates also underwent degradation through gluconeogenesis, lipogenesis, ketogenesis, or cholesterol synthesis pathway ( 7 ).…”

Identification of VLDL as a biomarker for prewarning of androgenic alopecia

“…This may be related to the fact that valine can be used as a marker for dyslipidemia metabolism. 6 To summarize, our findings suggest that Valine and three VLDL subfractions (M_VLDL_C, M_VLDL_P, S_VLDL_FC) are positively associated with AGA risk. Reverse MR analysis showed that AGA had no effect on these four circulating metabolites.…”

The BCKDH kinase inhibitor BT2 promotes BCAA disposal and mitochondrial proton leak in both insulin‐sensitive and insulin‐resistant C2C12 myotubes

“…Conversely, reductions in BCAA media content occurred without reduced BCKDHa phosphorylation. While this seems conflicting, BCAA metabolism is also dependent on substrate availability (including BCAA, NADH, acyl‐CoA, and others) in addition to enzyme activation (reviewed in detail elsewhere 29 ). Importantly, BT2 has previously been shown to reduce BCKDH phosphorylation in several tissues, but only increase BCAA metabolism in skeletal muscle 28 …”