Research

Hormonal

Pharmacological inhibition of BCKDK using BT2 reduces plasma branched-chain amino acid (BCAA) and branched-chain alpha-keto acid (BCKA) levels, thereby attenuating obesity-associated insulin resistance in obese mice.

In obese individuals, high levels of branched-chain amino acids (BCAAs) and their metabolites contribute to insulin resistance. This study suggests that enhancing the body's ability to break down BCAAs (via BCKDK inhibition) improves insulin sensitivity. While BT2 is a drug, the findings support the idea that managing BCAA metabolism is key to treating obesity-related metabolic issues.

GoodSupportsHIGH confidence
Restoring BCAA catabolic flux with a pharmacological inhibitor of BCKA dehydrogenase kinase (BCKDK) (a suppressor of BCKA dehydrogenase) reduced the abundance of BCAA and BCKA and markedly attenuated IR in ob/ob mice.
Meiyi Zhou et al. · Diabetes · 2019

Why this rating

Strong experimental evidence in genetically obese (ob/ob) and diet-induced obese (DIO) mouse models with consistent results across multiple metrics.

Source

Targeting BCAA Catabolism to Treat Obesity-Associated Insulin Resistance

Meiyi Zhou et al. · Diabetes · 2019

DOI 10.2337/db18-0927

mechanism_onlyCited 311×
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DOI resolved against Crossref · corpus check 2026-06-10

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