ArticlePhysiological reports2021
Effects of ketoisocaproic acid and inflammation on glucose transport in muscle cells.
Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Sex differences in cachexia outcomes and branched-chain amino acid metabolism following chemotherapy in aged mice.PloS one · 2026Article
- Myofibrillar protein accumulation but reduced protein synthesis in PDCD4-depleted myotubes.PloS one · 2026Article
- Primary Roles of Branched Chain Amino Acids (BCAAs) and Their Metabolism in Physiology and Metabolic Disorders.Molecules (Basel, Switzerland) · 2024Review
- Sex differences in cachexia and branched-chain amino acid metabolism following chemotherapy in mice.Physiological reports · 2024Article
- Elevated BCAA catabolism reverses the effect of branched-chain ketoacids on glucose transport in mTORC1-dependent manner in L6 myotubes.Journal of nutritional science · 2024Article
- Article
- Branched-Chain Amino Acids and Insulin Resistance, from Protein Supply to Diet-Induced Obesity.Nutrients · 2022Review
- Impact of Feeding Probiotics on Blood Parameters, Tail Fat Metabolites, and Volatile Flavor Components of Sunit Sheep.Foods (Basel, Switzerland) · 2022Article
- The mechanism of branched-chain amino acid transferases in different diseases: Research progress and future prospects.Frontiers in oncology · 2022Review
- Branched-chain Amino Acids: Catabolism in Skeletal Muscle and Implications for Muscle and Whole-body Metabolism.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Branched-chain amino acids (BCAAs) are regulators of protein metabolism. However, elevated levels of BCAAs and their metabolites are linked to insulin resistance. We previously demonstrated that the leucine metabolite, α-ketoisocaproate (KIC), inhibited insulin-stimulated glucose transport in myotubes. Like KIC, inflammatory factors are implicated in the development of insulin resistance. Here, we analyzed the effect of KIC and inflammatory factors (homocysteine [50 μM], TNF-α [10 ng/ml], and interleukin 6 (IL-6) [10 ng/ml]) on myotubes. Although KIC suppressed insulin-stimulated glucose transport, addition of the inflammatory factors did not worsen this effect. Depletion of branched-chain aminotransferase 2, the enzyme that catalyzes the conversion of leucine into KIC, abrogated the effect of KIC and the inflammatory factors. The effect of insulin on AKT
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.