Evidence map›Paper›PMID 40856815›Full record

ArticleActa diabetologica2026

The L-type amino acid transporter inhibitor, BCH, inhibits myotube BCAA uptake and mitochondrial function without altering myotube insulin sensitivity during insulin resistance in C2C12 myotubes.

Kipton B Travis, Kayla J Ragland, Emmalie R Spry, Toheed Zaman, Pamela M Lundin, Roger A Vaughan

Abstract read
PubMed Publisher
In one paragraph

Article in Acta diabetologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Kipton B TravisDepartment of Health and Human Performance, High Point University, One University Parkway, High Point, NC, 27262-3598, USA.
Kayla J RaglandDepartment of Health and Human Performance, High Point University, One University Parkway, High Point, NC, 27262-3598, USA.
Emmalie R SpryDepartment of Health and Human Performance, High Point University, One University Parkway, High Point, NC, 27262-3598, USA.
Toheed ZamanDepartment of Chemistry, High Point University, High Point, NC, USA.
Pamela M LundinDepartment of Chemistry, High Point University, High Point, NC, USA.
Roger A VaughanDepartment of Health and Human Performance, High Point University, One University Parkway, High Point, NC, 27262-3598, USA. rvaughan@highpoint.edu.ORCID http://orcid.org/0000-0002-4593-8807

Funding

Congdon School of Health Sciences Summer Undergraduate Research Fellowship (SURF) N/ADepartment of Health and Human Performance within the Congdon School of Health Sciences N/A
6 · The paper itself

Abstract

introductionBranched-chain amino acids (BCAA) are essential nutrients involved in protein synthesis. BCAA are absorbed via the L-type amino acid transporter (LAT1) in skeletal muscle where the majority of BCAA are metabolized. Higher circulating BCAA levels have been shown to correlate with insulin resistance. Some speculate that enhanced BCAA metabolism/disposal or reduced BCAA uptake may limit BCAA-mediated anabolic signaling and possibly improve insulin sensitivity.

aimsThis study investigated the effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), a LAT inhibitor, on metabolism and insulin sensitivity in a myotube model of insulin resistance. Because BCAA-mediated anabolic signaling has been linked with insulin resistance, we assessed if reduced BCAA uptake via LAT inhibition would improve insulin sensitivity.

methodsC2C12 myotubes were cultured in the presence and absence of insulin resistance and treated with and without BCH. Myotube metabolism was assessed via oxygen consumption, and associated gene and protein expression were assessed using qRT-PCR and Western blot, respectively. LC/MS was performed to assess the effect of each condition on extracellular BCAA accumulation. RESULTS AND

conclusionsBCH treatment and insulin resistance both increased extracellular BCAA levels which was associated with reduced protein expression/activity of BCAA catabolic enzymes. Additionally, BCH and insulin resistance were both independently associated with reduced mitochondrial function which occurred without significant changes in mitochondrial biogenesis signaling. Importantly, BCH did not alter myotube viability or insulin sensitivity, suggesting reduced metabolism was not a function of reduced viability. These observations demonstrate that reduction of BCAA uptake may not improve insulin resistance and may promote mitochondrial dysfunction.

Indexed as

Amino Acids, Branched-ChainAmino Acids, CyclicInsulin ResistanceLarge Neutral Amino Acid-Transporter 1MitochondriaMuscle Fibers, SkeletalAnimalsCell LineMice2-aminobicyclo(2,2,1)heptane-2-carboxylic acidAmino Acids, Branched-ChainAmino Acids, CyclicLarge Neutral Amino Acid-Transporter 1Amino acidsDiabetesMitochondrial dysfunctionMitochondrial metabolismSkeletal muscle

Identifiers

PMID40856815

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.