Skip to content

Study · Measured the body's own peptide · 2023

1 result

The specific mitochondrial unfolded protein response in fast- and slow-twitch muscles of high-fat diet-induced insulin-resistant rats.

Li C, Li N, Zhang Z, Song Y, Li J, Wang Z, Bo H, Zhang Y

Frontiers in endocrinology16 Mar 2023Cited by 5 (Europe PMC)

PMID37008907 (opens in a new tab)PMCIDPMC10061072 (opens in a new tab)DOI10.3389/fendo.2023.1127524 (opens in a new tab)PepBankPUB-37008907
Download PDFPubMedAsk about this study
Jump to 1 result

Summary

IntroductionSkeletal muscle insulin resistance (IR) plays an important role in the pathogenesis of type 2 diabetes mellitus. Skeletal muscle is a heterogeneous tissue composed of different muscle fiber types that contribute distinctly to IR development. Glucose transport shows more protection in slow-twitch muscles than in fast-twitch muscles during IR development, while the mechanisms involved remain unclear. Therefore, we investigated the role of the mitochondrial unfolded protein response (UPRmt) in the distinct resistance of two types of muscle in IR.MethodsMale Wistar rats were divided into high-fat diet (HFD) feeding and control groups. We measured glucose transport, mitochondrial respiration, UPRmt and histone methylation modification of UPRmt-related proteins to examine the UPRmt in the slow fiber-enriched soleus (Sol) and fast fiber-enriched tibialis anterior (TA) under HFD conditions.ResultsOur results indicate that 18 weeks of HFD can cause systemic IR, while the disturbance of Glut4-dependent glucose transport only occurred in fast-twitch muscle. The expression levels of UPRmt markers, including ATF5, HSP60 and ClpP, and the UPRmt-related mitokine MOTS-c were significantly higher in slow-twitch muscle than in fast-twitch muscle under HFD conditions. Mitochondrial respiratory function is maintained only in slow-twitch muscle. Additionally, in the Sol, histone methylation at the ATF5 promoter region was significantly higher than that in the TA after HFD feeding.ConclusionThe expression of proteins involved in glucose transport in slow-twitch muscle remains almost unaltered after HFD intervention, whereas a significant decline of these proteins was observed in fast-twitch muscle. Specific activation of the UPRmt in slow-twitch muscle, accompanied by higher mitochondrial respiratory function and MOTS-c expression, may contribute to the higher resistance to HFD in slow-twitch muscle. Notably, the different histone modifications of UPRmt regulators may underlie the specific activation of the UPRmt in different muscle types. However, future work applying genetic or pharmacological approaches should further uncover the relationship between the UPRmt and insulin resistance.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Other

    In rats fed a high-fat diet, MOTS‑c expression was higher in slow-twitch soleus muscle than in fast-twitch tibialis anterior muscle.

    In plain wordsIn rats fed a high-fat diet, the body's own MOTS‑c was higher in slow-twitch muscle than in fast-twitch muscle.

    Peptide
    MOTS-c
    Outcome
    IncreaseMOTS-c expression in slow-twitch vs fast-twitch muscle
    Study

    ratn: not reported in source

    High-fat diet-induced insulin resistance; soleus and tibialis anterior
    Comparator
    Fast-twitch muscle (tibialis anterior)
    Outcome group
    Mitochondrial function · Metabolic and weight

    Source sentences

    Summary
    The expression levels of UPRmt markers, including ATF5, HSP60 and ClpP, and the UPRmt-related mitokine MOTS-c were significantly higher in slow-twitch muscle than in fast-twitch muscle under HFD conditions.
    2 context sentences
    Summary · context
    Male Wistar rats were divided into high-fat diet (HFD) feeding and control groups.
    Summary · context
    We measured glucose transport, mitochondrial respiration, UPRmt and histone methylation modification of UPRmt-related proteins to examine the UPRmt in the slow fiber-enriched soleus (Sol) and fast fiber-enriched tibialis anterior (TA) under HFD conditions.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.