ArticleBMC biology2021
Age-related susceptibility to insulin resistance arises from a combination of CPT1B decline and lipid overload.
Article in BMC biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The crucial role and mechanism of insulin resistance in metabolic disease.Frontiers in endocrinology · 2023Pooled it
- Identification of Potential Biomarkers Associated with Impaired Fatty Acid Oxidation in Aged Skeletal Muscle Using Bioinformatics and Machine Learning Approaches.Biomolecules · 2026Article
- Combined Time-Restricted Feeding and Physical Exercise Attenuate ER Stress and Improve Liver Inflammation and Collagen Deposition in Aged Mice.Cell biochemistry and function · 2026Article
- Impact of sarcopenia and obesity on skeletal muscle size, gene expression, and mitochondrial function.GeroScience · 2026Article
- Integrating transcriptome and proteome profiles to compare carcass and meat quality traits between Songliao and Songlei black pigs.Frontiers in nutrition · 2026Article
- Sirt1 coordinates the mitochondrial UPR and myocellular proteostasis to preserve muscle integrity during muscle atrophy in zebrafish.Frontiers in cell and developmental biology · 2026Article
- Upregulated FASN-mediated lipogenesis in senescent macrophages contributes to liver fibrosis progression.Frontiers in immunology · 2026Article
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Modulation of endoplasmic reticulum stress-induced insulin resistance by the low-carbohydrate high-fat ketogenic diet.Frontiers in nutrition · 2025Review
- Intermedin Alleviates Diabetic Cardiomyopathy by Up-Regulating CPT-1β through Activation of the Phosphatidyl Inositol 3 Kinase/Protein Kinase B Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Saturated fatty acid concentrations are predictive of insulin sensitivity and beta cell compensation in dogs.Scientific reports · 2024Article
- Insulin Resistance: The Increased Risk of Cancers.Current oncology (Toronto, Ont.) · 2024Review
- Species-specific metabolic reprogramming in human and mouse microglia during inflammatory pathway induction.Nature communications · 2023Article
- meQTL mapping in the GENOA study reveals genetic determinants of DNA methylation in African Americans.Nature communications · 2023Article
- Age-Related Dysfunction in Proteostasis and Cellular Quality Control in the Development of Sarcopenia.Cells · 2023Review
- Increasing maternal age associates with lower placentalFrontiers in physiology · 2023Article
- AMPK as a Potential Therapeutic Target for Intervertebral Disc Degeneration.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe skeletal muscle plays a central role in glucose homeostasis through the uptake of glucose from the extracellular medium in response to insulin. A number of factors are known to disrupt the normal response to insulin leading to the emergence of insulin resistance (IR). Advanced age and a high-fat diet are factors that increase the susceptibility to IR, with lipid accumulation in the skeletal muscle being a key driver of this phenomenon. It is debated, however, whether lipid accumulation arises due to dietary lipid overload or from a decline of mitochondrial function. To gain insights into the interplay of diet and age in the flexibility of muscle lipid and glucose handling, we combined lipidomics, proteomics, mitochondrial function analysis and computational modelling to investigate young and aged mice on a low- or high-fat diet (HFD).
resultsAs expected, aged mice were more susceptible to IR when given a HFD than young mice. The HFD induced intramuscular lipid accumulation specifically in aged mice, including C18:0-containing ceramides and diacylglycerols. This was reflected by the mitochondrial β-oxidation capacity, which was upregulated by the HFD in young, but not in old mice. Conspicuously, most β-oxidation proteins were upregulated by the HFD in both groups, but carnitine palmitoyltransferase 1B (CPT1B) declined in aged animals. Computational modelling traced the flux control mostly to CPT1B, suggesting a CPT1B-driven loss of flexibility to the HFD with age. Finally, in old animals, glycolytic protein levels were reduced and less flexible to the diet.
conclusionWe conclude that intramuscular lipid accumulation and decreased insulin sensitivity are not due to age-related mitochondrial dysfunction or nutritional overload alone, but rather to their combined effects. Moreover, we identify CPT1B as a potential target to counteract age-dependent intramuscular lipid accumulation and thereby IR.
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