The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
The manifold role of the mitochondria in skeletal muscle insulin resistance
Open accessAbstract
PURPOSE OF REVIEW: The role of mitochondria in the development of skeletal muscle insulin resistance has been an area of intense investigation and debate for over 20 years. The mitochondria is a multifaceted organelle that plays an integral part in substrate metabolism and cellular signalling. This article aims to summarize the current findings and thought regarding the relationship between mitochondria and insulin resistance in skeletal muscle. RECENT FINDINGS: Skeletal muscle insulin resistance was earlier thought to result from deficiency in mitochondrial oxidative capacity and ectopic lipid accumulation. Recent evidence suggests that skeletal muscle insulin resistance in high-energy intake models (i.e. obesity) results primarily from disrupted mitochondrial bioenergetics and alterations in mitochondrial-associated cell signalling. These signalling pathways include reactive oxygen species and redox balance, fatty acid β-oxidation intermediates, mitochondrial derived peptides, sirtuins, microRNAs and novel nuclear-encoded, mitochondria-acting peptides. SUMMARY: The pathophysiology of skeletal muscle insulin resistance is likely multifactorial involving many coordinated physiological processes. However, it is apparent that the mitochondria play an essential role in skeletal muscle insulin sensitivity in health, ageing and in numerous metabolic diseases. Deciphering the manifold functions of the mitochondria will allow us to understand the complex relationship between mitochondria and skeletal muscle insulin resistance.
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A large number of studies have linked a reduced mitochondrial capacity to the aetiology of skeletal muscle insulin resistance and type 2 diabetes.
“Over the past decades, a large number of studies have linked a reduced mitochondrial capacity to the aetiology of skeletal muscle insulin resistance and type 2 diabetes (reviewed in [1–3]).”
From Human skeletal muscle mitochondrial dynamics in relation to oxidative capacity and insulin sensitivity (2021) · cites this paper as [1]
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“Recent evidence indicated that skeletal muscle insulin resistance in a high‐fat diet (HFD) model results from disrupted mitochondrial biogenesis and oxidative capacity (Cade, 2018).”
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“This is similar to what occurs in diabetic mice (Cade 2018; Nilsson et al. 2010) and Duchene’s muscular dystrophy (Comim et al. 2016).”
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“…that high-fat diet-induced mice exhibit a pro-inflammatory state in skeletal muscle, characterized by elevated levels of inflammatory cytokines such as TNF-α and IL-1β, along with activation of inflammatory pathways, which contribute to the progression of IR (Cade, 2018).”
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“Indeed, skeletal muscle insulin resistance in a HFD model disrupts mitochondrial biogenesis and oxidative capacity (Cade 2018).”
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“…relationship with insulin resistance: impaired mitochondrial respiration promotes intramyocellular lipid accumulation, while insulin resistance itself further depresses mitochondrial function through attenuated PGC-1 α signaling (Cade, 2018; Lee et al., 2017; Goodpaster, 2013; Holloszy, 2013).”
Metadata
- Authors
- Cade, W. T.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Cade, William Todd
- ORCID
- Cade, William Todd
- Venue
- Current Opinion in Clinical Nutrition & Metabolic Care
- Published
- 2018-07
- Volume
- 21
- Issue
- 4
- Pages
- 267-272
- ISSN
- 1363-1950 (ISSN-L)
- PMC
- PMC7001775
- OpenAlex
- W2805895816
- Cited by
- 21
- References
- 47
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 7 · 2019: 2 · 2018: 3
- FWCI
- 0.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Clinical Nutrition & Metabolic Care (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR002345)
- National Heart, Lung, and Blood Institute (R01HL107406)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK056341)
- National Center for Research Resources (UL1RR024992)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- mitochondrial dysfunction, skeletal muscle insulin resistance, mitochondrial bioenergetics, reactive oxygen species, redox homeostasis, fatty acid beta-oxidation, mitochondrial peptides, sirtuins, microRNA, obesity, ectopic fat deposition, mitochondrial oxidative capacity, aging
- MeSH terms
- Animals, Energy Metabolism, Fatty Acids, Humans, Insulin, Insulin Resistance, Mitochondria, Obesity, Peptides, Reactive Oxygen Species, Muscle, Skeletal, MicroRNAs, Sirtuins
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