Cited by 136Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

Adipokines as regulators of muscle metabolism and insulin sensitivityThis paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.

Dyck, David J.·2009·Applied Physiology, Nutrition, and Metabolism

Abstract

Skeletal muscle is the largest tissue responsible for the insulin-stimulated disposal of glucose. However, identifying the link between excess body fat and impaired insulin sensitivity in skeletal muscle has been difficult. Several adipose-derived cytokines (adipokines) have been implicated in the impairment of insulin sensitivity, while adipokines such as leptin and adiponectin exert an insulin-sensitizing effect. Leptin and adiponectin have each been shown to increase fatty acid (FA) oxidation and decrease triglyceride storage in muscle, which may explain, in part, the insulin-sensitizing effect of these cytokines. Recent evidence strongly implicates an increased localization of the FA transporters to the plasma membrane (PM) as an important factor in the accumulation of intramuscular lipids with high-fat diets and obesity. Perhaps suprisingly, relatively little attention has been paid to the ability of insulin-sensitizing compounds, such as leptin and adiponectin, to decrease the abundance of FA transporters in the PM, thereby decreasing lipid accumulation. In the case of both adipokines, there is also evidence that a resistance to their ability to stimulate FA oxidation in skeletal muscle develops during obesity. One of our recent studies indicates that this development can be very rapid (i.e., within days), and precedes the increase in lipid uptake and accumulation that leads to insulin resistance. It is noteworthy that leptin resistance can be modulated by both diet and training in rodents. Further studies examing the underlying mechanisms of the development of leptin and adiponectin resistance are warranted.

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Crossref · 10.1139/h09-037

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Authors
Dyck, D. J.
Affiliations
University of Guelph (CA)
Corresponding author
Dyck, David J.
Venue
Applied Physiology, Nutrition, and Metabolism
Published
2009-06
Volume
34
Issue
3
Pages
396-402
ISSN
  • 1715-5312 (ISSN-L)
  • 1715-5320
OpenAlex
W1494866272
Cited by
136
References
101
Citations by year
2026: 2 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 6 · 2020: 2 · 2019: 6 · 2018: 8 · 2017: 7 · 2016: 7 · 2015: 6 · 2014: 10 · 2013: 10 · 2012: 15
FWCI
2.37
Type
journal article
Language
en
Open access
closed
Locations
  • Applied Physiology, Nutrition, and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
adipokines, skeletal muscle metabolism, insulin sensitivity, leptin, adiponectin, insulin resistance, fatty acid oxidation, fatty acid transporters, obesity, leptin resistance, adiponectin resistance, high-fat diet, exercise training
MeSH terms
Fatty Acids, Glucose, Humans, Insulin, Muscle, Skeletal, Leptin, Adiponectin, Adipokines

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