Pathways leading to muscle insulin resistance – The muscle – fat connection
Abstract
Type 2 diabetes is a heterogeneous disease characterized by hyperglycemia and insulin resistance in peripheral tissues such as adipose tissue and skeletal muscle. This review focuses on obesity as one of the major environmental factors contributing to the development of diabetes. It has become evident that adipose tissue represents an active secretory organ capable of releasing a variety of cytokines such as TNFalpha, IL-6, adiponectin and other still unknown factors that might constitute the missing link between adipose tissue and insulin resistance. In fact, adipocyte-derived factors are significantly increased in obesity and represent good predictors of the development of type 2 diabetes. The negative crosstalk between adipocytes and skeletal muscle cells leads to disturbances in muscle cell insulin signalling and insulin resistance involving major pathways in inflammation, cellular stress and mitogenesis. Positive regulators of insulin sensitivity include the adipocyte hormone adiponectin and inhibitors of inflammatory pathways such as JNK-, IKK- and ERK-inhibitors. In summary, a better knowledge of intracellular and intercellular mechanisms by which adipose tissue affects skeletal muscle cell physiology may help to develop new strategies for diabetes treatment.
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Increased stress kinase activity has been implicated in contributing to serine phosphorylation of IRS-1 and subsequent impairment of tyrosine phosphorylation.
“Increased stress kinase activity also has been implicated in contribute to the serine phosphorylation of IRS-1 and subsequent impairment tyrosine phosphorylation [177, 178].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [178]
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- Authors
- Sell, H., Eckel, J., & Dietze-Schroeder, D.
- Affiliations
- Deutsches Diabetes-Zentrum e.V. (DE)
- Venue
- Archives of Physiology and Biochemistry
- Publisher
- Informa UK Limited
- Published
- 2006-01
- Volume
- 112
- Issue
- 2
- Pages
- 105-113
- ISSN
- 0778-3124 (ISSN-L)
- 1381-3455
- 1744-4160
- OpenAlex
- W2142811280
- Cited by
- 61
- References
- 97
- Citations by year
- 2026: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 4 · 2017: 1 · 2016: 1 · 2014: 3 · 2013: 8 · 2012: 4
- FWCI
- 4.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of Physiology and Biochemistry (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
- skeletal muscle insulin resistance, type 2 diabetes, obesity, adipose tissue, adipokines, adiponectin, TNF-α, interleukin-6, inflammation, insulin signaling, cellular stress, mitogenesis, JNK inhibitor, IKK inhibitor, ERK inhibitor, diabetes treatment
- MeSH terms
- Diabetes Mellitus, Type 2, Insulin Resistance, Models, Biological, Obesity, Cytokines, Adipocytes, Muscle, Skeletal
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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