Insulin signalling and the regulation of glucose and lipid metabolism
Abstract
The epidemic of type 2 diabetes and impaired glucose tolerance is one of the main causes of morbidity and mortality worldwide. In both disorders, tissues such as muscle, fat and liver become less responsive or resistant to insulin. This state is also linked to other common health problems, such as obesity, polycystic ovarian disease, hyperlipidaemia, hypertension and atherosclerosis. The pathophysiology of insulin resistance involves a complex network of signalling pathways, activated by the insulin receptor, which regulates intermediary metabolism and its organization in cells. But recent studies have shown that numerous other hormones and signalling events attenuate insulin action, and are important in type 2 diabetes.
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Phosphorylated tyrosine residues of IRS-1 mediate association with the 85-kDa regulatory subunit of PI3K, activating the enzyme.
“The phosphorylated tyrosine residues of IRS-1 mediate an association with the 85-kDa regulatory subunit of phosphatidylinositol 3-kinase (PI3K), leading to activation of the enzyme [138–140, 143, 144].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [138]
Insulin initiates its stimulatory effect on glucose metabolism by binding to specific receptors on the muscle cell surface.
“The cellular events via which insulin initiates its stimulatory effect on glucose metabolism start with binding of the hormone to specific receptors that are present on the muscle cell surface [2, 138–140].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [138]
PI3K inhibitors impair glucose transport and block activation of glycogen synthase and HK-II expression.
“Inhibitors of PI3K impair glucose transport and block the activation of glycogen synthase and hexokinase- (HK-) II expression [138–146]”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [138]
Inhibitors of PI3K inhibit glycogen synthase activity and abolish glycogen synthesis.
“Studies [138, 150] have demonstrated convincingly that inhibitors of PI3K inhibit glycogen synthase activity and abolish glycogen synthesis.”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [138]
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References 102 · Cited by 5,326
- Authors
- Saltiel, A. R., & Kahn, C. R.
- Affiliations
- University of Michigan (US)
- Joslin Diabetes Center (US)
- Venue
- Nature
- Published
- 2001-12
- Volume
- 414
- Issue
- 6865
- Pages
- 799-806
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2014887370
- Cited by
- 5,326
- References
- 102
- Citations by year
- 2026: 160 · 2025: 179 · 2024: 210 · 2023: 160 · 2022: 209 · 2021: 247 · 2020: 228 · 2019: 265 · 2018: 313 · 2017: 284 · 2016: 264 · 2015: 304 · 2014: 291 · 2013: 268 · 2012: 269
- FWCI
- 41.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- insulin signaling, insulin resistance, type 2 diabetes, impaired glucose tolerance, glucose metabolism, lipid metabolism, insulin receptor, intermediary metabolism, obesity, polycystic ovary syndrome, hyperlipidemia, hypertension, atherosclerosis
- MeSH terms
- Adipose Tissue, Animals, Cytoskeletal Proteins, Diabetes Mellitus, Type 2, Glucose, Insulin, Insulin Resistance, Proto-Oncogene Proteins, Receptor, Insulin, Signal Transduction, Phosphatidylinositol 3-Kinases, Ubiquitin-Protein Ligases, Lipid Metabolism, Proto-Oncogene Proteins c-cbl, Mice
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