The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Adiponectin and the metabolic syndrome: mechanisms mediating risk for metabolic and cardiovascular disease
Abstract
PURPOSE OF REVIEW: Adiponectin is secreted exclusively by adipocytes, aggregates in multimeric forms, and circulates at high concentrations in blood. This review summarizes recent studies highlighting cellular effects of adiponectin and its role in human lipid metabolism and atherosclerosis. RECENT FINDINGS: Adiponectin is an important autocrine/paracrine factor in adipose tissue that modulates differentiation of preadipocytes and favors formation of mature adipocytes. It also functions as an endocrine factor, influencing whole-body metabolism via effects on target organs. Adiponectin multimers exert differential biologic effects, with the high-molecular-weight multimer associated with favorable metabolic effects (i.e. greater insulin sensitivity, reduced visceral adipose mass, reduced plasma triglycerides, and increased HDL-cholesterol). Adiponectin influences plasma lipoprotein levels by altering the levels and activity of key enzymes (lipoprotein lipase and hepatic lipase) responsible for the catabolism of triglyceride-rich lipoproteins and HDL. It thus influences atherosclerosis by affecting the balance of atherogenic and antiatherogenic lipoproteins in plasma, and by modulating cellular processes involved in foam cell formation. SUMMARY: Recent studies emphasize the role played by adiponectin in the homeostasis of adipose tissue and in the pathogenesis of the metabolic syndrome, type 2 diabetes, and atherosclerosis. These pleiotropic effects make it an attractive therapeutic target for obesity-related conditions.
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Cites
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Self-citationInflammation in Atherosclerosis: From Vascular Biology to Biomarker Discovery and Risk Prediction
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“In addition, the secretion of an adipokine, adiponectin, which is associated with positive metabolic and vascular effects, is reduced in obesity and may contribute to the pathogenesis of metabolic syndrome, T2DM, and atherosclerosis (Lara-Castro et al., 2007).”
BackgroundSelf-citationCorcoran, S. M., Achamallah, N., Loughlin, J. O., Stafford, P., Dicker, P., Malone, F. D., & Breathnach, F. (2018) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2017.12.051 · Cited by 40
Wang, L., Yi, W., Ma, L., Lecea, E., Hazlehurst, L. A., Adjeroh, D. A., & Hu, G. (2023) · Cancers · doi:10.3390/cancers15215148 · Cited by 17
Metadata
- Authors
- Lara-Castro, C., Fu, Y., Chung, B. H., & Garvey, W. T.
- Venue
- Current Opinion in Lipidology
- Published
- 2007-06
- Volume
- 18
- Issue
- 3
- Pages
- 263-270
- ISSN
- 0957-9672 (ISSN-L)
- OpenAlex
- W2003828583
- Cited by
- 315
- References
- 9
- FWCI
- 15.70
- Type
- journal article
- Language
- en
- Open access
- closed
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