The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Update on Adipocyte Hormones
Abstract
Hormones produced by adipose tissue play a critical role in the regulation of energy intake, energy expenditure, and lipid and carbohydrate metabolism. This review will address the biology, actions, and regulation of three adipocyte hormones—leptin, acylation stimulating protein (ASP), and adiponectin—with an emphasis on the most recent literature. The main biological role of leptin appears to be adaptation to reduced energy availability rather than prevention of obesity. In addition to the well-known consequences of absolute leptin deficiency, subjects with heterozygous leptin gene mutations have low circulating leptin levels and increased body adiposity. Leptin treatment dramatically improves metabolic abnormalities (insulin resistance and hyperlipidemia) in patients with relative leptin deficiency due to lipoatrophy. Leptin production is primarily regulated by insulin-induced changes of adipocyte metabolism. Dietary fat and fructose, which do not increase insulin secretion, lead to reduced leptin production, suggesting a mechanism for high-fat/high-sugar diets to increase energy intake and weight gain. ASP increases the efficiency of triacylglycerol synthesis in adipocytes leading to enhanced postprandial lipid clearance. In mice, ASP deficiency results in reduced body fat, obesity resistance, and improved insulin sensitivity. Adiponectin production is stimulated by thiazolidinedione agonists of peroxisome proliferator-activated receptor-γ and may contribute to increased insulin sensitivity. Adiponectin and leptin cotreatment normalizes insulin action in lipoatrophic insulin-resistant animals. These effects may be mediated by AMP kinase-induced fat oxidation, leading to reduced intramyocellular and liver triglyceride content. The production of all three hormones is influenced by nutritional status. These hormones, the pathways controlling their production, and their receptors are promising targets for managing obesity, hyperlipidemia, and insulin resistance.
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Paradoxical Decrease of an Adipose-Specific Protein, Adiponectin, in Obesity
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Leptin-Replacement Therapy for Lipodystrophy
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Cited by
Makki, K., Froguel, P., & Wolowczuk, I. (2013) · ISRN Inflammation · doi:10.1155/2013/139239 · Cited by 1,085
Insulin resistance: a metabolic pathway to chronic liver disease
Bugianesi, E., McCullough, A. J., & Marchesini, G. (2005) · Hepatology · doi:10.1002/hep.20920 · Cited by 900
Adiponectin regulation and function
Fang, H., & Judd, R. L. (2018) · Comprehensive physiology · doi:10.1002/cphy.c170046 · Cited by 631
Havel, P. J. (2005) · Nutrition Reviews · doi:10.1111/j.1753-4887.2005.tb00132.x · Cited by 607
Self-citationLarson-Meyer, D. E., Heilbronn, L. K., Redman, L. M., Newcomer, B. R., Frisard, M. I., Anton, S., Smith, S. R., Alfonso, A., Ravussin, E., & the Pennington CALERIE Team (2006) · Diabetes Care · doi:10.2337/dc05-2565 · Cited by 504
Metadata
- Authors
- Havel, P. J.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2004-02-01
- Volume
- 53
- Issue
- suppl_1
- Pages
- S143-S151
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2133545915
- Cited by
- 626
- References
- 19
- FWCI
- 52.67
- Type
- journal article
- Language
- en
- Open access
- closed
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