The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
The adipoinsular axis: effects of leptin on pancreatic β-cells
Abstract
The prevalence of obesity and related diabetes mellitus is increasing worldwide. Here we review evidence for the existence of an adipoinsular axis, a dual hormonal feedback loop involving the hormones insulin and leptin produced by pancreatic β-cells and adipose tissue, respectively. Insulin is adipogenic, increases body fat mass, and stimulates the production and secretion of leptin, the satiety hormone that acts centrally to reduce food intake and increase energy expenditure. Leptin in turn suppresses insulin secretion by both central actions and direct actions on β-cells. Because plasma levels of leptin are directly proportional to body fat mass, an increase of adiposity increases plasma leptin, thereby curtailing insulin production and further increasing fat mass. We propose that the adipoinsular axis is designed to maintain nutrient balance and that dysregulation of this axis may contribute to obesity and the development of hyperinsulinemia associated with diabetes.
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Cited by
Adipocytes as regulators of energy balance and glucose homeostasis
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Mechanisms of β-Cell Death in Type 2 Diabetes
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Metadata
- Authors
- Kieffer, T. J., & Habener, J. F.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2000-01-01
- Volume
- 278
- Issue
- 1
- Pages
- E1-E14
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2123857763
- Cited by
- 418
- References
- 27
- FWCI
- 21.51
- Type
- journal article
- Language
- en
- Open access
- closed
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- Kieffer, T. J., & Habener, J. F. (2000). The adipoinsular axis: effects of leptin on pancreatic β-cells. American Journal of Physiology-Endocrinology and Metabolism. https://doi.org/10.1152/ajpendo.2000.278.1.e1
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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