The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Distinct Physiologic and Neuronal Responses to Decreased Leptin and Mild Hyperleptinemia1
Abstract
Leptin acts on specific populations of hypothalamic neurons to regulate feeding behavior, energy expenditure, and neuroendocrine function. It is not known, however, whether the same neural circuits mediate leptin action across its full biologic dose-response curve, which extends over a broad range, from low levels seen during starvation to high levels characteristic of obesity. Here, we show that the characteristic fall in leptin with fasting causes a rise in neuropeptide Y (NPY) messenger RNA (mRNA), as well as a fall in POMC and cocaine and amphetamine-regulated transcript (CART) mRNAs. Sc infusion of leptin sufficient to maintain plasma levels within the physiologic range during the fast prevents changes in the expression of these peptides, as well as changes in neuroendocrine function, demonstrating that multiple neural circuits are highly sensitive to small changes in leptin within its low physiologic range. In contrast, a modest elevation of plasma leptin above the normal fed range by constant sc infusion, which produced marked reduction in food intake and body weight, decreased NPY mRNA in the arcuate hypothalamic nucleus but did not affect the levels of mRNAs encoding the anorexigenic peptides alpha-MSH, CART or CRH. These results suggest that the dose response characteristics of leptin on hypothalamic target neurons at the level of mRNA expression are variable, with some neurons (e.g. NPY) responding across a broad dose range and others (e.g. POMC and CART) showing a limited response within the low range. These results further suggest that the central targets of leptin that mediate the transition from starvation to the fed state may be distinct from those that mediate the response to overfeeding and obesity.
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Cites
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Cited by
Adipose Tissue as an Endocrine Organ
Ahima, R. S., & Flier, J. S. (2000) · Trends in Endocrinology & Metabolism · doi:10.1016/s1043-2760(00)00301-5 · Cited by 1,608
Self-citationMetabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training
Roberts, C. K., Hevener, A. L., & Barnard, R. J. (2013) · Comprehensive Physiology · doi:10.1002/cphy.c110062 · Cited by 831
Leptin Regulation of Neuroendocrine Systems
Ahima, R. S., Saper, C. B., Flier, J. S., & Elmquist, J. K. (2000) · Frontiers in Neuroendocrinology · doi:10.1006/frne.2000.0197 · Cited by 767
Self-citationRosenbaum, M. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25977 · Cited by 575
Gonadal Hormones Determine Sensitivity to Central Leptin and Insulin
Clegg, D. J., Brown, L. M., Woods, S. C., & Benoit, S. C. (2006) · Diabetes · doi:10.2337/diabetes.55.04.06.db05-1339 · Cited by 552
Metadata
- Authors
- Ahima, R. S., Kelly, J., Elmquist, J. K., & Flier, J. S.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1999-11
- Volume
- 140
- Issue
- 11
- Pages
- 4923-4931
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2023555647
- Cited by
- 253
- References
- 39
- FWCI
- 6.94
- Type
- journal article
- Language
- en
- Open access
- closed
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