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Hyperleptinemia Is Required for the Development of Leptin Resistance
Open accessAbstract
Leptin regulates body weight by signaling to the brain the availability of energy stored as fat. This negative feedback loop becomes disrupted in most obese individuals, resulting in a state known as leptin resistance. The physiological causes of leptin resistance remain poorly understood. Here we test the hypothesis that hyperleptinemia is required for the development of leptin resistance in diet-induced obese mice. We show that mice whose plasma leptin has been clamped to lean levels develop obesity in response to a high-fat diet, and the magnitude of this obesity is indistinguishable from wild-type controls. Yet these obese animals with constant low levels of plasma leptin remain highly sensitive to exogenous leptin even after long-term exposure to a high fat diet. This shows that dietary fats alone are insufficient to block the response to leptin. The data also suggest that hyperleptinemia itself can contribute to leptin resistance by downregulating cellular response to leptin as has been shown for other hormones.
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“Following the switch to a HFD, wild-type and leptin-infused ob/ob mice displayed similar weight gain despite markedly higher plasma leptin levels in the former group (94).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [94]
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“wild-type mice exposed to a HFD were resistant to the ability of leptin to reduce food intake and body weight and to induce hypothalamic pSTAT3 relative to leptin-infused ob/ob mice fed a HFD.”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [94]
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Metadata
- Authors
- Knight, Z. A., Hannan, K. S., Greenberg, M. L., & Friedman, J. M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Friedman, Jeffrey M.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2010-06-29
- Volume
- 5
- Issue
- 6
- Pages
- e11376
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC2894068
- OpenAlex
- W1974838371
- Cited by
- 311
- References
- 53
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 17 · 2023: 16 · 2022: 21 · 2021: 21 · 2020: 31 · 2019: 21 · 2018: 20 · 2017: 22 · 2016: 19 · 2015: 23 · 2014: 19 · 2013: 14 · 2012: 15
- FWCI
- 7.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (DK083531)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK083531, R00DK083531, DK041096, K99DK083531, R01DK041096)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- hyperleptinemia, leptin resistance, diet-induced obesity, leptin signaling, high-fat diet, leptin sensitivity, obesity, energy homeostasis
- MeSH terms
- Animals, Energy Intake, Feeding Behavior, Mice, Inbred C57BL, Obesity, Leptin, Mice
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