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Roles for leptin receptor/STAT3-dependent and -independent signals in the regulation of glucose homeostasis
Open accessAbstract
Leptin activates the long form of the leptin receptor (LRb) to control feeding and neuroendocrine function and thus regulate adiposity. While adiposity influences insulin sensitivity, leptin also regulates glucose homeostasis independently of energy balance. Disruption of the LRb/STAT3 signal in s/s mice results in hyperphagia, neuroendocrine dysfunction, and obesity similar to LRb null db/db mice. Insulin resistance and glucose intolerance are improved in s/s compared to db/db animals, however, suggesting that LRb/STAT3-independent signals may contribute to the regulation of glucose homeostasis by leptin. Indeed, caloric restriction normalized glycemic control in s/s animals, but db/db mice of similar weight and adiposity remained hyperglycemic. These differences in glucose homeostasis were not attributable to differences in insulin production between s/s and db/db animals but rather to decreased insulin resistance in s/s mice. Thus, in addition to LRb/STAT3-mediated adiposity signals, non-LRb/STAT3 leptin signals mediate an important adiposity-independent role in promoting glycemic control.
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“However, the phenotype of these s/s mice does not completely mimic that of either ob/ob or db/db mice with respect to glucose metabolism, immune function or reproduction (13, 14), implying that other LepRb signals must also contribute to leptin action.”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [13]
In the citing paper
“leptin receptor-mediated STAT3 signaling appears to be critical for energy homeostasis, but not for glucose homeostasis.”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [13]
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Metadata
- Authors
- Bates, S. H., Kulkarni, R. N., Seifert, M., & Myers, M. G.
- Affiliations
- University of Michigan (US)
- Joslin Diabetes Center (US)
- Corresponding author
- Myers, Martin G.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2005-03
- Volume
- 1
- Issue
- 3
- Pages
- 169-178
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2122551774
- Cited by
- 173
- References
- 47
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 1 · 2021: 5 · 2020: 11 · 2019: 5 · 2018: 11 · 2017: 14 · 2016: 7 · 2015: 6 · 2014: 7 · 2013: 10 · 2012: 11
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service (56731)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 57768, R01DK057768)
- 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
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- leptin, leptin receptor, STAT3 signaling, glucose homeostasis, insulin resistance, impaired glucose tolerance, db/db mice, caloric restriction, hyperphagia, neuroendocrine dysfunction, obesity
- MeSH terms
- Animals, Body Composition, Body Weight, DNA-Binding Proteins, Glucose, Homeostasis, Hyperglycemia, Insulin Resistance, Male, Mice, Mutant Strains, Receptors, Cell Surface, Signal Transduction, Trans-Activators, Amino Acid Substitution, Caloric Restriction, STAT3 Transcription Factor, Mice, Receptors, Leptin
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