Enhanced leptin sensitivity and attenuation of diet-induced obesity in mice with haploinsufficiency of Socs3
Abstract
Leptin is an adipocyte-derived hormone that regulates energy balance and neuroendocrine function primarily by acting on specific hypothalamic pathways. Resistance to the weight reducing effects of leptin is a feature of most cases of human and rodent obesity, yet the molecular basis of leptin resistance is poorly understood. We have previously identified suppressor of cytokine signaling-3 (Socs3) as a leptin-induced negative regulator of leptin receptor signaling and potential mediator of leptin resistance. However, due to the non-viability of mice with targeted disruption of Socs3 (ref. 6), the importance of Socs3 in leptin action in vivo was unclear. To determine the functional significance of Socs3 in energy balance in vivo we undertook studies in mice with heterozygous Socs3 deficiency (Socs3(+/-)). We report here that Socs3(+/-) mice display greater leptin sensitivity than wild-type control mice: Socs3(+/-) mice show both enhanced weight loss and increased hypothalamic leptin receptor signaling in response to exogenous leptin administration. Furthermore, Socs3(+/-) mice are significantly protected against the development of diet-induced obesity and associated metabolic complications. The level of Socs3 expression is thus a critical determinant of leptin sensitivity and obesity susceptibility in vivo and this molecule is a potential target for therapeutic intervention.
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SOCS3 regulates leptin/pY-Jak2/pY-STAT3 signaling in the hypothalamus, causing leptin resistance.
“SOCS3 also regulates leptin/pY-Jak2/pY-STAT3 signaling in the hypothalamus, causing leptin resistance”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Howard et al., 2004
SOCS-3 induced via the IKKβ-NFκβ pathway during cellular inflammation can contribute to leptin resistance and has been implicated in the pathogenesis of diet-induced obesity.
“Since SOCS-3 can also be induced via the IKKβ-NFκβ pathway during cellular inflammation, this mechanism can contribute to leptin resistance in this setting (211) and has been implicated in the pathogenesis of diet-induced obesity (DIO) (87, 119, 211).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [87]
Heterozygous SOCS-3 deficient mice display increased leptin sensitivity and are protected against the development of obesity on a high-fat diet.
“heterozygous SOCS-3 deficient mice display increased leptin sensitivity and are protected against the development of obesity on a HF diet (87).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [87]
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- Authors
- Howard, J. K., Cave, B. J., Oksanen, L. J., Tzameli, I., Bjørbæk, C., & Flier, J. S.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Flier, Jeffrey S
- Venue
- Nature Medicine
- Published
- 2004-06-27
- Volume
- 10
- Issue
- 7
- Pages
- 734-738
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2024734221
- Cited by
- 490
- References
- 30
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 10 · 2023: 9 · 2022: 7 · 2021: 16 · 2020: 9 · 2019: 13 · 2018: 12 · 2017: 19 · 2016: 23 · 2015: 21 · 2014: 21 · 2013: 31 · 2012: 39
- FWCI
- 15.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- SOCS3, leptin resistance, leptin sensitivity, diet-induced obesity, energy balance, obesity susceptibility, metabolic complications
- MeSH terms
- Suppressor of Cytokine Signaling 3 Protein, Animals, Blood Glucose, Energy Intake, Dietary Fats, Energy Metabolism, Mice, Inbred C57BL, Obesity, Receptors, Cell Surface, Repressor Proteins, Transcription Factors, Leptin, Suppressor of Cytokine Signaling Proteins, Mice, Receptors, Leptin
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