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Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up
Open accessAbstract
Obesity induced by high-fat (HF) feeding is associated with low-grade inflammation in peripheral tissues that predisposes to insulin resistance. Recent evidence suggests the occurrence of a similar process in the hypothalamus, which favors weight gain through impairment of leptin and insulin signaling. In addition to its implications for obesity pathogenesis, this hypothesis suggests that centrally targeted antiinflammatory therapies may prove effective in prevention and treatment of this disorder. This article highlights molecular and cellular mechanisms by which hypothalamic inflammation predisposes to diet-induced obesity.
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“Neuroinflammation in the hypothalamus has been extensively implicated in the pathogenesis of various metabolic disorders, including obesity, insulin resistance, and type 2 diabetes [1, 2].”
From The Resistin/TLR4/miR-155-5p axis: a novel signaling pathway in the onset of hypothalamic neuroinflammation (2025) · cites this paper as [1]
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“Recent evidence suggests that consumption of a HFD also induces inflammation in the hypothalamus, an effect that itself could favor weight gain by impairing the neuronal response to input from leptin and insulin (184).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [184]
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Metadata
- Authors
- Thaler, J. P., & Schwartz, M. W.
- Affiliations
- University of Washington (US)
- Corresponding author
- Schwartz, Michael W.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2010-07-23
- Volume
- 151
- Issue
- 9
- Pages
- 4109-4115
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC2940486
- OpenAlex
- W1998525855
- Cited by
- 313
- References
- 58
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 11 · 2023: 10 · 2022: 14 · 2021: 19 · 2020: 21 · 2019: 21 · 2018: 16 · 2017: 12 · 2016: 27 · 2015: 24 · 2014: 34 · 2013: 34 · 2012: 31
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrinology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association (DK052989)
- University of Washington (DK007247)
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-083042, DK068384, DK052989, R01DK052989, DK-007247, P01DK068384, R01DK090320, R01DK083042, T32DK007247)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- hypothalamic inflammation, diet-induced obesity, high-fat feeding, insulin resistance, leptin signaling, insulin signaling, obesity pathogenesis, anti-inflammatory therapy, low-grade inflammation
- MeSH terms
- Animals, Humans, Hypothalamus, Inflammation, Insulin Resistance, Models, Biological, Obesity, Weight Gain, Glucose Intolerance, Leptin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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