Obesity is associated with hypothalamic injury in rodents and humans.
Open accessAbstract
Rodent models of obesity induced by consuming high-fat diet (HFD) are characterized by inflammation both in peripheral tissues and in hypothalamic areas critical for energy homeostasis. Here we report that unlike inflammation in peripheral tissues, which develops as a consequence of obesity, hypothalamic inflammatory signaling was evident in both rats and mice within 1 to 3 days of HFD onset, prior to substantial weight gain. Furthermore, both reactive gliosis and markers suggestive of neuron injury were evident in the hypothalamic arcuate nucleus of rats and mice within the first week of HFD feeding. Although these responses temporarily subsided, suggesting that neuroprotective mechanisms may initially limit the damage, with continued HFD feeding, inflammation and gliosis returned permanently to the mediobasal hypothalamus. Consistent with these data in rodents, we found evidence of increased gliosis in the mediobasal hypothalamus of obese humans, as assessed by MRI. These findings collectively suggest that, in both humans and rodent models, obesity is associated with neuronal injury in a brain area crucial for body weight control.
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Multiple studies have demonstrated that microglia number increases within the mediobasal hypothalamus during diet induced obesity.
“Multiple studies have demonstrated that microglia number increases within the mediobasal hypothalamus during diet induced obesity (Thaler et al., 2012; de Kloet et al., 2014; Valdearcos et al., 2014; Schur et al., 2015; Waise et al., 2015; Baufeld et al., 2016; Guillemot-Legris et al., 2016).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Thaler et al., 2012
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References 45 · Cited by 1,857
Research works printed but not linked: 1
- [20]Posey K, et al. Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet. Am J Physiol Endocrinol Metab. 2009;296(5):E1003–E1012. doi: 10.1152/ajpendo.90377.2008. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
- Authors
- Thaler, J. P., Yi, C.-X., Schur, E. A., Guyenet, S. J., Hwang, B. H., Dietrich, M. O., Zhao, X., Sarruf, D. A., Izgur, V., Maravilla, K. R., Nguyen, H. T., Fischer, J. D., Matsen, M. E., Wisse, B. E., Morton, G. J., Horvath, T. L., Baskin, D. G., Tschöp, M. H., & Schwartz, M. W.
- Affiliations
- University of Washington (US)
- University of Cincinnati (US)
- Yale University (US)
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2012-01-03
- Volume
- 122
- Issue
- 1
- Pages
- 153-162
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3248304
- OpenAlex
- W2154696002
- Cited by
- 1,857
- References
- 45
- Citations by year
- 2026: 104 · 2025: 118 · 2024: 140 · 2023: 128 · 2022: 139 · 2021: 175 · 2020: 154 · 2019: 153 · 2018: 139 · 2017: 132 · 2016: 116 · 2015: 113 · 2014: 107 · 2013: 87 · 2012: 48
- FWCI
- 35.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Site cant be reached (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs
- Office of Research and Development
- University of Washington (DK‐035816)
- Novo Nordisk
- National Institutes of Health (1u24dk076126-01, 5r01dk077975-05, DK-035816, DK077975, DK017047, DK076126)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK074758, DK-083042, DK017047, U24-DK076126, DK068384, DK 035816, DK052989, DP1DK098058, DK-077975, DK-080000, R01DK052989, K08DK088872, P01DK068384, R01DK080000, R01-DK-077975, R01DK090320, DK088872, P30DK035816, P30DK017047, R01DK083042)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- obesity, hypothalamus, hypothalamic inflammation, high-fat diet, reactive gliosis, neuronal injury, arcuate nucleus, mediobasal hypothalamus, energy homeostasis, neuroinflammation
- MeSH terms
- Adolescent, Adult, Animals, Base Sequence, Female, Gliosis, Humans, Hypothalamus, Inflammation, Male, Mice, Inbred C57BL, Middle Aged, Neurons, Obesity, RNA, Messenger, Time Factors, Signal Transduction, Cytokines, NF-kappa B, Rats, Long-Evans, Mice, Rats, Young Adult, Diet, High-Fat
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