Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome
Abstract
The relationship between stress and obesity remains elusive. In response to stress, some people lose weight, whereas others gain. Here we report that stress exaggerates diet-induced obesity through a peripheral mechanism in the abdominal white adipose tissue that is mediated by neuropeptide Y (NPY). Stressors such as exposure to cold or aggression lead to the release of NPY from sympathetic nerves, which in turn upregulates NPY and its Y2 receptors (NPY2R) in a glucocorticoid-dependent manner in the abdominal fat. This positive feedback response by NPY leads to the growth of abdominal fat. Release of NPY and activation of NPY2R stimulates fat angiogenesis, macrophage infiltration, and the proliferation and differentiation of new adipocytes, resulting in abdominal obesity and a metabolic syndrome-like condition. NPY, like stress, stimulates mouse and human fat growth, whereas pharmacological inhibition or fat-targeted knockdown of NPY2R is anti-angiogenic and anti-adipogenic, while reducing abdominal obesity and metabolic abnormalities. Thus, manipulations of NPY2R activity within fat tissue offer new ways to remodel fat and treat obesity and metabolic syndrome.
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Weight-related metabolic shifts may increase allostatic load with increased autonomic basal tone and altered HPA axis activity to affect food reward and food seeking.
“weight-related metabolic shifts may increase allostatic load with increased autonomic basal tone and altered HPA axis activity to affect food reward and food seeking”
From Role of addiction and stress neurobiology on food intake and obesity (2018) · cites this paper as Kuo et al., 2007
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- Authors
- Kuo, L. E., Kitlinska, J. B., Tilan, J. U., Li, L., Baker, S. B., Johnson, M. D., Lee, E. W., Burnett, M. S., Fricke, S. T., Kvetnansky, R., Herzog, H., & Zukowska, Z.
- Affiliations
- Georgetown University Medical Center (US)
- University of California, Los Angeles (US)
- MedStar Heart & Vascular Institute (US)
- Garvan Institute of Medical Research (AU)
- Venue
- Nature Medicine
- Published
- 2007-07
- Volume
- 13
- Issue
- 7
- Pages
- 803-811
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2085792819
- Cited by
- 656
- References
- 49
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 12 · 2023: 24 · 2022: 22 · 2021: 33 · 2020: 31 · 2019: 24 · 2018: 31 · 2017: 34 · 2016: 38 · 2015: 48 · 2014: 46 · 2013: 42 · 2012: 54
- FWCI
- 33.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health (1r03de016050-01a1)
- National Heart, Lung, and Blood Institute (HL055310, HL067357, R01HL067357)
- National Institute of Dental and Craniofacial Research (DE016050)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- neuropeptide Y, NPY2 receptor, metabolic syndrome, diet-induced obesity, glucocorticoids, sympathetic nervous system, macrophage infiltration, cold stress, aggression, obesity treatment
- MeSH terms
- Animals, Cold Temperature, Diet, Dietary Fats, Gene Expression Regulation, Male, Mice, Inbred C57BL, Mice, Nude, Neuropeptide Y, Obesity, Stress, Physiological, Up-Regulation, Gene Deletion, Receptors, Neuropeptide Y, Metabolic Syndrome, 3T3-L1 Cells, Mice, Adipose Tissue, White
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