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Cited by 322Adipokines, Inflammation, and Metabolic DiseasesRegulation of Appetite and ObesityTryptophan and brain disorders

The DOI matches its Crossref record; 225 of the 225 references it cites were found in a registry or an index.

Metabolic disturbances connecting obesity and depression

Open access
Hryhorczuk, Cecile, Sharma, Sandeep, Fulton, Stephanie E.·2013·Frontiers in Neuroscience
DOI 10.3389/fnins.2013.00177PMC PMC3791387
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Abstract

Obesity markedly increases the odds of developing depression. Depressed mood not only impairs motivation, quality of life and overall functioning but also increases the risks of obesity complications. Abdominal obesity is a better predictor of depression and anxiety risk than overall adipose mass. A growing amount of research suggests that metabolic abnormalities stemming from central obesity that lead to metabolic disease may also be responsible for the increased incidence of depression in obesity. As reviewed here, a higher mass of dysfunctional adipose tissue is associated with several metabolic disturbances that are either directly or indirectly implicated in the control of emotions and mood. To better comprehend the development of depression in obesity, this review pulls together select findings addressing the link between adiposity, diet and negative emotional states and discusses the evidence that alterations in glucocorticoids, adipose-derived hormones, insulin and inflammatory signaling that are characteristic of central obesity may be involved.

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Crossref · 10.3389/fnins.2013.00177

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Figure 1 Metabolic signals and disturbances linking obesity and abdominal adiposity with depression. Central obesity and related metabolic changes correlate positively with depression. Excessive intake of foods high in saturated fat promotes weight gain, visceral fat accumulation and increased risk of depressed mood. Endocrine changes associated with abdominal obesity include hypothalamic-pituitary-adrenal (HPA) dysregulation and altered plasma levels of cortisol, leptin, adiponectin, resistin and insulin—hormones implicated in the central control of emotion and mood. Obesity-induced impairments in brain glucocorticoids (GCs), leptin and insulin receptor signaling are posited to link hypercortisolemia and leptin and insulin resistance to depression. Central fat accumulation also stimulates the release of inflammatory cytokines (e.g., tumour necrosis factor-α, interleukin-1β) and signals (C-reactive protein) that can promote neuroinflammatory responses and depressive behavior. Increased entry of saturated free fatty acids into the brain may also propagate neuroinflammation, leptin/insulin resistance and, consequently, depression. In parallel, increased vulnerability to external stressors, negative emotional states and adverse cognitive style (e.g., poor self-image) associated with overweight and obesity can potentiate consumption of energy-dense “comfort” foods to fuel a vicious cycle of central obesity, metabolic dysfunction and depression. This figure was produced using Servier Medical Art.
Figure 1 Metabolic signals and disturbances linking obesity and abdominal adiposity with depression. Central obesity and related metabolic changes correlate positively with depression. Excessive intake of foods high in saturated fat promotes weight gain, visceral fat accumulation and increased risk of depressed mood. Endocrine changes associated with abdominal obesity include hypothalamic-pituitary-adrenal (HPA) dysregulation and altered plasma levels of cortisol, leptin, adiponectin, resistin and insulin—hormones implicated in the central control of emotion and mood. Obesity-induced impairments in brain glucocorticoids (GCs), leptin and insulin receptor signaling are posited to link hypercortisolemia and leptin and insulin resistance to depression. Central fat accumulation also stimulates the release of inflammatory cytokines (e.g., tumour necrosis factor-α, interleukin-1β) and signals (C-reactive protein) that can promote neuroinflammatory responses and depressive behavior. Increased entry of saturated free fatty acids into the brain may also propagate neuroinflammation, leptin/insulin resistance and, consequently, depression. In parallel, increased vulnerability to external stressors, negative emotional states and adverse cognitive style (e.g., poor self-image) associated with overweight and obesity can potentiate consumption of energy-dense “comfort” foods to fuel a vicious cycle of central obesity, metabolic dysfunction and depression. This figure was produced using Servier Medical Art.CC BY · PubMed Central

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  1. Liu J. Garza J. C. Bronner J. Kim C. S. Zhang W. Lu X. Y. (2010b). Acute administration of leptin produces anxiolytic-like effects: a comparison with fluoxetine. Psychopharmacology (Berl.) 207, 535– 545 10.1007/s00213-009-1684-3 19823809 PMC4057895 · DOI

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Metadata

Authors
Hryhorczuk, C., Sharma, S., & Fulton, S. E.
Affiliations
Université de Montréal (CA)
Corresponding author
Fulton, Stephanie E.
ORCID
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2013
Volume
7
Pages
177-177
ISSN
1662-453X (ISSN-L)
DOI
10.3389/fnins.2013.00177
PMC
PMC3791387
OpenAlex
W2100391099
Cited by
322
References
225
Citations by year
2026: 18 · 2025: 30 · 2024: 22 · 2023: 20 · 2022: 28 · 2021: 27 · 2020: 32 · 2019: 35 · 2018: 17 · 2017: 21 · 2016: 20 · 2015: 26 · 2014: 26
FWCI
2.85
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
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 › Biological Psychiatry › Tryptophan and brain disorders
Keywords
obesity, depression, abdominal obesity, metabolic disorders, glucocorticoids, adipokines, insulin resistance, inflammation, diet, mood regulation, anxiety

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