CoChat
Sign Up
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
Open this paper in CoChat — free accountOpen PDF

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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fnins.2013.00177

Cites

225 of 225 references verified0 citation errors · 0 not checkable

Statistics

Figures

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

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

1 retracted

Show all 225 references

Research works printed but not linked: 1

  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

Cited by

Sorted by citations

Related

See all

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

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 ›

Are you an author, or do you see a problem with this page? Request a review