The menace of obesity to depression and anxiety prevalence

Trends in Endocrinology and Metabolism, Journal Year: 2021, Volume and Issue: 33(1), P. 18 - 35

Published: Nov. 5, 2021

Obesity increases the incidence of depression and anxiety as a function extent metabolic dysfunction.Diets that include excess saturated fat sugar intake promote dysfunction, neuroinflammation, mental health impairments.Adipose- gut-derived inflammation changes in brain nutrient composition stimulate neuroinflammation.Neuroinflammation alters structure, excitability, connectivity corticolimbic networks controlling mood, motivation, emotion. The is amplified by obesity. Mounting evidence reveals psychiatric consequences obesity stem from poor diet, inactivity, visceral adipose accumulation. Resulting vascular including inflammation, insulin leptin resistance, hypertension, have emerged key risks to development. Recent research advancements are exposing important contribution these different corollaries their impact on neuroimmune status neural circuits mood emotional states. Along lines, this review connects clinical manifestations our current understanding origins biology immunometabolic threats central nervous system behavior. peril disorders receiving increasing attention beyond psychological practice, an expansion encouraging constructive awareness discussion public forums. centrality overall wellbeing substantial external stressors has never been more apparent. major influence internal, biological originating alterations energy metabolism also earned significant consideration. In keeping with its extensive physiology health, growing accentuating threat risk illness. Depression prevalent disabling conditions increased hazard they pose for obese individuals far-reaching. Beyond hindering personal welfare quality life, depressed can diminish will seek out adhere therapeutic interventions. interchange between dysfunction perpetuate cycle despair, overeating physical inactivity enhances severity numerous associated risks. view limitations available therapies, it critical improve knowledge dietary, metabolic, neurobiological effectors development progression implement better preventative treatment strategies. An elevated body mass index (BMI) predictive chronic course depressive symptoms [1.Zhao G. et al.Depression among US adults: associations index.Int. J. Obes. 2009; 33: 257-266Crossref PubMed Scopus (161) Google Scholar,2.Milaneschi Y. obesity: shared mechanisms.Mol. Psychiatry. 2019; 24: 18-33Crossref (157) Scholar]. odds developing disorder (MDD) increase number coexisting impairments, such those characteristic syndrome [3.Jokela M. al.Association metabolically healthy symptoms: pooled analysis eight studies.Mol. 2014; 19: 910-914Crossref (60) Scholar,4.Tang F. syndrome: systematic meta-analysis epidemiological studies.Psychoneuroendocrinology. 2017; 77: 112-121Crossref (0) coupled various structural functional remarkably similar observed disorders, region-specific cell density compromised excitability [5.Rapuano K.M. al.Nucleus accumbens cytoarchitecture predicts weight gain children.Proc. Natl. Acad. Sci. U. S. A. 2020; 117: 26977-26984Crossref (8) Scholar,6.Opel N. al.Brain abnormalities relation age, genetic risk, common disorders: through univariate multivariate mega-analysis 6420 participants ENIGMA MDD working group.Mol. 2021; 26: 4839-4852Crossref (15) Several lines suggest prolonged caused dietary lifestyle resulting required outcomes. Clinical observations combined rodent models exhibiting depressive- anxiety-like behaviors proving valuable uncovering mechanisms involved. review, we focus how (for cognitive corollaries, see [7.Farruggia M.C. Small D.M. Effects adiposity cognition: review.Physiol. Behav. 208: 112578Crossref (25) Scholar,8.Kendig M.D. al.Unravelling impacts western-style diets brain, gut microbiota cognition.Neurosci. Biobehav. Rev. 128: 233-243Crossref Scholar]), aim illuminate diverse culprits behavioral processes giving rise deficits. (or depression) debilitating condition genetic, epigenetic, environmental contributions. manifest ways, modulating homeostatic functions appetite sleep turn further alter mood. Anxiety accompanies most cases indicative poorer prognosis. Melancholic depression, form, distinguished hypophagia, hyposomnia, anhedonia (decreased capacity experience anticipate pleasure). addition anhedonia, characteristics atypical subtype hyperphagia, lethargy, hypersomnia. Obese individuals, particularly presenting attributes (abdominal obesity, hyperglycemia, triglycerides), tend develop [9.Milaneschi al.Genetic association features obesity-related dysregulations.JAMA 74: 1214-1225Crossref (90) Scholar] (Box 1). This form stronger links peripheral [10.Rudolf al.Elevated IL-6 levels patients but not typical depression.Psychiatry Res. 217: 34-38Crossref (31) Scholar,11.Yoon H.K. al.Role cytokines depression.Nord. 2012; 66: 183-188Crossref [12.Woelfer al.The role subtypes within neuroinflammation hypothesis disorder.Neuroscience. 403: 93-110Crossref (46) inflammation. Individuals often unrelenting [13.Thase M.E. Recognition diagnosis depression.J. 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Language: Английский

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Inter-organ cross-talk in metabolic syndrome

Nature Metabolism, Journal Year: 2019, Volume and Issue: 1(12), P. 1177 - 1188

Published: Dec. 9, 2019

Language: Английский

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Insulin-like growth factors: Ligands, binding proteins, and receptors

Molecular Metabolism, Journal Year: 2021, Volume and Issue: 52, P. 101245 - 101245

Published: May 4, 2021

The insulin-like growth factor family of ligands (IGF-I, IGF-II, and insulin), receptors (IGF-IR, M6P/IGF-IIR, insulin receptor [IR]), IGF-binding proteins (IGFBP-1-6) play critical roles in normal human physiology disease states. Insulin are the focus other chapters this series will therefore not be discussed further. Here we review basic components IGF system, their role pathology's. While concentrates on IGFs physiology, animal models have been essential providing understanding its regulation, briefly described. IGF-I has effects via circulation locally within tissues to regulate cellular growth, differentiation, survival, thereby controlling overall body growth. IGF-II levels highest prenatally when it important In adults, plays tissue-specific roles, including maintenance stem cell populations. Although IGF-IR is closely related IR distinct physiological both surface nucleus. contrast, acts as a scavenger by mediating internalization degradation IGF-II. IGFBPs bind prolong half-lives modulate tissue access, function. also ligand-independent effects.

Language: Английский

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Insulin action at a molecular level – 100 years of progress

Molecular Metabolism, Journal Year: 2021, Volume and Issue: 52, P. 101304 - 101304

Published: July 15, 2021

The discovery of insulin 100 years ago and its application to the treatment human disease in since have marked a major turning point history medicine. availability purified allowed for establishment physiological role regulation blood glucose ketones, determination amino acid sequence, solving structure. Over last 50 years, function has been applied into receptor signaling cascade reveal impaired signaling—or resistance—in progression type 2 diabetes. It also become clear that can impact not only classical insulin-sensitive tissues, but all tissues body, many these regulates unexpected functions. Despite remarkable advances, much remains be learned about both how use this molecular knowledge advance diabetes other insulin-resistant states.

Language: Английский

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The brain as an insulin-sensitive metabolic organ

Molecular Metabolism, Journal Year: 2021, Volume and Issue: 52, P. 101234 - 101234

Published: April 16, 2021

The brain was once thought of as an insulin-insensitive organ. We now know that the insulin receptor is present throughout and serves important functions in whole-body metabolism function. Brain signaling involved not only homeostatic processes but also neuropathological such cognitive decline Alzheimer's disease.

Language: Английский

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Impaired insulin signalling and allostatic load in Alzheimer disease

Nature reviews. Neuroscience, Journal Year: 2022, Volume and Issue: 23(4), P. 215 - 230

Published: Feb. 28, 2022

Language: Английский

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Brain insulin signalling in metabolic homeostasis and disease

Nature Reviews Endocrinology, Journal Year: 2021, Volume and Issue: 17(8), P. 468 - 483

Published: June 9, 2021

Language: Английский

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Glucose metabolic crosstalk and regulation in brain function and diseases

Progress in Neurobiology, Journal Year: 2021, Volume and Issue: 204, P. 102089 - 102089

Published: June 10, 2021

Language: Английский

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Insulin action in the brain: cell types, circuits, and diseases

Trends in Neurosciences, Journal Year: 2022, Volume and Issue: 45(5), P. 384 - 400

Published: March 28, 2022

Language: Английский

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IGF1 enhances memory function in obese mice and stabilizes the neural structure under insulin resistance via AKT-GSK3β-BDNF signaling

Biomedicine & Pharmacotherapy, Journal Year: 2025, Volume and Issue: 183, P. 117846 - 117846

Published: Jan. 12, 2025

Language: Английский

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