Dataset Information

Anxiety independently contributes to elevated inflammation in humans with obesity.

ABSTRACT:

Objective

Anxious and depressive states are associated with increased cardiovascular disease (CVD) risk and a proinflammatory phenotype, although the latter appears to be at least partially explained by adiposity. It was hypothesized that depression and anxiety would be associated with elevated inflammation independent of adiposity in persons with obesity at high risk of CVD.

Methods

This study explored the relation between baseline anxiety as measured by the Beck Anxiety Inventory and depression as measured by the Beck Depression Inventory-II and baseline serum c-reactive protein (CRP) in a cross-sectional sample of 100 participants [mean (SD) age 57.8 (7.7) years; 64% female] with obesity [mean (SD) body mass index, BMI 37.3 (5.5) kg/m² ] enrolled in a clinical trial for pharmacological weight loss.

Results

Beck Anxiety Inventory, but not Beck Depression Inventory-II, scores were significantly correlated with CRP (??=?0.28, P?=?0.005). BMI was also highly correlated with CRP (??=?0.42, P?ConclusionsAnxiety, but not depression, was associated with elevated inflammation in persons with obesity beyond that attributable to higher BMI. Further study is warranted to assess whether anxiety represents a potential therapeutic target to mitigate corresponding CVD risk associated with elevated inflammation in persons with obesity.

SUBMITTER: Pierce GL

PROVIDER: S-EPMC5269606 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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Publications

Anxiety independently contributes to elevated inflammation in humans with obesity.

Pierce Gary L GL Kalil Graziela Z GZ Ajibewa Tiwaloluwa T Holwerda Seth W SW Persons Jane J Moser David J DJ Fiedorowicz Jess G JG

Obesity (Silver Spring, Md.) 20161221 2

<h4>Objective</h4>Anxious and depressive states are associated with increased cardiovascular disease (CVD) risk and a proinflammatory phenotype, although the latter appears to be at least partially explained by adiposity. It was hypothesized that depression and anxiety would be associated with elevated inflammation independent of adiposity in persons with obesity at high risk of CVD.<h4>Methods</h4>This study explored the relation between baseline anxiety as measured by the Beck Anxiety Inventor ...[more]

PMID: 28000423

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Project description:Glycogen metabolism has emerged as a mediator in the control of energy homeostasis and studies in murine models reveal that adipose tissue might contain glycogen stores. Here we investigated the physio(patho)logical role of glycogen in human adipose tissue in the context of obesity and insulin resistance.We studied glucose metabolic flux of hypoxic human adipoctyes by nuclear magnetic resonance and mass spectrometry-based metabolic approaches. Glycogen synthesis and glycogen content in response to hypoxia was analyzed in human adipocytes and macrophages. To explore the metabolic effects of enforced glycogen deposition in adipocytes and macrophages, we overexpressed PTG, the only glycogen-associated regulatory subunit (PP1-GTS) reported in murine adipocytes. Adipose tissue gene expression analysis was performed on wild type and homozygous PTG KO male mice. Finally, glycogen metabolism gene expression and glycogen accumulation was analyzed in adipose tissue, mature adipocytes and resident macrophages from lean and obese subjects with different degrees of insulin resistance in 2 independent cohorts.We show that hypoxia modulates glucose metabolic flux in human adipocytes and macrophages and promotes glycogenesis. Enforced glycogen deposition by overexpression of PTG re-orients adipocyte secretion to a pro-inflammatory response linked to insulin resistance and monocyte/lymphocyte migration. Furthermore, glycogen accumulation is associated with inhibition of mTORC1 signaling and increased basal autophagy flux, correlating with greater leptin release in glycogen-loaded adipocytes. PTG-KO mice have reduced expression of key inflammatory genes in adipose tissue and PTG overexpression in M0 macrophages induces a pro-inflammatory and glycolytic M1 phenotype. Increased glycogen synthase expression correlates with glycogen deposition in subcutaneous adipose tissue of obese patients. Glycogen content in subcutaneous mature adipocytes is associated with BMI and leptin expression.Our data establish glycogen mishandling in adipose tissue as a potential key feature of inflammatory-related metabolic stress in human obesity.

Dataset Information

Anxiety independently contributes to elevated inflammation in humans with obesity.

Objective

Methods

Results

Publications

Anxiety independently contributes to elevated inflammation in humans with obesity.

Similar Datasets

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