Special Issue "Biomarker of Stress, Metabolic Syndrome and Human Health"

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 10 December 2021.

Special Issue Editors

Prof. Dr. Frederic Dutheil
E-Mail Website
Guest Editor
CNRS, LaPSCo, Physiological and Psychosocial Stress, University Hospital of Clermont-Ferrand, Occupational and Environmental Medicine, WittyFit, Clermont Auvergne University, Clermont-Ferrand, Auvergne-Rhône-Alpes, France
Interests: stress; biomarkers; metabolic syndrome; well-being; exercise
Dr. Jean-Baptiste Bouillon-Minois
E-Mail Website
Guest Editor
Physiological and Psychosocial Stress, Université Clermont Auvergne, CNRS, LaPSCo, Emergency Medicine, CHU Clermont-Ferrand, Clermont-Ferrand, France
Interests: stress; biomarkers; metabolic syndrome; emergency medicine; trauma brain injury; exercise

Special Issue Information

Dear Colleagues,

Metabolic syndrome is a significant public health concern linked to the obesity pandemic. Even if glycemia, triglycerides, and HDL are mandatory to assess the metabolic syndrome, other biomarkers have recently been proposed to be part of the metabolic syndrome. Recent studies indicate that both chronic and (repeated) acute stress are involved in developing metabolic syndrome. Furthermore, both oxidative and psychosocial stress are linked to heart disease and metabolic syndrome. The main hypothesis is the disruption of the hypothalamic–pituitary–adrenal axis (HPA axis). Indeed, a dysfunction in the HPA axis increases cortisol levels in blood, increasing both glucose and insulin levels, so the apparition of insulin resistance leads to the promotion of dyslipidemia, high blood pressure, and visceral adiposity. Secondly, HPA axis dysfunction has an impact on bones, cardiovascular diseases, and psychiatric disorders.

To conclude, this Special Issue should review all aspects concerning the impact of biomarkers to assess, prevent, or monitor the link between stress and metabolic syndrome. We welcome original papers, including randomized controlled trials and observational studies, systematic reviews, and meta-analyses.

Prof. Dr. Frederic Dutheil
Dr. Jean-Baptiste Bouillon-Minois
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • stress
  • biomarkers
  • metabolic syndrome
  • HPA axis
  • insulin
  • exercise
  • leptin
  • obesity

Published Papers (4 papers)

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Research

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Article
Stress Responsiveness and Emotional Eating Depend on Youngsters’ Chronic Stress Level and Overweight
Nutrients 2021, 13(10), 3654; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103654 - 19 Oct 2021
Viewed by 507
Abstract
The persistent coexistence of stress and paediatric obesity involves interrelated psychophysiological mechanisms, which are believed to function as a vicious circle. Here, a key mechanistic role is assumed for stress responsiveness and eating behaviour. After a stress induction by the Trier Social Stress [...] Read more.
The persistent coexistence of stress and paediatric obesity involves interrelated psychophysiological mechanisms, which are believed to function as a vicious circle. Here, a key mechanistic role is assumed for stress responsiveness and eating behaviour. After a stress induction by the Trier Social Stress Test in youngsters (n = 137, 50.4% boys, 6–18 years), specifically those high in chronic stress level and overweight (partial η2 = 0.03–0.07) exhibited increased stress vulnerability (stronger relative salivary cortisol reactivity and weaker happiness recovery) and higher fat/sweet snack intake, compared to the normal-weight and low-stress reference group. Stress responsiveness seems to stimulate unhealthy and emotional eating, i.e., strong cortisol reactivity was linked to higher fat/sweet snack intake (β = 0.22) and weak autonomic system recovery was linked to high total and fat/sweet snack intake (β = 0.2–0.3). Additionally, stress responsiveness acted as a moderator. As a result, stress responsiveness and emotional eating might be targets to prevent stress-induced overweight. Full article
(This article belongs to the Special Issue Biomarker of Stress, Metabolic Syndrome and Human Health)
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Article
Pancreatic β-Cell Dysfunction Is Associated with Nonalcoholic Fatty Liver Disease
Nutrients 2021, 13(9), 3139; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13093139 - 09 Sep 2021
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Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is associated with decreased insulin sensitivity. However, the association between NAFLD and pancreatic β-cell function is still ambiguous. Here, we assessed whether pancreatic β-cell function is associated with NAFLD. Method: The data of NHANES III from 1988 [...] Read more.
Background: Nonalcoholic fatty liver disease (NAFLD) is associated with decreased insulin sensitivity. However, the association between NAFLD and pancreatic β-cell function is still ambiguous. Here, we assessed whether pancreatic β-cell function is associated with NAFLD. Method: The data of NHANES III from 1988 to 1994 were used. NAFLD was diagnosed when subjects had ultrasonographically hepatic steatosis without other liver diseases. Disposition index (DI) was employed to assess pancreatic β-cell function. A total of 6168 participants were included in this study. Results: NAFLD participants had much higher HOMA2-%B (weighted mean, 124.1; standard error, 1.8) than the non-NAFLD participants (weighted mean, 100.7; standard error, 0.9). However, when evaluating the β-cell function in the context of insulin resistance by using DI index, DI levels were much lower in NAFLD subjects (weighted mean, 79.5; standard error, 1.0) compared to non-NAFLD (weighted mean, 95.0; standard error, 0.8). Multivariate logistic regression analyses showed that DI was inversely associated with NAFLD prevalence. The adjusted OR (95% CI) for quartile 1 versus quartile 4 was 1.81 (1.31–2.50) (p < 0.001 for trend). Moreover, DI was also inversely associated with the presence of moderate to severe hepatic steatosis. The multivariable-adjusted ORs across quartiles of DI were 2.47, 1.44, 0.96 and 1.00 for the presence of moderate to severe hepatic steatosis (p < 0.001 for trend). Conclusions: Pancreatic β-cell function might be a new predictor for the presence of NAFLD, and insufficient compensatory β-cell function is associated with NAFLD. Full article
(This article belongs to the Special Issue Biomarker of Stress, Metabolic Syndrome and Human Health)

Review

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Review
Metabolic Syndrome and Sarcopenia
Nutrients 2021, 13(10), 3519; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103519 - 07 Oct 2021
Viewed by 891
Abstract
Skeletal muscle is a major organ of insulin-induced glucose metabolism. In addition, loss of muscle mass is closely linked to insulin resistance (IR) and metabolic syndrome (Met-S). Skeletal muscle loss and accumulation of intramuscular fat are associated with a variety of pathologies through [...] Read more.
Skeletal muscle is a major organ of insulin-induced glucose metabolism. In addition, loss of muscle mass is closely linked to insulin resistance (IR) and metabolic syndrome (Met-S). Skeletal muscle loss and accumulation of intramuscular fat are associated with a variety of pathologies through a combination of factors, including oxidative stress, inflammatory cytokines, mitochondrial dysfunction, IR, and inactivity. Sarcopenia, defined by a loss of muscle mass and a decline in muscle quality and muscle function, is common in the elderly and is also often seen in patients with acute or chronic muscle-wasting diseases. The relationship between Met-S and sarcopenia has been attracting a great deal of attention these days. Persistent inflammation, fat deposition, and IR are thought to play a complex role in the association between Met-S and sarcopenia. Met-S and sarcopenia adversely affect QOL and contribute to increased frailty, weakness, dependence, and morbidity and mortality. Patients with Met-S and sarcopenia at the same time have a higher risk of several adverse health events than those with either Met-S or sarcopenia. Met-S can also be associated with sarcopenic obesity. In this review, the relationship between Met-S and sarcopenia will be outlined from the viewpoints of molecular mechanism and clinical impact. Full article
(This article belongs to the Special Issue Biomarker of Stress, Metabolic Syndrome and Human Health)
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Review
Leptin as a Biomarker of Stress: A Systematic Review and Meta-Analysis
Nutrients 2021, 13(10), 3350; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103350 - 24 Sep 2021
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Abstract
Background: Leptin is a satiety hormone mainly produced by white adipose tissue. Decreasing levels have been described following acute stress. Objective: To conduct a systematic review and meta-analysis to determine if leptin can be a biomarker of stress, with levels decreasing following acute [...] Read more.
Background: Leptin is a satiety hormone mainly produced by white adipose tissue. Decreasing levels have been described following acute stress. Objective: To conduct a systematic review and meta-analysis to determine if leptin can be a biomarker of stress, with levels decreasing following acute stress. Methods: PubMed, Cochrane Library, Embase, and ScienceDirect were searched to obtain all articles studying leptin levels after acute stress on 15 February 2021. We included articles reporting leptin levels before and after acute stress (physical or psychological) and conducted random effects meta-analysis (DerSimonian and Laird approach). We conducted Meta-regressions and sensitivity analyses after exclusion of groups outside the metafunnel. Results: We included seven articles—four cohort and three case-control studies—(28 groups) from 27,983 putative articles. Leptin levels decreased after the stress intervention (effect size = −0.34, 95%CI −0.66 to −0.02) compared with baseline levels, with a greater decrease after 60 min compared to mean decrease (−0.45, −0.89 to −0.01) and in normal weight compared to overweight individuals (−0.79, −1.38 to −0.21). There was no difference in the overweight population. Sensitivity analyses demonstrated similar results. Levels of leptin after stress decreased with sex ratio—i.e., number of men/women—(−0.924, 95%CI −1.58 to −0.27) and increased with the baseline levels of leptin (0.039, 0.01 to 0.07). Conclusions: Leptin is a biomarker of stress, with a decrease following acute stress. Normal-weight individuals and women also have a higher variation of leptin levels after stress, suggesting that leptin may have implications in obesity development in response to stress in a sex-dependent manner. Full article
(This article belongs to the Special Issue Biomarker of Stress, Metabolic Syndrome and Human Health)
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