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Despite the available literature on the consequences of night shiftwork on stress and food intake, its impact on leptin and ghrelin has never been studied. We previously demonstrated that leptin and ghrelin were biomarkers related to stress, and acute stress-induced a decrease in leptin levels and an increase in ghrelin levels. We performed a prospective observational study to assess the influence of night work, nutrition, and stress on the levels of ghrelin and leptin among emergency healthcare workers (HCWs). We took salivary samples at the beginning of a day shift and/or at the end of a night shift. We also monitored stress using the job demand-control-support model of Karasek. We recorded 24-h food intake during the day shift and the consecutive night shift and during night work and the day before. We included 161 emergency HCWs. Emergency HCWs had a tendency for decreased levels of leptin following the night shift compared to before the dayshift (p = 0.067). Furthermore, the main factors explaining the decrease in leptin levels were an increase in job-demand (coefficient −54.1, 95 CI −99.0 to −0.92) and a decrease in job control (−24.9, −49.5 to −0.29). Despite no significant changes in ghrelin levels between shifts, social support was the main factor explaining the increase in ghrelin (6.12, 0.74 to 11.5). Food intake (kcal) also had a negative impact on leptin levels, in addition to age. Ghrelin levels also decreased with body mass index, while age had the opposite effect. In conclusion, we confirmed that ghrelin and leptin as biomarkers of stress were directly linked to the job demand-control-support model of Karasek, when the main cofounders were considered.

Background: Psychosocial stress is a significant public health problem inducing consequences for quality of life. Results about the use of dehydroepiandrosterone (DHEA) as a biomarker of acute stress are conflicting. We conducted a systematic review and meta-analysis to demonstrate that DHEA levels could be a biomarker of stress.Methods: PubMed, Cochrane Library, Embase, and ScienceDirect databases were searched on March 19, 2021 using the keywords “acute stress” AND “DHEA” OR “Dehydroepiandrosterone.” Articles needed to describe our primary outcome, i.e., induction of acute stress and at least two measures of DHEA.Results: We included 14 studies, with a total of 631 participants, in our meta-analysis. The DHEA levels increased overtime after acute stress [standardized mean difference (SMD) = 1.56, 95%CI = 1.13–1.99]. Stratification by time showed a main peak at the end of stress (SMD = 2.43, 95%CI = 1.59–3.27), followed by a progressive decrease (coefficient = −0.11, 95%CI = −0.19 to −0.17, p = 0.020). There was no significant change 1 h after the end of acute stress. Metaregressions showed an impact of mental stress (SMD = 2.04, 95%CI = 1.43–2.65), sex (SMD = 0.02, 95%CI = 0.00–0.04), age (SMD = −0.12, 95%CI = −0.2 to −0.05), and obesity (SMD = 0.31, 95%CI = −0.00 to 0.63). There was no difference whatever the type of fluid (blood or saliva) and the measurement technique used.Conclusions: DHEA is a biomarker of acute stress, with a short-term increase (1 h). DHEA increases following acute mental stress, whatever the type and duration of mental stress. Women, young people, and obese individuals had a higher response. Blood and saliva measures were comparable.

Insulin resistance decreases the ability of insulin to inhibit hepatic gluconeogenesis, a key step in the development of metabolic syndrome. Metabolic alterations, fat accumulation, and fibrosis in the liver are closely related and contribute to the progression of comorbidities, such as hypertension, type 2 diabetes, or cancer. Omega 3 (n-3) polyunsaturated fatty acids, such as eicosapentaenoic acid (EPA), were identified as potent positive regulators of insulin sensitivity in vitro and in animal models. In the current study, we explored the effects of a transgenerational supplementation with EPA in mice exposed to an obesogenic diet on the regulation of microRNAs (miRNAs) and gene expression in the liver using high-throughput techniques. We implemented a comprehensive molecular systems biology approach, combining statistical tools, such as MicroRNA Master Regulator Analysis pipeline and Boolean modeling to integrate these biochemical processes. We demonstrated that EPA mediated molecular adaptations, leading to the inhibition of miR-34a-5p, a negative regulator of Irs2 as a master regulatory event leading to the inhibition of gluconeogenesis by insulin during the fasting&ndash, feeding transition. Omics data integration provided greater biological insight and a better understanding of the relationships between biological variables. Such an approach may be useful for deriving innovative data-driven hypotheses and for the discovery of molecular&ndash, biochemical mechanistic links.

The authors acknowledge the staff from Auvergne University Experimental Animal Laboratory and Christophe Del’Homme, Philippe Denis, Anne Terisse-Lottier and Alexandre Teynie from the Experimental Animal Facility of the Human Nutrition Unit (INRA of Clermont-Ferrand) for their assistance throughout the animal protocol. We thank Celine Bobby for her help for TaqMan gene expression assays. We gratefully acknowledge financial support and doctoral fellowship (to A.P.) fromLesieur and Avril; Impact of ALA, EPA and DHA on obesity and metabolic complications were studied in mice fed a high-fat high-sucrose diet (HF). HF diets were supplemented with ALA, EPA or DHA (1%w/w) and given to C57BL/6J mice for 16 weeks and to Ob/Ob mice for 6 weeks. In C57BL/6J mice, EPA reduced plasma cholesterol (-20%), limited fat mass accumulation (-23%), adipose cell hypertrophy (-50%), and reduced plasma leptin concentration (-60%), compared to HF fed mice. Furthermore, mice supplemented with EPA exhibited a higher insulin sensitivity (+24%) and glucose tolerance (+20%) compared to HF fed mice. Similar effects were observed in EPA supplemented Ob/Ob mice, although fat mass accumulation was not prevented. By contrast in comparison to HF fed mice, DHA did not prevent fat mass accumulation, increased plasma leptin concentration (+128%) in C57BL/6J mice and did not improve glucose homeostasis in C57BL/6J and Ob/Ob mice. In 3T3-L1 adipocytes, DHA stimulated leptin expression whereas EPA induced adiponectin expression, suggesting that improved leptin / adiponectin balance may contribute to the protective effect of EPA. In conclusion, supplementation with EPA, but not ALA and DHA, could preserve glucose homeostasis in an obesogenic environment and limit fat mass accumulation in the early stage of weight gain.

Insulin resistance (IR) favors the progression of metabolic syndrome (MetS) and increases the risk of type 2 diabetes. IR results from metabolic dysfunctions, oxidative stress and inflammation caused by ectopic fat depots. We studied the effect of canola oil enriched with micronutrients naturally present in canola seed on IR and MetS during a high fat (HF)-challenge. Rats were fed with a HF diet containing 30% of lipids, mainly derived from palm oil (diet P), or from a mixture of palm and canola oils (60:40, diet C). In 2 groups of animals, diet C was further supplemented with alpha tocopherol, CoQ with or without Canolol, (diets CMC & CM respectively). Insulin sensitivity and glucose tolerance were assessed after 10 weeks. HF animals were compared to control animals receiving a standard diet. All groups receiving a HF diet gained significantly more weight compared to control. Similar results were obtained for fat depots. Glucose tolerance was altered in P and C groups and improved in CM and CMC. Insulin sensitivity was not different between control and P groups, but was higher in CMC group compared to controls. A reduced activation of PDK4 and Srebp1c expression was observed in skeletal muscle in CM group. In conclusion, the proportion of AGPI could not prevent metabolic disturbance induced by a HF meal. Enrichment with natural micronutrients could prevent insulin resistance and glucose intolerance which could be mediated by a better glucose oxidation in skeletal muscle

Contexte En 2009, des travaux de bitumage du toit-terrasse d’un laboratoire ont ete realises. Suite a ces travaux, des salaries ont ressentis differents symptomes subjectifs. Malgre des prelevements atmospheriques normaux et des travaux d’etancheite, les symptomes ont persiste chez ses salaries. Le Centre de consultations de pathologies professionnelles a ete sollicite fin 2014, une expertise ergonomique a ete realisee. Une des preconisations etait de realiser des travaux de ventilation. Aucun lien n’avait ete etabli entre les symptomes et une eventuelle exposition professionnelle. Aucune evaluation psychologique n’avait ete realisee. Objectifs Evaluer les symptomes et leur retentissement chez ces salaries avant et apres travaux de ventilation. Methode Etude descriptive d’une population comprenant deux groupes, un expose dont les bureaux etaient a proximite du toit-terrasse et un non expose, a distance. Les salaries de chaque groupe ont evalue les symptomes ressentis avant et apres les travaux de ventilation a l’aide d’echelles visuelles analogiques avec 4 temps de mesure pour rechercher une chronologie professionnelle. Le retentissement psychologique a ete evalue avant et apres travaux par un questionnaire d’anxiete depression (HAD), le questionnaire de Karasek, et l’estime de soi (Rosenberg). Resultats 36 salaries ont ete inclus dans l’etude. Le groupe expose (n = 21) et le groupe non expose (n = 15) ne differaient pas en termes de caracteristiques socio-demographiques. Avant les travaux de ventilation, le groupe expose avait plus de symptomes que le groupe non expose (effet groupe : sensibilite a la lumiere (p = 0,042), gene olfactive (p = 0,029), capacite a se concentrer (p = 0,023), fatigue mentale (p = 0,004) ; et a une tendance a differer du groupe non expose pour les symptomes suivants : demangeaisons oculaires (p = 0,081), brulures oculaires (p = 0,091), fatigue visuelle (p = 0,077), maux de tete (p = 0,090), et fatigue physique (p = 0,065)), avec une chronologie professionnelle des symptomes (Effet temps ; p 0,05) pour aucun des symptomes recherches avec une diminution des symptomes dans le groupe expose (effet travaux, p Conclusion Avant les travaux, le groupe expose avait plus de symptomes, avec une chronologie professionnelle. Les travaux de ventilation ont permis de normaliser les symptomes. La cause initiale des symptomes etait liee de facon sure a une ventilation non aux normes. Le lien avec le bitumage du toit terrasse reste hypothetique.