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–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–biochemical mechanistic links.