Sex differences in the association of vital exhaustion with regional fat deposition and subclinical cardiovascular disease risk

Vital exhaustion (VE) is more strongly associated with cardiovascular disease (CVD) risk for women than men. This study examined whether sex differences in associations of VE with CVD risk markers are accounted for by unique associations of VE with regional adiposity. The study enrolled 143 persons (18–55 years) without diagnosed conditions. VE was assessed by the Maastricht questionnaire. CVD indices were measured using the euglycemic-hyperinsulinemia clamp, resting blood pressure, and blood draws. Regional adiposity was measured using computed tomography and 2-D echocardiography. This cross-sectional study employed a path analysis approach, including relevant covariates. Of the cohort, aged 38.7 ± 8.4 years, 65% were men, and 41% were obese. The final model had excellent fit (χ2(36) = 36.5, p = .45; RMSEA = 0.009, CFI = 0.999). For women, but not men, the model indicated paths from VE to: 1) lower insulin sensitivity (B = −0.10, p = .04), and higher total cholesterol to HDL ratio (B = 0.12, p = .09), triglycerides (B = 0.10, p = .08), and C-reactive protein (B = 0.08, p = .09) through visceral adiposity; 2) higher mean arterial pressure (B = 0.14, p = .04), lower insulin sensitivity (B = −0.09, p = .08), and higher C-reactive protein (B = 0.12, p = .07) through subcutaneous adiposity; 3) lower insulin sensitivity (B = −0.07, p = .08) and higher total cholesterol to HDL ratio (B = 0.16, p = .03) through liver adiposity; and 4) higher C-reactive protein (B = 0.08, p = .09) through epicardial adiposity. Results extend prior evidence by showing that the association of VE with CVD risk in women is linked with specific regional adiposity elevation. Further study of adiposity-related mechanisms in women who experience early decline in vitality may inform clinical targets for CVD prevention. •Prior evidence for specific link of vital exhaustion with CVD risk in women.•For women only, associations emerged between vital exhaustion and CVD risk markers.•These associations were mediated by elevations in distinct regional fat depots.•Results suggest an early decline in vitality for women may be a CVD risk indicator.•Further study of adiposity-related mechanisms in women with vital exhaustion needed

Ecogenomics and potential biogeochemical impacts of globally abundant ocean viruses

Tara Oceans CoordinatorsInternational audienceOcean microbes drive biogeochemical cycling on a global scale. However, this cycling is constrained by viruses that affect community composition, metabolic activity, and evolutionary trajectories. Owing to challenges with the sampling and cultivation of viruses, genome-level viral diversity remains poorly described and grossly understudied, with less than 1% of observed surface-ocean viruses known. Here we assemble complete genomes and large genomic fragments from both surface- and deep-ocean viruses sampled during the Tara Oceans and Malaspina research expeditions, and analyse the resulting ‘global ocean virome’ dataset to present a global map of abundant, double-stranded DNA viruses complete with genomic and ecological contexts. A total of 15,222 epipelagic and mesopelagic viral populations were identified, comprising 867 viral clusters (defined as approximately genus-level groups. This roughly triples the number of known ocean viral populations and doubles the number of candidate bacterial and archaeal virus genera, providing a near-complete sampling of epipelagic communities at both the population and viral-cluster level. We found that 38 of the 867 viral clusters were locally or globally abundant, together accounting for nearly half of the viral populations in any global ocean virome sample. While two-thirds of these clusters represent newly described viruses lacking any cultivated representative, most could be computationally linked to dominant, ecologically relevant microbial hosts. Moreover, we identified 243 viral-encoded auxiliary metabolic genes, of which only 95 were previously known. Deeper analyses of four of these auxiliary metabolic genes (dsrC, soxYZ, P-II (also known as glnB) and amoC) revealed that abundant viruses may directly manipulate sulfur and nitrogen cycling throughout the epipelagic ocean. This viral catalog and functional analyses provide a necessary foundation for the meaningful integration of viruses into ecosystem models where they act as key players in nutrient cycling and trophic networks