Sucrose Counteracts the Anti-Inflammatory Effect of Fish Oil in Adipose Tissue and Increases Obesity Development in Mice

BACKGROUND: Polyunsaturated n-3 fatty acids (n-3 PUFAs) are reported to protect against high fat diet-induced obesity and inflammation in adipose tissue. Here we aimed to investigate if the amount of sucrose in the background diet influences the ability of n-3 PUFAs to protect against diet-induced obesity, adipose tissue inflammation and glucose intolerance. METHODOLOGY/PRINCIPAL FINDINGS: We fed C57BL/6J mice a protein- (casein) or sucrose-based high fat diet supplemented with fish oil or corn oil for 9 weeks. Irrespective of the fatty acid source, mice fed diets rich in sucrose became obese whereas mice fed high protein diets remained lean. Inclusion of sucrose in the diet also counteracted the well-known anti-inflammatory effect of fish oil in adipose tissue, but did not impair the ability of fish oil to prevent accumulation of fat in the liver. Calculation of HOMA-IR indicated that mice fed high levels of proteins remained insulin sensitive, whereas insulin sensitivity was reduced in the obese mice fed sucrose irrespectively of the fat source. We show that a high fat diet decreased glucose tolerance in the mice independently of both obesity and dietary levels of n-3 PUFAs and sucrose. Of note, increasing the protein∶sucrose ratio in high fat diets decreased energy efficiency irrespective of fat source. This was accompanied by increased expression of Ppargc1a (peroxisome proliferator-activated receptor, gamma, coactivator 1 alpha) and increased gluconeogenesis in the fed state. CONCLUSIONS/SIGNIFICANCE: The background diet influence the ability of n-3 PUFAs to protect against development of obesity, glucose intolerance and adipose tissue inflammation. High levels of dietary sucrose counteract the anti-inflammatory effect of fish oil in adipose tissue and increases obesity development in mice

SARS-CoV-2 specific immune responses in overweight and obese COVID-19 patients

Obesity is a known risk factor for severe respiratory tract infections. In this prospective study, we assessed the impact of being obese or overweight on longitudinal SARS-CoV-2 humoral and cellular responses up to 18 months after infection. 274 patients provided blood samples at regular time intervals up to 18 months including obese (BMI ≥30, n=32), overweight (BMI 25-29.9, n=103) and normal body weight (BMI 18.5-24.9, n=134) SARS-CoV-2 patients. We determined SARS-CoV-2 spike-specific IgG, IgA, IgM levels by ELISA and neutralising antibody titres by neutralisation assay. RBD- and spike-specific memory B cells were investigated by ELISpot, spike- and non-spike-specific IFN-γ, IL-2 and IFN-γ/IL-2 secreting T cells by FluoroSpot and T cell receptor (TCR) sequencing was performed. Higher BMI correlated with increased COVID-19 severity. Humoral and cellular responses were stronger in overweight and obese patients than normal weight patients and associated with higher spike-specific IgG binding titres relative to neutralising antibody titres. Linear regression models demonstrated that BMI, age and COVID-19 severity correlated independently with higher SARS-CoV-2 immune responses. We found an increased proportion of unique SARS-CoV-2 specific T cell clonotypes after infection in overweight and obese patients. COVID-19 vaccination boosted humoral and cellular responses irrespective of BMI, although stronger immune boosting was observed in normal weight patients. Overall, our results highlight more severe disease and an over-reactivity of the immune system in overweight and obese patients after SARS-CoV-2 infection, underscoring the importance of recognizing overweight/obese individuals as a risk group for prioritisation for COVID-19 vaccination

Diversity of hard-bottom fauna relative to environmental gradients in Kongsfjorden, Svalbard

A baseline study of hard-bottom zoobenthos in relation to environmental gradients in Kongsfjorden, a glacial fjord in Svalbard, is presented, based on collections from 1996 to 1998. The total species richness in 62 samples from 0 to 30 m depth along five transects was 403 species. Because 32 taxa could not be identified to species level and because 11 species are probably new to science, the total number of identified species was 360. Of these, 47 species are new for Svalbard waters. Bryozoa was the most diverse group. Biogeographic composition revealed features of both Arctic and sub-Arctic properties of the fauna. Species richness, frequency of species occurrence, mean abundance and biomass generally decreased towards the tidal glaciers in inner Kongsfjorden. Among eight environmental factors, depth was most important for explaining variance in the composition of the zoobenthos. The diversity was consistently low at shallow depths, whereas the non-linear patterns of species composition of deeper samples indicated a transitional zone between surface and deeper water masses at 15–20 m depth. Groups of “colonial” and “non-colonial” species differed in diversity, biogeographic composition and distribution by location and depth as well as in relation to other environmental factors. “Non-colonial” species made a greater contribution than “colonial” species to total species richness, total occurrence and biomass in samples, and were more influenced by the depth gradient. Biogeographic composition was sensitive to variation of zoobenthic characteristics over the studied depth range. A list of recorded species and a description of sampling sites are presented

Quantitative evaluation of respiration induced metabolic oscillations in erythrocytes

International audienceThe changes in the partial pressures of oxygen and carbon dioxide (P and P) during blood circulation alter erythrocyte metabolism, hereby causing flux changes between oxygenated and deoxygenated blood. In the study we have modeled this effect by extending the comprehensive kinetic model by Mulquiney and Kuchel (1999) with a kinetic model of hemoglobin oxy/deoxygenation transition based on an oxygen dissociation model developed by Dash and Bassingtwaighte (2004). The system has been studied during transitions from the arterial to the venous phases by simply forcing P and P to follow the physiological values of venous and arterial blood. The investigations show that the system passively follows a limit cycle driven by the forced oscillations of P and is thus inadequately described solely by steady state consideration. The metabolic system exhibits a broad distribution of time scales. Relaxations of modes with hemoglobin and Mg binding reactions are very fast, while modes involving glycolytic, membrane transport and 2,3-BPG shunt reactions are much slower. Incomplete slow mode relaxations during the 60 s period of the forced transitions cause significant overshoots of important fluxes and metabolite concentrations – notably ATP, 2,3-BPG, and Mg. The overshoot phenomenon arises in consequence of a periodical forcing and is likely to be widespread in nature – warranting a special consideration for relevant systems

Limited Colocalization of Microbleeds and Microstructural Changes after Severe Traumatic Brain Injury

Severe traumatic brain injury (TBI) produces shearing forces on long-range axons and brain vessels, causing axonal and vascular injury. To examine whether microbleeds and axonal injury co-localize after TBI, we performed whole-brain susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI) in 14 patients during the subacute phase after severe TBI. SWI was used to determine the number and volumes of microbleeds in five brain regions: the fronto-temporal lobe, parieto-occipital lobe, mid-sagittal region (cingular cortex, parasagittal white matter and corpus callosum), deep nuclei (basal ganglia and thalamus), and brainstem. Averaged fractional anisotropy (FA) and mean diffusivity (MD) were measured to assess microstructural changes in the normal appearing white matter due to axonal injury in the same five regions. Regional expressions of microbleeds and microstructure was used in a partial least squares model to predict the impairment of consciousness in the subacute stage after TBI as measured with the Coma Recovery Scale-Revised (CRS-R). Only in the midsagittal region, expression of microbleeds correlated with regional changes in microstructure as revealed by DTI. Microbleeds and microstructural DTI-based metrics of deep but not superficial brain regions were able to predict individual CRS-R. Our results suggest that microbleeds are not strictly related to axonal pathology in other that the midsagittal region. While each measure alone was predictive, the combination of both metrics scaled best with individual CRS-R. Structural alterations in deep brain structures are relevant in terms of determining the severity of impaired consciousness in the acute stage after TBI