Perchlorate exposure does not induce obesity or non-alcoholic fatty liver disease in zebrafish

Perchlorate is a water-soluble contaminant found throughout the United States and many other countries. Perchlorate competitively inhibits iodide uptake at the sodium/iodide symporter, reducing thyroid hormone synthesis, which can lead to hypothyroidism and metabolic syndromes. Chronic perchlorate exposure induces hepatic steatosis and non-alcoholic fatty liver disease (NAFLD) in developing threespine stickleback (Gasterosteus aculeatus). We hypothesized that perchlorate would also induce zebrafish (Danio rerio) to develop phenotypes consistent with NAFLD and to accumulate lipids throughout the body. We exposed zebrafish embryos to four concentrations of perchlorate treated water (10μg/L, 10mg/L, 30mg/L, and 100mg/L) and a control (0mg/L) over the course of 133 days. Adult zebrafish were euthanized, sectioned, H&E and Oil Red-O stained, and analyzed for liver morphology and whole body lipid accumulation. In a representative section of the liver, we counted the number of lipid droplets and measured the area of each droplet and the total lipid area. For whole body analysis, we calculated the ratio of lipid area to body area within a section. We found that zebrafish exposed to perchlorate did not differ in any measured liver variables or whole body lipid area when compared to controls. In comparison to stickleback, we see a trend that control stickleback accumulate more lipids in their liver than do control zebrafish. Differences between the species indicate that obesogenic effects due to perchlorate exposure are not uniform across fish species, and likely are mediated by evolutionary differences related to geographic location. For example, high latitude fishes such as stickleback evolved to deposit lipid stores for over-winter survival, which may lead to more pronounced obesogenic effects than seen in tropical fish such as zebrafish.

Nutrigenetic comparison of two Varroa-resistant honey bee stocks fed pollen and spirulina microalgae

We tested the influence of genetic variation on responses to natural and artificial diets in Varroa-resistant Pol-line and Russian honey bee stocks. Newly emerged workers from six colonies per stock were fed pollen, spirulina (blue-green microalgae), and sucrose-only diets in 144 total cages. Diet type had a strong effect on sugar intake, body weight, fat body lipid content, and vitellogenin (vg) expression. Spirulina consumption was approximately half that of pollen, but led to higher head weights, equivalent thorax weights and vg levels, and marginally reduced fat body lipids. Bee stock and colony had a significant impact on nutritional response. Despite equivalent diet intakes, Pol-line bees accumulated higher lipid levels and consumed less sugar overall than Russian bees. Furthermore, pollen-fed bees sourced from Pol-line colonies had significantly higher vg levels. These differences in nutrient and energy allocation may reflect life history-related physiological tradeoffs. Our results suggest that genotype-dependent nutritional responses are present in honey bees, with promising implications for breeding efforts and tailored approaches to diet and health in a changing global climate.

Fat and Happy: Profiling Mosquito Fat Body Lipid Storage and Composition Post-blood Meal

The fat body is considered the insect analog of vertebrate liver and fat tissue. In mosquitoes, a blood meal triggers a series of processes in the fat body that culminate in vitellogenesis, the process of yolk formation. Lipids are stored in the fat body in specialized organelles called lipid droplets that change in size depending on the nutritional and metabolic status of the insect. We surveyed lipid droplets in female Aedes aegypti fat body during a reproductive cycle using confocal microscopy and analyzed the dynamic changes in the fat body lipidome during this process using LC/MS. We found that lipid droplets underwent dynamic changes in volume after the mosquito took a blood meal. The lipid composition found in the fat body is quite complex with 117 distinct lipids that fall into 19 classes and sublcasses. Our results demonstrate that the lipid composition of the fat body is complex as most lipid classes underwent significant changes over the course of the vitellogenic cycle. This study lays the foundation for identifying unknown biochemical pathways active in the mosquito fat body, that are high-value targets for the development of novel mosquito control strategies.

Biochemical composition of tropical eel Anguilla bicolor McClelland,1844 in Freshwater and Estuary

During migration, Anguilla bicolor will stop its feeding activity and use energy from its body lipid stores. Therefore, information on changes in the body lipid content of eels is essential to know the preparation of spawning migration. Thus, it is interesting to study the body composition of A. bicolor in freshwater and estuaries. This research conducted a survey method. The eel was obtained from the Serayu River (freshwaters) and Segara Anakan (Estuary). The observed variables were water, dry weight, lipid, protein, crude fiber, ash, and BETN of eel. Oneway ANOVA analyzed data. The results show that freshwater eels' average body length and weight were 457.875 cm ± 153.8552 and 224.4375 g ± 165.3735. The body length and weight of the estuary eels were smaller than freshwater eels, which are 372.5714 cm ± 152.6467 and 109.6429 g ± 134.6054, respectively. The body composition of eel, except for lipid content, was similar for both habitats (p>0.05). However, the body lipid content of freshwater eels and the estuarine eel differed (p<0.05), namely 40.15% ± 9.63 and 27.33% ± 9.93, respectively. In conclusion, the lipid body content of freshwater eels was higher than the estuary eel, while another is relatively the same.

Remodeling of whole-body lipid metabolism and a diabetic-like phenotype caused by loss of CDK1 and hepatocyte division

Cell cycle progression and lipid metabolism are well-coordinated processes required for proper cell proliferation. In liver diseases that arise from dysregulated lipid metabolism, proliferation is diminished. To study the outcome of CDK1 loss and blocked hepatocyte proliferation on lipid metabolism and the consequent impact on whole-body physiology, we performed lipidomics, metabolomics, and RNA-seq analyses on a mouse model. We observed reduced triacylglycerides in liver of young mice, caused by oxidative stress that activated FOXO1 to promote expression of Pnpla2/ATGL. Additionally, we discovered that hepatocytes displayed malfunctioning β-oxidation, reflected by increased acylcarnitines (ACs) and reduced β-hydroxybutyrate. This led to elevated plasma free fatty acids (FFAs), which were transported to the adipose tissue for storage and triggered greater insulin secretion. Upon aging, chronic hyperinsulinemia resulted in insulin resistance and hepatic steatosis through activation of LXR. Here, we demonstrate that loss of hepatocyte proliferation is not only an outcome but also possibly a causative factor for liver pathology.