Invading species along with increased anthropogenization may lead to hybridization events between wild species and closely related domesticates. As a consequence, wild species may carry introgressed a Show more
Invading species along with increased anthropogenization may lead to hybridization events between wild species and closely related domesticates. As a consequence, wild species may carry introgressed alleles from domestic species, which is generally assumed to yield adverse effects in wild populations. The opposite evolutionary consequence, adaptive introgression, where introgressed genes are positively selected in the wild species, is possible but has rarely been documented. Grey wolves (Canis lupus) are widely distributed across the Holarctic and frequently coexist with their close relative, the domestic dog (C. familiaris). Despite ample opportunity, hybridization rarely occurs in most populations. Here we studied the geographically isolated grey wolves of the Iberian Peninsula, who have coexisted with a large population of loosely controlled dogs for thousands of years in a human-modified landscape. We assessed the extent and impact of dog introgression on the current Iberian grey wolf population by analysing 150 whole genomes of Iberian and other Eurasian grey wolves as well as dogs originating from across Europe and western Siberia. We identified almost no recent introgression and a small (< 5%) overall ancient dog ancestry. Using a combination of single scan statistics and ancestry enrichment estimates, we identified positive selection on six genes (DAPP1, NSMCE4A, MPPED2, PCDH9, MBTPS1, and CDH13) for which wild Iberian wolves carry alleles introgressed from dogs. The genes with introgressed and positively selected alleles include functions in immune response and brain functions, which may explain some of the unique behavioural phenotypes in Iberian wolves such as their reduced dispersal compared to other wolf populations. Show less
Consumption of beverages that contain fructose favors the increasing prevalence of metabolic syndrome alterations in humans, including non-alcoholic fatty liver disease (NAFLD). Although the only effe Show more
Consumption of beverages that contain fructose favors the increasing prevalence of metabolic syndrome alterations in humans, including non-alcoholic fatty liver disease (NAFLD). Although the only effective treatment for NAFLD is caloric restriction and weight loss, existing data show that atorvastatin, a hydroxymethyl-glutaryl-CoA reductase inhibitor, can be used safely in patients with NAFLD and improves hepatic histology. To gain further insight into the molecular mechanisms of atorvastatin's therapeutic effect on NAFLD, we used an experimental model that mimics human consumption of fructose-sweetened beverages. Control, fructose (10% w/v solution) and fructose+atorvastatin (30 mg/kg/day) Sprague-Dawley rats were sacrificed after 14 days. Plasma and liver tissue samples were obtained to determine plasma analytes, liver histology, and the expression of liver proteins that are related to fatty acid synthesis and catabolism, and inflammatory processes. Fructose supplementation induced hypertriglyceridemia and hyperleptinemia, hepatic steatosis and necroinflammation, increased the expression of genes related to fatty acid synthesis and decreased fatty acid β-oxidation activity. Atorvastatin treatment completely abolished histological signs of necroinflammation, reducing the hepatic expression of metallothionein-1 and nuclear factor kappa B binding. Furthermore, atorvastatin reduced plasma (x 0.74) and liver triglyceride (x 0.62) concentrations, decreased the liver expression of carbohydrate response element binding protein transcription factor (x 0.45) and its target genes, and increased the hepatic activity of the fatty acid β-oxidation system (x 1.15). These effects may be related to the fact that atorvastatin decreased the expression of fructokinase (x 0.6) in livers of fructose-supplemented rats, reducing the metabolic burden on the liver that is imposed by continuous fructose ingestion. Show less