The effects of cadmium and high fructose diet on metabolic and reproductive health in female CD-1 mice.

Background: Evaluation of the combined effects of endocrine-disrupting chemicals and dietary factors provides critical information for cumulative health risk assessment. Herein, we investigated the effects of cadmium (Cd) exposure and high fructose (HFr) diet on metabolic and reproductive health in female mice.

Methods: Female CD-1 mice were exposed to cadmium chloride (CdCl) (0.

Fructose regulates the pentose phosphate pathway and induces an inflammatory and resolution phenotype in Kupffer cells.

Over-consumption of fructose in adults and children has been linked to increased risk of non-alcoholic fatty liver disease (NAFLD). Recent studies have highlighted the effect of fructose on liver inflammation, fibrosis, and immune cell activation. However, little work summarizes the direct impact of fructose on macrophage infiltration, phenotype, and function within the liver.

Myeloid cell MHC I expression drives CD8 T cell activation in nonalcoholic steatohepatitis.

Background & Aims: Activated CD8 T cells are elevated in Nonalcoholic steatohepatitis (NASH) and are important for driving fibrosis and inflammation. Despite this, mechanisms of CD8 T cell activation in NASH are largely limited. Specific CD8 T cell subsets may become activated through metabolic signals or cytokines.

Beneficial effects of eicosapentaenoic acid on the metabolic profile of obese female mice entails upregulation of HEPEs and increased abundance of enteric Akkermansia muciniphila.

Eicosapentaenoic acid (EPA) ethyl esters are of interest given their clinical approval for lowering circulating triglycerides and cardiometabolic disease risk. EPA ethyl esters prevent metabolic complications driven by a high fat diet in male mice; however, their impact on female mice is less studied. Herein, we first investigated how EPA influences the metabolic profile of female C57BL/6J mice consuming a high fat diet.