Fig. 6. Schematic overview of potential IL-4Rα contribution to HF + HC-driven obesity and obesity-associated metabolic derangements.

Schematic overview of the potentially impact of IL-4Rα-deficiency on hepatic fructose metabolism in mice fed high-fat + high carbohydrate diet. IL-4Rα-deficient mice on HF + HC diet show protection from weight gain, adiposity, insulin dysmetabolism and hepatocellular damage. Fructose is metabolized in the intestine and the liver. KHK-C is the first/key enzyme in fructolysis. KHK-C impacts de novo lipogenesis (DNL) and suppress fatty acid oxidation (FAO). Our data shows that IL-4Rα-deficient mice potentially have lower KHK-C expression which can explain their increased expression of genes related to FAO and could represent an underlying mechanism explaining their protection from weight gain and associated metabolic derangements.