Abstract:
Background: The growing rate of obesity, metabolic syndrome and infertility is a significant health issue. Over recent years, maternal diet has been exposed as a driving force for predisposing chronic adult-onset conditions in offspring. These outcomes are associated with a state of chronic low-grade inflammation. IL-1R1, an important signalling mediator links these inflammatory and metabolic systems. Previous studies show IL-1R1 knockout (IL-1R1-/-) male mice are protected against metabolic abnormalities associated with a high-fat diet (HFD). This study will further examine the role of IL-1R1 depletion in the context of HFD-induced developmental programming of male adult offspring metabolic and reproductive function. Methods: Control C57BL/6 mice and weight and age-matched IL-1R1-/- were assigned either a control diet (10%kcal from fat) or high-fat diet (45%kcal from fat) in which body weight and food intake were assessed. Age of puberty onset and puberty weight were recorded in the male offspring of these mice. Glucose tolerance tests were administered to assess metabolic function, and the expression of genes in the testes was determined by RT-PCR. Results: IL-1R1-/- in maternal mice showed a reduction in weight gain during pregnancy; this reduction was furthered by a HFD. Male offspring of HFD fed IL-1R1-/- mice demonstrated no significant differences in body weight and glucose tolerance. However, IL-1R1-/- male offspring mice displayed a reduction in the expression of genes involved in reproduction in the testes. Discussion: Results indicate that depletion of IL-1R1 does not provide protective effects against HFD-induced weight gain and glucose intolerance in adult male offspring. Despite this, removal of IL-1R1 signalling has positive effects on the reproductive function of male offspring of maternal HFD-induced obesity mice.
