Neonatal administration of fenofibrate had no developmental programming effect on the lipid profile and relative leucocyte telomere lengths of adolescent rats fed a high-fructose diet postnatally.

INTRODUCTION Telomere length, a marker of ageing is susceptible to developmental programming that may cause its accelerated attrition. Metabolic syndrome triggers telomere attrition. Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist is protective against telomere attrition. We investigated the impact of fenofibrate administered during suckling on the lipid profile and leucocyte telomere lengths of rats fed a high fructose diet post-weaning. METHODS Suckling Sprague-Dawley pups (n=119) were allocated to four groups and gavaged with either 10ml.kg-1 body mass 0.5% dimethyl sulfoxide, 100mg.kg-1 body mass fenofibrate, fructose (20%, w/v) or a combination of fenofibrate and fructose for 15 days. Upon weaning, each of the initial groups was split into two subgroups: one had plain water while the other had fructose solution (20%, w/v) to drink for six weeks. Blood was collected for DNA extraction and relative leucocyte telomere length determination by real-time PCR. Plasma triglycerides and cholesterol were also quantified. RESULTS The treatments had no effect (p>0.05) on body mass, cholesterol concentration, and relative leucocyte telomere lengths in both sexes. Post-weaning fructose increased triglyceride concentrations (p<0.05) in female rats. CONCLUSION Fenofibrate administered during suckling, did not affect ageing nor did it prevent high fructose-induced hypertriglyceridaemia in female rats.