Abstract:Epidemiologically, metabolic disorders have garnered much attention, perhaps due to the predominance of obesity. The early postnatal life represents a critical period for programming multifactorial metabolic disorders of adult life. Though, altricial rodents are prime subjects for investigating neonatal programming, there is still no sufficiently generalised literature on their usage and methodology. This review focuses on establishing five approach-based models of neonatal rodents adopted for studying metabol… Show more
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.
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.
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