A potential mechanism for impaired vasorelaxation in a dietary model of metabolic syndrome

Poor early growth confers an increased risk of developing type 2 diabetes, hypertension, and other features of the metabolic syndrome in later life. This may result from a mismatch during early life exerting permanent effects on the structure and function of key metabolic organ systems, including the vasculature. Mice (C57BL/J) were exposed to either a high fat (HF, 45% kcal fat) or standard animal chow (C, 21% kcal fat) diet throughout pregnancy and lactation. Male offspring were then continued on the same diet as their dams or crossed over onto the alternative diet, for 10 to 12 weeks post weaning. Those fed the HF diet post weaning (HF/HF and C/HF groups) gained more weight and had a higher blood pressure than the C/C and HF/C animals. They also showed an impaired endothelium-dependent relaxation to ACh and higher basal NO production (P<0.05). Our preliminary data demonstrate the impact of an in utero and postnatal HF diet on vascular function through an impairment of NO production and/or bioavailability. It further suggests that both predisposition to disease, acquired in early life, and later lifestyle may contribute to the development of cardiovascular disease which are sustained into adulthood