Our findings suggest that increased SBP, DBP and resting HR as well as increased insulin and resistin plasma levels and decreased adiponectin plasma levels pre-exist in young healthy offspring with positive family history for essential hypertension.
Furthermore, CT KO mice exhibited significantly decreased fat contents in the liver, lipid droplets in adipose tissues, serum glucose, and lipid levels, and significantly increased insulin sensitivity and serum adiponectin levels.
Subsequently, in vitro studies in 3T3-L1 (white) and T37i (brown) adipocytes suggest that the increased leptin and adiponectin levels were mainly driven by the elevated insulin levels.
The observed association between higher adiponectin levels and increased insulin sensitivity is likely to represent a causal relationship partly mediated by reduced adiposity.
When the data were analyzed by adiponectin tertiles, an elevated adiponectin level was associated with high total, oxidative, and nonoxidative glucose disposal and high energy expenditure during hyperinsulinemia; low levels of free fatty acids and low rates of lipid oxidation during hyperinsulinemia; as well as low levels of inflammatory cytokines; and a low amount of intraabdominal fat evaluated by computed tomography.
GE treated groups improved the glucose tolerance, attenuated hyperglycemia and hyperinsulinemia in the mice by up-regulating the adiponectin and GLUT-4 gene expressions.