Early-life factors are associated with nocturnal cortisol and glucose effectiveness in Afro-Caribbean young adults.

CONTEXT: Early-life factors (including intrauterine growth retardation) may influence the development of type 2 diabetes. We postulated that birth size is associated with cortisol levels, which itself could alter serum adipomyokines (i.e. adiponectin, IGF-I, myostatin) and glucose metabolism. DESIGN: An observational study with 60 Afro-Caribbean young adults from a birth cohort. MEASUREMENTS: Fasting blood was drawn for serum adiponectin, IGF-I and myostatin. A frequently sampled intravenous glucose tolerance test measured insulin sensitivity (SI), acute insulin response (AIRg), disposition index (DI) and glucose effectiveness (Sg). Body composition was assessed by dual-energy X-ray absorptiometry. Salivary cortisol was collected at home at 0800 and 2300 h. Sex-adjusted correlations were used to explore the relationships between birth size, cortisol and the metabolic variables. RESULTS: The participants were 55% male, mean age 23·1 ± 0·5 years. Birth weight correlated positively with 2300-h cortisol (P = 0·04), although not after adjusting for gestational age. Gestational age was correlated with 2300 h cortisol (r = 0·38, P = 0·03), even after adjusting for birth weight (P = 0·02). 2300 h cortisol was not associated with adiponectin, IGF-I, myostatin, SI, AIRg or DI, but was negatively correlated with Sg (r = -0·30, P = 0·05) even after adjusting for birth and adult anthropometry. Adiponectin, IGF-I and myostatin were unrelated to glucose metabolism. CONCLUSIONS: Gestational age is associated with higher nocturnal cortisol, which in turn is associated with lower glucose effectiveness in adulthood. Higher glucose effectiveness could therefore be a compensatory mechanism to improve glucose uptake.

A potential indicator of denervated muscle atrophy: the ratio of myostatin to follistatin in peripheral blood.

Myostatin is a secreted negative regulator of muscle mass, and follistatin antagonizes the function of several members of the TGF-b family, including myostatin. Previously, myostatin expression was found to be closely associated with atrophy of the gastrocnemius muscle, showing a linear correlation, after sciatic nerve injury. In this study, we investigated the possibility of myostatin being an indicator of denervated muscle atrophy. ELISA was used to detect the concentration of myostatin and follistatin in sera collected from individual rats at different times after sciatic nerve crush. A strong correlation was shown between the expression level of secreted myostatin in circulation and the wet weight ratio of the gastrocnemius muscle. The ratio of follistatin/myostatin could be used to monitor the progress of target muscle atrophy and recovery. Our study provides a potential serological test to detect denervated muscle atrophy for clinical purposes.