ESPE2014 Free Communications Programming & Early Endocrinology (6 abstracts)
aGirona Institute for Biomedical Research, Girona, Spain; bDr Josep Trueta Hospital, Girona, Spain; cUniversitat de Barcelona, Barcelona, Spain; dUniversity of Leuven, Leuven, Belgium; eSant Joan de Déu Childrens Hospital, Esplugues, Barcelona, Spain
Background: STK11 regulates glucose and lipid metabolism. In adult rats, excessive fat deposition and dysfunctional metabolism are related to low STK11 expression in adipose tissue. It is unknown if low STK11 expression in adipose tissue relates also to catch-up growth and fat deposition after intrauterine growth restriction.
Objective and Hypotheses: To assess the expression of STK11 in adipose tissue and its relation to body weight gain and visceral fat mass in prenatally growth-restricted rats.
Method: We used a Wistar rat model of intrauterine growth retardation induced by calorie restriction throughout gestation. Dams fed ad libitum delivered control pups (C), and dams on a 50% calorie-restricted diet delivered growth-restricted pups with low birth weight (R). Restricted offspring fed a standard rat chow after birth showed catch-up growth (RC) whereas restricted offspring kept on a calorie-restricted diet did not show catch-up growth (RR). Body weight gain, visceral fat mass and relative expression of STK11 in retroperitoneal white adipose tissue (WAT) were postnatally assessed in the offspring (n=10 pups/group) at day 42.
Results: Postnatal body weight gain was higher in RC pups compared with RR and control pups (P<0.0001). RC pups showed higher percentages of visceral fat mass (P<0.0001) and retroperitoneal WAT (P<0.0001) and lower STK11 expression in adipose tissue (P<0.005) than RR pups. In RC pups, STK11 expression in adipose tissue was negatively related to postnatal body weight gain (r=−0.652, P=0.012), visceral fat mass (r=−0.584, P=0.028) and retroperitoneal WAT (r=−0.682, P=0.007).
Conclusion: Impaired STK11 expression in adipose tissue could be among the mechanisms involved in catch-up growth and fat mass accumulation following fetal growth restriction in rats. If STK11 expression in adipose tissue is also reduced in low-birthweight children, then this may be one of mechanisms underpinning the beneficial effects of metformin therapy that are observed in such children.