Ligation of the uterine arteries in rats (LIG) serves as a model of intrauterine growth restriction (IUGR) and subsequent developmental programming of impaired glucose tolerance, hyperinsulinemia and adiposity in the offspring. Its impact on lipid metabolism has been less well investigated.

We compared parameters of glucose and lipid metabolism and glucocorticoid levels in the offspring of dams which underwent either LIG or sham operation (SOP) with those of untreated controls (C). Blood parameters including insulin, leptin and visfatin as well as body weight, food intake and creatinine clearance were recorded up to an age of 30 weeks, glucose tolerance tests were performed and both leptin and visfatin expression in liver, muscle, epididymal and mesenteric fat was quantified by RT-PCR. After catch-up growth, weight gain of all groups was similar, despite lower food intake of the LIG rats. LIG offspring showed impaired glucose tolerance from the age of 15 weeks as well as elevated glycosylated hemoglobin and corticosterone levels. However, the body fat content of both LIG and SOP animals increased relative to C, and both showed elevated triglyceride, total cholesterol and leptin levels as well as a reduced proportion of HDL cholesterol. Thus, use of the LIG model requires both SOP and C controls. While only LIG is associated with impaired glucose tolerance, pathogenic programming of the lipid metabolism can also be induced by SOP. Visfatin does not appear to be involved in the disturbed glucose metabolism following IUGR and may only represent a marker of fat accumulation.