Calcium plays important roles in lipid metabolism and adipogenesis, but whether its status in early life affects later
lipid profiles needs to be clarified. Three to four-week old C57BL/6J female mice were fed with three different reproductive diets containing normal, low (insufficient) and high (excessive)
calcium concentrations respectively throughout pregnancy and lactation. At postnatal 21 days, the weaning male and female pups from each group were sacrificed for experiments and the remaining were fed with the normal chow diet for 16 weeks. Meanwhile, some of the weaning female pups from maternal low
calcium diet group were fed with the normal
calcium, low
calcium and high
calcium mature diets respectively for 8 weeks. Maternal insufficient or excessive
calcium status during pregnancy and lactation programmed an abnormal expression of hepatic and adipose genes (
PPAR-γ, C/EBP-α, FABP4, Fasn, UCP2,
PPAR-α, HMG-Red1, Acc1, and
SREBP-1c) in the offspring and this may lead to
dyslipidemia and accumulation of hepatic
triglyceride (TG) and total
cholesterol (TC) in later life. The effects of maternal
calcium status on lipid metabolism were found only in the female adult offspring, but were similar between offspring males and females at postnatal 21 days. Additionally, the
dyslipidemia and hepatic
lipid accumulation caused by insufficient
calcium status in early life may be reversed to some extent by
dietary calcium supplementation in later life.