Maternal prolactin inhibition during lactation programs for metabolic syndrome in adult progeny. The Journal of physiology [J Physiol] Journal article

Neonatal malnutrition is associated with metabolic syndrome in adulthood. Maternal hypoprolactinemia at the end of lactation (a precocious weaning model) caused obesity, leptin resistance and hypothyroidism in adult offspring, suggesting an association of PRL and programming of metabolic dysfunctions. Metabolic syndrome pathogenesis is still unclear, but abdominal obesity, higher triglycerides, lower HDL-c and insulin resistance have been proposed to be important factors involved. Then, we studied the consequences of maternal hypoprolactinemia during lactation on parameters associated with metabolic syndrome. Lactating Wistar rats were treated with bromocriptine (BRO, 1mg/2x/day) or saline on days 19, 20 and 21 of lactation and their offspring were followed from weaning until 180 days-old. Adult BRO offspring had higher body weight (+10%, p<0.05), total body fat (+41%, p<0.05), visceral fat (+20%, p<0.05), subcutaneous fat (+ 3 times, p<0.05) and total body protein (+24%, p<0.05). BRO group presented hyperglycemia (+16%, p<0.05), lower muscle glycogen (-51%, p<0.05), higher cholesterol (+30%, p<0.05), higher LDL-c (+ 1.5 times, p<0.05), higher triglycerides (+49%, p<0.05), lower HDL-c (-28%, p<0.05), hyperleptinemia (+ 2.9 times, p<0.05), hypoadiponectinemia (-16%, p<0.05) and hypoprolactinemia (-54%, p<0.05) as well as higher insulin resistance index (+24%, p<0.05). Regarding adrenal function, BRO rats showed hypercorticosteronemia (+46%, p<0.05) and higher total catecholamine (+37%, p<0.05). In hypothalamus, no change was observed in proteins expression of leptin signalling pathway. Thus, neonatal malnutrition induced by maternal PRL inhibition during late lactation programs for obesity, dyslipidemia and insulin resistance in adult offspring increasing the risk for metabolic syndrome development.

The Journal of physiology [J Physiol]