Abstract: SAT 456

Decreased Prolactin Levels Induced By an Obesogenic Diet in Lactating Mothers Contribute to Metabolic Alterations in Their Offspring

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Abstract


Abstract. Maternal obesity during lactation generates insulin resistance (IR) in the offspring1,2. We have shown that prolactin (PRL), a critical hormone for the regulation of lactation, is reduced in the circulation of adult obese rats, and treatment with the hormone improves IR in those animals3; however, little is known about the effects of PRL on the offspring metabolism during lactation. In this study, we evaluated whether a 60% high fat diet (OD) in lactating mothers reduced PRL levels in serum and milk, and if this diminution contributes to IR in their offspring. view more

Abstract. Maternal obesity during lactation generates insulin resistance (IR) in the offspring1,2. We have shown that prolactin (PRL), a critical hormone for the regulation of lactation, is reduced in the circulation of adult obese rats, and treatment with the hormone improves IR in those animals3; however, little is known about the effects of PRL on the offspring metabolism during lactation. In this study, we evaluated whether a 60% high fat diet (OD) in lactating mothers reduced PRL levels in serum and milk, and if this diminution contributes to IR in their offspring. Lactating Wistar rats fed with control diet (CD) or OD throughout the 21 days of lactation were treated or not with PRL delivered by subcutaneous osmotic mini-pumps (OD+PRL). Additionally, the offspring from OD dams were treated orally with vehicle or PRL (oPRL) during the lactation period, in an equivalent concentration of that present in milk4. We found that OD in mothers generated a significant reduction in milk PRL levels of 39% and 46% at days 7 and 21 of lactation, respectively, whereas the OD+PRL group showed higher levels of milk PRL at day 7 (similar to the CD group) and increased serum PRL levels at day 21 (p<0.05) compared to OD group. In addition, offspring from mothers on OD showed 23% higher body weight gain and 46% higher visceral adipose tissue (VAT) mass compared to offspring from CD-fed mothers, whereas PRL treatment in mothers and PRL given orally to the offspring lead to 35% and 31% lower VAT mass in the offspring, respectively, compared to those from mothers on OD. Furthermore, an OD in mothers generated IR in their offspring, as shown by higher glucose levels during an insulin tolerance test compared to offspring from CD-fed mothers, whereas both types of PRL treatment resulted in an amelioration of offspring IR. In conclusion, maternal obesity during lactation results in reduced milk PRL levels and IR in their offspring. PRL treatment restores milk PRL levels, reduces visceral adiposity, and promotes insulin sensitivity in the offspring from OD-fed mothers, suggesting an important function of milk PRL on the offspring metabolic health.

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