Abstract
Delay in the onset of lactogenesis has been shown to occur in women who are obese, however the mechanism altered within the mammary gland causing the delay remains unknown. Consumption of high fat diets (HFD) has been previously determined to result decreased litters and litter numbers in rodent models due to a decrease in fertility. We examined the effects of feeding a HFD (60% kcal from fat) diet versus a low-fat diet (LFD; 10% kcal from fat) to female Wistar rats on lactation outcomes. Feeding of HFD diet resulted in increased pup weights compared to pups from LFD fed animals for 4 d post-partum. Lactation was delayed in mothers on HFD but they began to produce copious milk volumes beginning 2 d post-partum, and milk yield was similar to LFD by day 3. Mammary glands collected from lactating animals on HFD diet, displayed a disrupted morphologies, with very few and small alveoli. Consistently, there was a significant decrease in the mRNA expression of milk protein genes, glucose transporter 1 (GLUT1) and keratin 5 (K5), a luminobasal cell marker in the mammary glands of HFD lactating animals. Expression of tryptophan hydroxylase 1 (TPH1), the rate-limiting enzyme in serotonin (5-HT) biosynthesis, and the 5-HT7 receptor (HTR7), which regulates mammary gland involution, were significantly increased in mammary glands of HFD animals. Additionally, we saw elevation of the inflammatory markers interleukin-6 (IL-6) and tumor necrosis factor-α (TNF- α). These results indicate that consumption of HFD impairs mammary parenchymal tissue and impedes its ability to synthesize and secrete milk, possibly through an increase in 5-HT production within the mammary gland leading to an inflammatory process.
Highlights
Obesity has profound negative impacts on numerous physiological processes
In addition to elevated tryptophan hydroxylase 1 (TPH1) expression, we demonstrated an increase in HTR7 mRNA expression in the high fat diets (HFD)-lactating animals compared to low-fat diet (LFD)-lactating and HFD-non lactating animals (Figure 4f)
Several studies have indicated that maternal obesity contributes to delayed onset of lactogenesis, reduced breast-feeding duration, as well increased birth weights [6,26,27]
Summary
Obesity has profound negative impacts on numerous physiological processes. Prevalence of obesity of adult women in the United States from 1999–2008 is approximately 36%, with approximately 60% of women of a reproductive age (20–39 years of age) being either overweight or obese [1]. Excessive weight gain during pregnancy increases the mother’s risk of developing breast cancer [3]. Delayed lactogenesis (failure to lactate for .72 h post-partum) is correlated with a shorter duration of breast-feeding [8]. In dairy cattle over-feeding during the pre-pubertal period has been determined to cause a permanent decrease in milk yield potential [9]. In studies in rat models, pre-pregnancy overweight and obesity has been determined to decrease the response to suckling induced prolactin and disrupt normal mammary gland development during pregnancy [10]. Consumption of high-fat diets during pregnancy has been determined to decrease the amount of myoepithelium in the mammary gland, which is thought to increase breast cancer risk [11]
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