Abstract
The role of fructose in the global obesity and metabolic syndrome epidemic is widely recognized. However, its consumption is allowed during pregnancy. We have previously demonstrated that maternal fructose intake in rats induces detrimental effects in fetuses. However, these effects only appeared in adult descendants after a re-exposure to fructose. Pregnancy is a physiological state that leads to profound changes in metabolism and hormone response. Therefore, we wanted to establish if pregnancy in the progeny of fructose-fed mothers was also able to provoke an unhealthy situation. Pregnant rats from fructose-fed mothers (10% w/v) subjected (FF) or not (FC) to a fructose supplementation were studied and compared to pregnant control rats (CC). An OGTT was performed on the 20th day of gestation, and they were sacrificed on the 21st day. Plasma and tissues from mothers and fetuses were analyzed. Although FF mothers showed higher AUC insulin values after OGTT in comparison to FC and CC rats, ISI was lower and leptinemia was higher in FC and FF rats than in the CC group. Accordingly, lipid accretion was observed both in liver and placenta in the FC and FF groups. Interestingly, fetuses from FC and FF mothers also showed the same profile observed in their mothers on lipid accumulation, leptinemia, and ISI. Moreover, hepatic lipid peroxidation was even more augmented in fetuses from FC dams than those of FF mothers. Maternal fructose intake produces in female progeny changes that alter their own pregnancy, leading to deleterious effects in their fetuses.
Highlights
In the present work, we wanted to answer two questions: (1) given that pregnancy is a physiological state that produces profound changes in lipids and glucose metabolism and insulin and leptin responses in dams, would pregnancy alone be sufficiently able to reveal the programmed phenotype hidden in females from fructose-fed dams? and (2) since we observed in non-pregnant rats that the programmed phenotype was initially hidden but appeared when fructose was offered to descendants of fructose-fed mothers [28], what effects would this re-exposure to fructose produce in females from fructose-fed dams when they were pregnant? we evaluated whether this situation could affect their fetuses and we studied how the placenta was involved in this process
The body weight (BW) at the beginning of the experiment was different between descendants from fructose-fed mothers and those from control mothers (FC and fructose-fed dams (FF) vs. compared to controls (CC)), no changes in maternal BW increase throughout gestation were found between the three groups evaluated (Table 1)
Despite the increased amount of calories ingested by the FF mothers, no changes in the conceptus weight, the number or the BW of their fetuses were observed when compared to CC and fructose supplementation (FC) dams (Table 1)
Summary
Many studies have demonstrated how an inappropriate nutrition and/or diseases such as obesity and diabetes during pregnancy can promote metabolic and cardiovascular disturbances in the offspring when adults [1] The mechanism underlying this effect is called fetal programming [2]. The placenta plays a key role in this process, since it regulates the correct supply of nutrients and protects the fetus ensuring correct fetal development [3]. Both mother malnutrition and overnutrition during pregnancy can cause deleterious effects in the progeny such as defective hormonal responses, oxidative stress and epigenetic modifications [4,5]. A higher risk of cardiovascular diseases and diabetes in descendants from obese or diabetic mothers has been well-described in the bibliography [6,7]
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