Maternal hypertriglyceridemia during late pregnancy does not affect the increase in circulating triglycerides caused by the long-term consumption of a sucrose-rich diet by rats

Citation
Ma. Munilla et E. Herrera, Maternal hypertriglyceridemia during late pregnancy does not affect the increase in circulating triglycerides caused by the long-term consumption of a sucrose-rich diet by rats, J NUTR, 130(12), 2000, pp. 2883-2888
Citations number
35
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
00223166 → ACNP
Volume
130
Issue
12
Year of publication
2000
Pages
2883 - 2888
Database
ISI
SICI code
0022-3166(200012)130:12<2883:MHDLPD>2.0.ZU;2-4
Abstract
Feeding a sucrose-rich diet (SRD) during pregnancy enhances maternal hypert riglyceridemia. The goal of this study was to investigate whether this effe ct is modified when pregnancy is initiated in rats at different times durin g feeding of a SRD (63 g sucrose/100 g). One group of rats was fed the SRD; another group received the same diet except that the sucrose was replaced by an equal amount of cornstarch. At different times during the feeding of the diets, i.e., 5, 45 or 90 d, half of the rats were mated; after serial r ail blood collections, rats were studied at d 20 of pregnancy. Virgin rats fed the same diets were always studied in parallel. Plasma triglycerides In creased progressively in virgin rats fed the SRD from d 1 to 35, declined t hereafter up to d 50, increased again to attain the highest level at d 65-7 0, partially declined at d 100 and increased again at d 110. During late pr egnancy, rats fed the control diet (CD) always had greater plasma triglycer ide concentrations than virgin rats, whereas triglyceride levels did not di ffer between pregnant and virgin rats fed the SRD. These intergroup differe nces were similar to those seen for plasma VLDL-triglycerides. The liver tr iglyceride concentration in virgin rats fed the SRD was always significantl y higher than that of rats fed the CD, whereas it did not differ in pregnan t rats fed the SRD for either 25 or 65 d from those fed the CD. However, in those fed the SRD for 110 d, values were higher than in either pregnant or virgin rats fed the CD. We propose that the known capability of the liver to enhance triglyceride secretion during pregnancy protects dams from devel oping a fatty liver when fed a SRD for short periods of time, although not for long-term treatments.