Hyperlipidemias: Herrera E

Herrera E, Amusquivar E, López-Soldado I, Ortega H. · Department of Biochemistry, Molecular and Cellular Biology, University San Pablo-CEU, Madrid, Spain. · Horm Res. · Pubmed #16612115 No free full text.

Abstract: During early pregnancy, long-chain polyunsaturated fatty acids (LC-PUFA) may accumulate in maternal fat depots and become available for placental transfer during late pregnancy, when the fetal growth rate is maximal and fetal requirements for LC-PUFAs are greatly enhanced. During this late part of gestation, enhanced lipolytic activity in adipose tissue contributes to the development of maternal hyperlipidaemia; there is an increase in plasma triacylglycerol concentrations, with smaller rises in phospholipid and cholesterol concentrations. Besides the increase in plasma very-low-density lipoprotein, there is a proportional enrichment of triacylglycerols in both low-density lipoproteins and high-density lipoproteins. These lipoproteins transport LC-PUFA in the maternal circulation. The presence of lipoprotein receptors in the placenta allows their placental uptake, where they are hydrolysed by lipoprotein lipase, phospholipase A(2) and intracellular lipase. The fatty acids that are released can be metabolized and diffuse into the fetal plasma. Although present in smaller proportions, maternal plasma non-esterified fatty acids are also a source of LC-PUFA for the fetus, their placental transfer being facilitated by the presence of a membrane fatty acid-binding protein. There is very little placental transfer of glycerol, whereas the transfer of ketone bodies may become quantitatively important under conditions of maternal hyperketonaemia, such as during fasting, a high-fat diet or diabetes. The demands for cholesterol in the fetus are high, but whereas maternal cholesterol substantially contributes to fetal cholesterol during early pregnancy, fetal cholesterol biosynthesis rather than cholesterol transfer from maternal lipoproteins seems to be the main mechanism for satisfying fetal requirements during late pregnancy.

Herrera E. · Facultad de Ciencias Experimentales y de la Salud, Universidad San Pablo-CEU, Madrid, Spain. · Endocrine. · Pubmed #12583601 No free full text.

Abstract: During early pregnancy there is an increase in body fat accumulation, associated with both hyperphagia and increased lipogenesis. During late pregnancy there is an accelerated breakdown of fat depots, which plays a key role in fetal development. Besides using placental transferred fatty acids, the fetus benefits from two other products: glycerol and ketone bodies. Although glycerol crosses the placenta in small proportions, it is a preferential substrate for maternal gluconeogenesis, and maternal glucose is quantitatively the main substrate crossing the placenta. Enhanced ketogenesis under fasting conditions and the easy transfer of ketones to the fetus allow maternal ketone bodies to reach the fetus, where they can be used as fuels for oxidative metabolism as well as lipogenic substrates. Although maternal cholesterol is an important source of cholesterol for the fetus during early gestation, its importance becomes minimal during late pregnancy, owing to the high capacity of fetal tissues to synthesize cholesterol. Maternal hypertriglyceridemia is a characteristic feature during pregnancy and corresponds to an accumulation of triglycerides not only in very low-density lipoprotein but also in low- and high-density lipoprotein. Although triglycerides do not cross the placental barrier, the presence of lipoprotein receptors in the placenta, together with lipoprotein lipase, phospholipase A2, and intracellular lipase activities, allows the release to the fetus of polyunsaturated fatty acids transported as triglycerides in maternal plasma lipoproteins. Normal fetal development needs the availability of both essential fatty acids and long chain polyunsaturated fatty acids, and the nutritional status of the mother during gestation has been related to fetal growth. However, excessive intake of certain long chain fatty acids may cause both declines in arachidonic acid and enhanced lipid peroxidation, reducing antioxidant capacity.

Otero P, Bonet B, Herrera E, Rabano A. · Facultad de Ciencias Experimentales y de la Salud, Universidad San Pablo-CEU, Madrid, Spain. · Atherosclerosis. · Pubmed #16159598 No free full text.

Abstract: The aim of the present study was to determine in the BALB/c mice, a model of development of atherosclerosis when both hyperglycemia and hypercholesterolemia are present, whether the atherogenic effects of these parameters could be decreased with the administration of Vitamin E. BALB/c mice were made diabetic and divided in three groups: one fed the standard rodent chow diet (D); the other two fed an atherogenic diet (D+A); one of them supplemented with Vitamin E (D+A+E). Two groups of non diabetic animals were also performed, one fed the standard diet (C) and the other the atherogenic diet (C+A). After 16 weeks of treatment all the control animals survived, in contrast, a mortality rate of 12, 70 and 37% was observed, respectively, in the D, D+A and D+A+E groups. Neither fatty deposits nor macrophages were observed in the arterial wall of the animals fed the standard diet (D and C animals). In contrast, this finding was observed in 25% of the C+A, 71% of the D+A and 33% of the D+A+E. In conclusion, diabetic mice fed an atherogenic diet showed in the aorta a higher number of fatty deposits and macrophages than the control animals. These effects were partially reversed with the administration of Vitamin E, supporting in this model the role of oxidative stress in the development of atherosclerosis.

Munilla MA, Herrera E. · Facultad de Ciencias Experimentales y Técnicas, Universidad San Pablo-CEU, E-28668 Boadilla del Monte, Madrid, Spain. · J Nutr. · Pubmed #11110841 links to  free full text

Abstract: Feeding a sucrose-rich diet (SRD) during pregnancy enhances maternal hypertriglyceridemia. The goal of this study was to investigate whether this effect is modified when pregnancy is initiated in rats at different times during 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 tail blood collections, rats were studied at d 20 of pregnancy. Virgin rats fed the same diets were always studied in parallel. Plasma triglycerides increased progressively in virgin rats fed the SRD from d 1 to 35, declined thereafter up to d 50, increased again to attain the highest level at d 65-70, partially declined at d 100 and increased again at d 110. During late pregnancy, rats fed the control diet (CD) always had greater plasma triglyceride concentrations than virgin rats, whereas triglyceride levels did not differ between pregnant and virgin rats fed the SRD. These intergroup differences were similar to those seen for plasma VLDL-triglycerides. The liver triglyceride concentration in virgin rats fed the SRD was always significantly higher than that of rats fed the CD, whereas it did not differ in pregnant 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 developing a fatty liver when fed a SRD for short periods of time, although not for long-term treatments.