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not metabolized in fetal tissues of domestic animals. The activities of glucose 6 phosphate dehydrogenase, malic enzyme and acetyl CoA carboxylase in liver are stimulated by glucose in adult rats which increases lipogenesis and fructose enters adipocytes by both GSK525762 insulin independent and insulin insensitive mechanisms. It is of interest that researchers focused on intra uterine growth restriction too as subsequent adult onset of metabolic disease in various ungulate spe cies have not deemed fructose to be an essential metabolic substrate. This seems to be so simply because fruc tose is not metabolized through the glycolytic pathway or Krebs cycle within the placenta, fetus or neonate. In ewes, for instance, the maximum con centration of glucose in allantoic fluid is 1.
1 mmol/L be tween Days 35 and 140 of pregnancy, whereas the concentration of fructose is amongst 11. 1 and 33 mmol/L throughout the identical period of pregnancy. For that reason, fructose is exerting effects on cell proliferation at molar concentrations well beneath those in allantoic fluid. Glu cose, GSK525762 on the other hand, exerts effects at concentrations well above those in allantoic fluid. Fructose may be one of the most likely hexose sugar to stimulate MTOR nutrient sensing cell signaling and synthesis of glycosaminogly cans from fructose and glutamine through the hexosamine pathway to stimulate growth T0901317  and develop ment with the conceptus. Fructose is also the main sugar in blood, allantoic fluid and amniotic fluid with the fetal pig to about Day 80 of gestation, but it decreases thereafter as glucose increases amongst Days 82 and 112 with the 114 day period of gesta tion.
The fast clearance of fructose from blood of piglets by 24 h post partum indicates that the neonatal piglet is unable to utilize fructose as an energy source. Based on the lack of understanding with the role of fruc tose, one of the most abundant hexose sugar within the pregnant uterus, we conducted experiments to learn that fruc tose is actively involved in stimulating cell proliferation and Ribonucleotide mRNA translation through activation of MTOR cell sig naling and synthesis of glycosaminoglycans through the hex osamine metabolic pathway. Glucose induces proliferation of human trophoblast cells through MTOR signaling in a PI3K independent mechanism that involves activation of MTOR by metabolites with the GFPT1 path way, particularly UDP N acetylglucosamine.
UDP GlcNAC is responsible for phosphorylation of TSC2, a GTPase T0901317  activating protein, and p70S6K1, a pro tein kinase downstream of MTOR, to stimulate tropho blast cell proliferation in response to metabolism of glucose to glucose 6 PO4, fructose 6 PO4 and glucosa mine 6 PO4. Glucose and fructose can also be applied within the hexosamine pathway for synthesis of hyaluronic acid that may have an effect on angiogenesis along with other aspects of fetal placental development throughout pregnancy. The pig pla centa contains substantial amounts of hyaluronic acid and hyaluronidase, both of which improve within the uterine lumen of pigs in response to progesterone. Hyalur onic acid could stimulate angiogenesis and/or stimulate angiogenesis, morphogenesis and tissue remodeling with the placenta as reported for the human placenta.
The accumulation of Whartons Jelly occurs within the placentae of most mammals and localizes to the umbilical cord primar ily, but to a lesser extent to placental blood vessels and it really is composed mainly of hyaluronic acid that also supports fibroblasts and stem cells. It is clear that angiogenesis is essential to conceptus GSK525762 development in all species and results with the present study indicate that fruc tose is applied for synthesis of glycosaminoglycans like hyaluronic acid that support angiogenesis, particularly within the placenta. There's altered glucose metabolism in ewes with fetuses that encounter intrauterine growth retardation on account of placental insufficiency which affects T0901317  concentra tions of myo inositol, sorbitol and fructose.
The redirec tion of placental glucose into myo inositol is likely on account of decreased sorbitol and fructose production GSK525762 within the placenta through aldose reductase that demands NADPH. The abundance of fructose is likely on account of high hepatic sorbitol dehydrogenase activity and high placental aldose reductase activity for conversion of glucose to sorbitol. Glucose is transported into T0901317  and out of cells by both facili tative and sodium dependent transporters. The glucose transporters SLC2A1 and SLC5A1 are most abundant in ovine endometria and SLC2A1, SLC2A3, SLC2A4, SLC5A1 and SLC5A11 are most abundant in trophectoderm and endoderm of ovine conceptuses. A portion of glucose transported into trophoblast cells is converted to fructose which is unable to return to the maternal circulation, but does enter the fetal circulation. Fructose may be converted to fructose 6 phosphate after which to glucosamine 6 phosphate by glutamine fructose 6 phosphate amido transferase 1. Glucosamine 6 phosphate is needed for production of glycosaminoglycans like hyaluronans necessary for formation with the fetal placen