Glucose placenta

P2Y14 Placenta, adipose tissue, stomach, intestine, discrete brain regions UDP glucose = UDP-galactose Gq/Gu... 

Facilita GLUT1 ive bidirectionai transporters Brain, kidney, colon, placenta, erythrocyte Uptake of glucose... 

A. Ericsson, B. Hamark, T.L. Powell, and T. Jansson. Glucose transporter isoform 4 is expressed in the syncytiotrophoblast of first trimester human placenta. Hum Reprod. 20 521-530 (2005). 

P.A. Vardhana and N.P. Ulsley. Transepithelial glucose transport and metabolism in BeWo choriocarcinoma cells. Placenta. 23 653-660 (2002). 

T FIGURE 10-19 Steroids derived from cholesterol. Testosterone, the male sex hormone, is produced in the testes. Estradiol, one of the female sex hormones, is produced in the ovaries and placenta. Cortisol and aldosterone are hormones synthesized in the cortex of the adrenal gland they regulate glucose metabolism and salt excretion, respectively. Prednisolone and prednisone are synthetic steroids used as antiinflammatory agents. 

Out of this concept grew the cardinal idea of carrier mediated transport. Necessary for this was the development of a more coherent theoretical analysis built upon the general notion of facilitated diffusion. The major insight here came from Widdas who proposed in 1952 that carrier mediated transport would explain earlier data such as the transport of glucose across the sheep placenta, as well as his own observations on glucose entry into the erythrocyte. There were three assumptions made in developing this quantitative hypothesis ... 

Polyol DH (Aldose Human placenta D-Sorbitol D-Glucose NADP A... 

The maternal glucose concentration is extremely critical in determining fetal glucose supply, and a normal fetal endocrine environment is important in modulating the way the fetus uses this supply of glucose. The endocrine milieu of the fetus provides an anabolic environment within which the fetus can produce complex macromolecules from simpler precursors. Although the placenta is essentially impermeable to maternal insulin, the fetal pancreas releases insulin in response to increases in fetal blood glucose concentration. 

Chlorothiazide readily crosses the placenta (149), but there have been few studies of the effects of diuretic treatment on the fetus. There are case reports of abnormalities of glucose handling (150) and severe electrolyte disturbances (151) in pregnant women taking diuretics. 

GLUT3 (brain) Wide distribution, especially neurons, placenta, and testis Glucose transport in neurons... 

GLUT 3 Brain, placenta, fetal muscle Low provide glucose for tissue cells metabolically dependent on glucose... 

As noted above, there have been reports that link some cases of APLP with a defect in fatty acid metabolism in the fetus. These include fetal deficiencies of long chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD), carnitine-palmitoyl transferase 1 (CPT 1), and medium chain acyl-coenzyme A dehydrogenase (MCAD). The mechanism by which defective fetal fatty acid oxidation causes maternal illness is not known. However, since the fetus uses primarily glucose metabolism for its energy needs, it is likely that toxic products from the placenta, which does use fatty acid oxidation, cause the maternal liver failure. 

Before birth, the chief source of energy for the fetus is glucose obtained from the mother via the placenta. Any excess glucose is stored as liver glycogen. Free fatty acids cross the placenta and are stored in fat. At birth, the baby must switch to gluconeogenesis and glyco-... 

---