Glucose Fetus

The high demand for glucose by the fetus and fot synthesis of lactose in lactation can lead to ketosis. This may be seen as mild ketosis with hypoglycemia in women, but in lactating cattle and in ewes cattying twins thete may be vety pronounced ketosis and profound hypoglycemia. 

Rogers JM, Morelli L, Grabowski CT. 1984. Plasma glucose and protein concentrations in rat fetuses and neonates exposed to cataractogenic doses of mirex. Environ Res 34 155-161. 

Acarbose is a glucopyranose derivative that acts by inhibiting intestinal a-gluco-sidase. This delays carbohydrate absorption and reduces the postprandial (1.5 hours after food) blood glucose levels and is used in combination with other sulfonyl-ureas. Acarbose may cause GI disturbances, flatulence, abdominal distortion, diarrhea, and pain. Acarbose should be avoided during pregnancy, as it affects the fetus. Acarbose is contraindicated in inflammatory bowel disease and hepatic dysfunction. 

An eight-month pregnant medical student complains of lower abdominal pain and a 48-hour history of dysuria. She does not have any fever an analysis of her urine shows protein, but no blood or glucose. A culture is taken. Which of the following is useful for treating this urinary tract infection orally without causing risks to the fetus ... 

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. 

With the above discussion in mind, it is possible to predict at least some of the consequences to the fetus and newborn of an elevated maternal blood glucose concentration, such as occurs in diabetes nielli tus (Cowett, 1998). As the maternal blood glucose level increases, the gradient between fetal and maternal blood glucose... 

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. 

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. 

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