Since the homeostasis of carbohydrate-lipid metabolism during normal pregnancy resembles to the metabolic state of mild diabetes mellitus, pregnancy is often called “diabetogenic”, and, as the foetus depends upon a large and constant glucose supply from the maternal body for its rapid growth and energy demand, it may be called “a glucose dependent parasite”. Therefore, alterations in maternal metabolism will directly lead to changes in fetal metabolism and growth.
The authors investigated the concentrations of blood glucose, serum free fatty acids, triglycerides, β-lipoprotein, insulin, human chorionic somatomammotropin (hCS), plasma glucagon after an overnight fast and the changes of these polypeptide hormones' levels by intravenous or oral G. T. T. in normal women at early, mid and late pregnancy.
In total, 140 normal women from 7th to 40th gestation week who visited the department of obstetrics and gynecology, Kobe University, school of medicine volunteered for this study. Blood was drawn from vein of 70 normal pregnant women after an overnight fast and the other volunteers were subjected to 50 grams O-G. T. T. or 25 grams I. V.-G. T. T.
Serum insulin and hCS were measured by radioimmunoassay of double antibody method, plasma glucagon by radioimmunoassay of charcoal method utilizing antiserum 30K, blood glucose by Hoffman's method, serum FFA by Ui-Itaya's method, serum TG by enzymatic method, and serum β-lipoprotein by the turbidity method of dextran sulfate. All samples were systematically measured simultaneously. All data obtained by these experiments were statistic ally analyzed by student's t test.
The maternal carbohydrate-lipid metabolism and function of pancreas during normal pregnancy are characterized as follows.
1. The basal levels of insulin and glucagon increase as pregnancy advances although there is a slightly lower basal glucose level during pregnancy.
2. Normal women gradually become hyperlipemic from mid toward late pregnancy.
3. At early pregnancy there is a good glucose tolerance, and the response of α and β cells in pancreas is sensitive to hyperglycemia. But from mid toward late pregnancy there is a gradually impaired glucose tolerance, and the hyperglycemic response of α and β cells in pancreas become gradually insensitive.
These alterations of carbohydrate-lipid metabolism during pregnancy have been thought for the causes of insulin insensitivity at peripheral tissues. Among many insulin antagonists, hCS seems to play a leading role.
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