Fetal metabolic response to phloridzin-induced hypoglycemia in pregnant rats.
Phloridzin, an inhibitor of renal sugar transport, produces an important loss of glucose in urine of treated animals. In order to reduce severely the maternal glucose supply to the fetuses in short-term experiments, we have combined phloridzin administration to pregnant rats with 18 h starvation. Fetuses from starved phloridzin-treated mothers were compared with fetuses from starved mothers. Combined treatment markedly decreases fetal blood glucose concentration (-36%) and fetal liver glycogen stores (-76%). These changes are associated with a decrease in plasma insulin (-25%), a rise in plasma glucagon (+120%) and a marked increase of hepatic PEPCK activity (+400%). It appears from these results that phloridzin treatment for a short duration is able to induce glycogenolysis and the premature appearance of PEPCK in the liver of rat fetuses.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005333:Fetus / Q000378:metabolism*; D005934:Glucagon / Q000097:blood; D006029:Glycosuria / Q000378:metabolism; D007003:Hypoglycemia / Q000139:chemically induced*; D007328:Insulin / Q000097:blood; D007657:Ketone Bodies / Q000097:blood; D008112:Liver Glycogen / Q000378:metabolism; D010695:Phlorhizin; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications / Q000139:chemically induced*; D051381:Rats
D001786:Blood Glucose; D007328:Insulin; D007657:Ketone Bodies; D008112:Liver Glycogen; D005934:Glucagon; D010695:Phlorhizin; D010729:Phosphoenolpyruvate Carboxykinase (GTP)