Development of Hepatic Acetyl Coenzyme A Carboxylase in Hormone-Treated Chicks

Abstract

It has been suggested that the carbohydrate-rich diet of chicks after hatching is responsible for the emergence of hepatic enzymes involved in lipogenesis; the injection of glucose to newly hatched chicks gives rise to an appreciable elevation on the activities of acetyl coenzyme A carboxylase and fatty acid synthetase. The present study shows that during the first hours after hatching, there is a natural elevation of glycemia which parallels the increase in acetyl coenzyme A carboxylase activity. However, the administration of hormones which alter the blood glucose levels considerably (insulin, tolbutamide, glucagon and hydrocortisone) did not influence the enzyme activity. The administration of thyroxine, estradiol and cyclic AMP, was also without effect. These results do not support the theory that the increased amount of blood glucose is the natural effector of the induction of acetyl coenzyme A carboxylase. They also show that different lipogenic enzymes are not regulated via the same ‘operon’ since thyroxine or glucagon which alter the level of some enzymes on this pathway did not modify that of the acetyl coenzyme A carboxylase.

Prenatal tolbutamide treatment alters plasma glucose and insulin concentrations and negatively affects the postnatal performance of chickens

“…The prolonged hypoglycemic state from 4 h PI to 36 h PI after a single injection of tolbutamide, associated with a profound rise in plasma insulin concentrations at 0.5 h PI, is in agreement with in vitro and in vivo studies on layer and broiler chickens at different ages [9,[14][15][16][17][18][25][26][27][28] and with in vitro and in vivo studies on mice, rats, dogs, and hamsters [29][30][31][32][33]. Indeed, tolbutamide is a potent hypoglycemic agent in mammals and birds and stimulates insulin secretion from pancreatic b-cells, principally by inhibiting adenosine triphosphatesensitive K þ channels in the cell membrane, consequently, causing a membrane depolarization and an activation of voltage-gated Ca 2þ influx [34][35][36].…”