Abstract
Glycogen storage in the fetal liver obeys a hormonal control (Jost, Harvey Lect. 55: 201, 1961). In rabbits it is prevented by decapitating the fetus before day 25; it is restored by giving a corticosteroid + prolactine or GH to the decapitate. In rats glycogen storage is prevented in fetuses decapitated on or before day 18 on condition that the mother is adrenalectomized; it is restored simply by giving a corticosteroid. It was studied whether these variations in liver glycogen are paralleled by variations in plasma immunoreactive insulin (IRI). Rabbits:fetuses decapitated on day 24 and studied day 29 (number in brackets): glycogen= 2.8 + 0.2(lO)mg/g fresh tissue;IRI:173±6 (12) uU/ml (human standard); controls:glycogen=26±3 (11); IRI=45±4(17). Rats:1) mother adrenalectomized on day 14, fetuses decapitated on day 18 and studied on day 21:glycogen = 10.0 ± 6(8) mg/g; IRI=113±16(8)uU/ml(rat standard); 2) same treatment + lOOug cortisol acetate 24hr before: glycogen = 58.4±4 (10); IRI=95±29 (10); 3) controls:glycogen = 91.3±2 (4); IRI = 138±21(16). The striking differences in liver glycogen are not paralleled by similar variations in plasma insulin. If insulin is required for glycogen deposition in the liver, it is not the limiting factor in decapitated fetuses.
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