Protein Malnutrition in the Domestic Fowl Induces Alterations in Adrenocortical Function*

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Abstract
Adrenocortical function was investigated in immature, dietary protein-restricted domestic fowl (Gallus gallus domesticus). White Leghorn cockerels (2 weeks old) were fed isocaloric semipurified diets containing either 8% [low (L)] or 20% [normal (N)] soy protein for 4 weeks ad libitum. Cockerels were quickly killed by decapitation and exsanguination. Trunk plasma corticosterone (B) and ACTH levels were measured by RIA. Maximal B-binding capacity (CBC) of plasma was also measured. In addition, in randomly selected cockerels, a rough index of the B clearance rate was determined. Finally, to determine the influence of protein malnutrition on adrenocortical cell function per se, we measured the acute (2-h) B responses of highly enriched adrenocortical cell populations to various ACTH analogs, 8-bromo-cAMP (8-Br-cAMP), and cellular B production maximally supported with 25-hydroxycholesterol. Plasma B and ACTH concentrations of L cockerels were, respectively, 160% greater and 32% less than those of N cockerels. In addition, plasma B clearance rate of L birds was 85% greater than that of N birds, thus suggesting a greater B secretion rate in L birds. However, maximal plasma CBC of L cockerels was 59% less than that of N cockerels. Thus, the free plasma B concentration of L birds was greater than that of N birds. The increase in the plasma B concentration of L cockerels is explained in part by the relative adrenal weight of these birds which was 88% greater than that of N cockerels. In addition, there were differences at the adrenocortical cell level. On an equal cell concentration basis, basal and maximal B production values (stimulated by ATCH analogs and 8-Br-cAMP, and supported by 25-hydroxycholesterol) of L cockerel adrenocortical cells were, respectively, 73% and 139% greater than those of N cockerel adrenocortical cells. In addition, maximal ACTH-induced aldosterone production of L bird cells was 104% greater than that of N bird cells, such that the ratio of aldosterone production to B production was not altered by protein deprivation. The data suggest that the greater steroidogenic capacity of L cockerel cells was due to an increase in intracellular steroidogenic enzyme content and/or activity and not to an alteration in the composition of adrenocortical cell types within the populations of isolated cells. Furthermore, ACTH analog ED50 values for B, aldosterone, and cAMP production by L bird cells were about one third to one fifth the values for N bird cells, thus indicating that L bird cells were about 3-5 times more sensitive to ACTH than were N bird cells. However, ED50 values of 8-Br-cAMP and 25-hydroxycholesterol were not different between L and N cockerel cells. THese data suggest that the differences in cellular sensitivity to ACTH analogs between L and N cockerel cells were due to differences in corticosteroidogenic steps before the generation of cAMP. The present study indicates that persistent protein malnutrition increases circulating B concentrations in growing domestic fowl by operating through the following mechanisms: 1) an increase in relative adrenal weight, 2) an increase in adrenocortical cell steroidogenic capacity, and 3) an increase in cellular sensitivity to ACTH. In addition, the data suggest that protein malnutrition alters ACTH-adrenocortical cell interaction, possibly including ACTH receptors and/or ACTH transmembrane signaling events.

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