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Summary. A kinetic study of the conversion of blood cholesterol into hydrocortisone was carried out in two patients through prolonged infusions of cholesterol-4-14C. The following points appear to be established by our observations:1) The infused tracer behaved metabolically like endogenous cholesterol; it could therefore serve as a means of labeling plasma cholesterol for investigating its utilization by the adrenal cortex.2) At rest, about 80% of hydrocortisone derived from plasma cholesterol, the other 20% thus being synthesized in situ from acetate and other unlabeled precursors.3) Under ACTH stimulation the participation of plasma cholesterol in the synthesis of hydrocortisone was the same as at rest; the conversion of plasma cholesterol into hydrocortisone was thus proportional to the production of glucocorticosteroids by the adrenal glands.4) The specific activities of hydrocortisone allowed us to trace its adrenal precursors including adrenal cholesterol. The kinetics of the replacement of adrenal cholesterol by plasma cholesterol underlined the functional heterogeneity of the former. The experimental data were compatible with the following model: A fraction of plasma cholesterol entering the adrenal cell is immediately available for metabolism and conversion into steroid hormones, and another fraction turns over slowly, representing some form of storage.

The effect of glucose upon the handling of 22Na+ by pancreatic islets was investigated. Using a triple-isotope technique, the apparent concentration of Na+ in islet cells was estimated at 50--75 mM. The pattern of 22Na+ efflux from perifused islets indicates that this intracellular Na+ load is compartmentalized among a small, possibly organelle-bound pool characterized by a low fractional turnover rate (5%/min) and a large, presumably cystosolic pool displaying a much higher fractional turnover rate (20--34%/min). Glucose provokes a rapid, pronounced and sustained increase in the fractional outflow rate of Na+ across the plasma membrane and, under steady-state conditions, moderately reduces the concentration of Na+ inside the islet cells. The glucose-induced increase in Na+ outflow rate, which is also observed in response to glyceraldehyde and dose not require the presence of extracellular Ca2+, might be mediated, in part at least, by an ouabain-resistant ionophoretic system. The experimental data suggest that glucose also increases the inward transport of Na+ in islet cells by a veratridine-sensitive channel.

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