The Role of the Endocrine Glands in Ketosis. Ii. Ketonemia Following Insulin Hypoglycemia*

Interrelationships of blood sugar and ketones in insulin-treated diabetics

“…The release of several ketogenic hormones, including adrenaline, cortisol, and growth hormone, is known to occur in response to hypogiycaemia or even to a rapid fall of blood sugar. Amatruda et al (1962), however, have shown that hyperketonaemia still follows hypoglycaemia in hypophysectomized and adrenalectomized animals, suggesting that these hormones are not responsible for this phenomenon. Release of catecholamines may be more important in this regard, but the evidence is not con-Diabetes-Watkins et al M SJUL 651 vincing.…”

“…Other mechanisms may be important in effecting these responses to hypoglycaemia. Relative insulin deficiency during hypoglycaemia has been suggested (Amatruda et al, 1962;Engel and AmatFruda, 1963;Scow et al, 1964) but disputed by others (Armstrong et al, 1961). Glucagon release also follows hypoglycaemia, but its effect on ketogenesis is not well established (Penhos et al, 1966).…”

“…Ketonuria has also been described in cases of hypoglycaemia due to glycogen storage diseases (Hsia, 1964) and in infantile hypoglycaemia (Stephenson and Hainsworth, 1966). The ketogenic effect of hypoglycaemia has now been well established under carefully controlled experimental conditions, and the responsibility of the liver for the increased ketogenesis has been shown (McPherson et al, 1958 ;Amatruda et al, 1962).…”

Afternoon Glucose Tolerance Testing: A Key to the Pathogenesis, Early Diagnosis and Prognosis of Diabetogenic Hyperinsulinism

“…In referring to this hypothesis, Mirsky and associates (46) have stated that such diabetes “is attributed to a relative insufficiency in the capacity of the pancreas to meet the increased peripheral requirements for insulin.” ) In patients who have been operated upon for insulinoma, the postoperative hyperglycemia may disappear in association with a decline in the level of plasma insulin. Such hyperglycemia can be explained as readily by the high‐output failure of insulin release as by the usual explanation of “compensatory islet‐cell atrophy.” The decompensation in glucose tolerance associated with organic hyperinsulinism is exemplified by Watkins and Traylor's (47) case of a 4‐year‐old boy with a single islet‐cell adenoma which was successfully resected. The results of the first preoperative glucose tolerance test in this patient were as follows: blood glucose values (mg per 100 ml)—fasting, 22 mg; 30 minutes, 175 mg; 60 minutes, 182 mg; 90 minutes, 187 mg; 120 minutes, 123 mg; 150 minutes, 150 mg; 180 minutes, 55 mg; and 210 minutes, 22 mg. Another preoperative study sixteen months later gave the following results: fasting, 75 mg; 30 minutes, 320 mg; 60 minutes, 65 mg; 90 minutes, 162 mg; 120 minutes, 160 mg; and 180 minutes, 147 mg. Diabetes mellitus also has followed subtotal pancreatectomy for islet‐cell adenoma, either shortly after such surgery (48) or after a hiatus of several decades (49).…”

Effect of Glucagon on the Metabolism of Lipids and on Urea Formation by the Perfused Rat Liver

“…in length. The middle part of (C) is an aeration chamber that receives a mixture of O 2 (95 per cent) plus CO, (5 per cent) through (K) and allows the gas mixture to pass out through (L) into a trap for CO 2 . The lower part of (C) is the reservoir of blood from which it is possible to take samples via the arm (M) occluded with a cork.…”