Biomedical subjects
Publications and source records attributed to J P Assal.
Are long-term complications secondary to diabetes or do they appear independently? This question has an important bearing, particularly for the physician and the patient who must achieve optimum control of hyperglycemia. Over the last 10 years, many epidemiological and biochemical studies have shown close links between hyperglycemia and the wide range of factors involved in the development of long-term complications.
Glucagon immunoreactivity (IRG) was measured in plasma of 8 duodenopancreatectomized patients with antiserum 30-K. Arginine infusions failed to raise plasma IRG, whereas in control subjects IRG rose 3-fold. Column chromatography revealed that the basal IRG measured in these plasmas was not due to glucagon (molecular weight 3485) but to other plasma factors, mainly of high molecular weight. This suggests that diabetes mellitus does not require the presence of glucagon to produce the clinical picture, as suggested by other authors. Plasma levels of the amino acids alanine, serine, ornithine, and arginine were significantly (p less than 0.05) elevated, the former two being gluconeogenic substrates and the latter two constituents of the urea cycle. This amino acid abnormality may be a consequence of glucagon deficiency.
Glucogon immunoreactivity (IRG) was measured in plasma of duodenopancreatectomized subjects with a nonspecific (K-4023) and a specific (30-K) glucagon antiserum. After an overnight fast, plasma IRG (K-4023) was significantly (P < 0.05) higher in the subjects without pancreas, averaging 782+/-79 (SEM) pgeq/ml, than in the controls (482+/-80 pgeq/ml). IRG (30-K) of 162+/-68 pg/ml did not change during an infusion of arginine (450 mg/kg per 40 min). Insulin deprivation during 3 d in one patient did not restore the IRG response to arginine as reported in depancreatized dogs.Bio-Gel P-30 column chromatography revealed that virtually all IRG (30-K) measured in whole plasma was of different molecular weight than glucagon, and primarily of a mol wt >/= 40,000. Intravenous arginine did not significantly alter the chromatographic pattern of these plasmas. Thus, as postulated by others, duodeno-pancreatectomized humans have virtually no circulating 3,500-dalton glucagon. Hence, the presence of 3,500-dalton glucagon in plasma is not a condition for the diabetic state. It might, nevertheless, when present in normal or excessive amounts, worsen the metabolic state of diabetic patients. Among 14 amino acids measured in plasma of these patients, the concentrations of alanine, serine, ornithine, and arginine were significantly (P < 0.05) elevated to approximately twice that of normal: alanine and serine are both substrates for gluconeogenesis, whereas ornithine and arginine are involved in the formation of urea, the second product of hepatic gluconeogenesis. As the concentrations of branched chain amino acids were not grossly altered, it is hypothesized that this amino acid pattern is a consequence of glucagon deficiency rather than secondary to the diabetic state of these patients.
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The renin-angiotensin-aldosterone system was evaluated in two types of uncontrolled diabetes: a) diabetic ketoacidosis, and b) nonketotic hyperglycemia. In thirteen patients with ketoacidosis, mean plasma renin activity (PRA) was 58 plus or minus 12 (S.E.M.) ng. per milliliter per hour and in four patients, plasma aldosterone was 82 plus or minus 17 ng. per 100 ml. Corresponding values for upright salt-depleted subjects were 13 plus or minus 2 and 62 plus or minus 8. In eleven diabetics with nonketotic hyperglycemia (mean glucose 318 plus or minus 19 mg. per cent), mean blood volume was 4,660 ml. and PRA 2.1 plus or minus .7. After control of the diabetes (mean glucose 129 plus or minus 13) blood volume was 4,553 ml. and PRA 3.3 plus or minus 1 (NS). The results suggest that: 1) diabetic ketoacidosis is a state of severe secondary aldosteronism, 2) no significant change in blood volume or PRA occurs during short periods of hyperglycemia, and 3) insulin is not necessary for renin release.
The goal of the present study is to compare the pedagogic involvement of two groups of doctors, both of which were in charge of teaching the same courses to diabetic patients. Important structural differences were-shown exit between the two series of courses. The first group of ten doctors (who not undergone any pedagogic training) applied either ex-catedra teaching methods or proceeded by systematically asking questions to the patients. These scholastic methods led to passive attitudes in their patients in listening and replies to a large number of questions. In the second group of ten doctors (who had undergone pedagogic training) learning practices and a stimulating didactic material were used which resulted in more diversified and more attractive responses in the participation of the patients. Providing improved didactic means on the behalf of the doctors is aimed at obtaining better knowledge from patients who have themselves to assume the self-management of their treatment.