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Biomedical subjects

S Podolsky

Publications and source records attributed to S Podolsky.

At least 37 records · Page 2Linked to original sources
PubMed1979

Effects of long term sulfonylurea therapy on plasma insulin and fasting lipid levels.

Insulin secretion was studied before and after the control of hyperglycemia in fourteen maturity onset male non-obese diabetics. Optimum control of hyperglycemia was achieved by the addition of the sulfonylurea chlorpropamide to dietary treatment. One patient was a primary treatment failure, but nine out of thirteen had excellent control of hyperglycemia. A standardized oral glucose tolerance test (GTT) was performed before and after eight months of individualized therapy with the sulfonylurea. The GTT was repeated with each patient taking his usual dose of chlorpropamide 90 min prior to the administrationo f the glucose load. In the baseline test glucose levels rose from 135.6 +/- 9.9 mg/dl to a peak level of 268.8 +/- 17.7 mg/dl at 120 min. After control of hyperglycemia glucose levels were significantly lower at 0, 30 and 60 min, and rose from 106.8 +/- 8.5 mg/dl to a maximum of 224.5 +/- 17.3 mg/dl at 120 min. Plasma insulin response was unchanged. Fasting serum cholesterol, triglyceride and total lipid levels changed only minimally during therapy. It is concluded that lowered serum glucose levels after long term treatment with chlorpropamide occured while plasma insulin response to glucose was no greater than before treatment. These findings may be explained by an extrapancreatic effect of the drug or by an indirect result of chlorpropamide induced insulin release which occured earlier in the course of therapy.

Aged↗
PubMed1978

Hyperosmolar nonketotic coma in the elderly diabetic.

The gravity of this syndrome of severe diabetic stupor without ketosis may not be recognized because patients are usually middle-aged or elderly with mild diabetes. A lack of urgency in treating these patients is probably the cause of the widely reported mortality of 40 to 70 per cent.

Aged↗
PubMed1977

Abnormal glucose tolerance and arginine tolerance tests in Huntington's disease.

Neuropathological studies of Huntington's disease reveal neuronal atrophy, lipofuscin accumulation and other findings characteristic of the aged brain, although the onset of disease is only the fourth decade. The pathology is limited to specific areas such as the caudate nucleus, cerebral cortex and hypothalamus. 14 patients with documented Huntington's disease (mean age of 44.4 years with a range of 27-79 years) were studied by oral glucose tolerance tests (GTT) and intravenous arginine tolerance tests performed under standardized metabolic conditions. Seven of the 14 patients had impaired carbohydrate tolerance. Mean plasma glucose level at 2h was 90.4+/-6.2 mg/100 ml in the patients with a normal GTT and 148.1+/-8.9 mg/100 ml in the patients with a diabetic type GTT. Mean peak insulin level in the nondiabetic group occurred at 1/2 h and was 60.2+/-10.1 muU/ml, but in the diabetic group the peak insulin level occurred at 2h and was 155.9+/-33.8 mgU/ml. There was failure of suppression of growth hormone during the GTT, with a rise to abnormally high levels at 5h (18.6+/-5.6 ng/ml). Arginine infusion resulted in normal glucose and insulin rise in the nondiabetic patients with Huntington's disease. However, arginine infusion provoked an elevated insulin response in those with a diabetic GTT, and an exaggerated growth hormone response in the majority of the patients. It is uncertain whether these observations are related to abnormal cerebral aging per se, direct hypothalamic neuronal degeneration, or perhaps a relative imbalance of intracerebral neurotransmitters including dopamine.

Adult↗
PubMed1977

Absence of sleep-related growth hormone elevations in myotonic dystrophy.

There is evidence that in myotonic dystrophy, the endocrine and central nervous systems are affected. To study a possible relationship between both defects, we investigated nocturnal sleep patterns and associated growth hormone secretion in two men and three women with myotonic dystrophy. In three patients who were clinically the most severely affected by myotonic dystrophy, plasma growth hormone elevations related to the slow-wave phase of sleep were absent. The two least severely affected patients had plasma growth hormone increases of low magnitude and brief duration (from 0.4 ng per milliliter to 13.0 ng per milliliter). These data suggest a failure of integration at a subcortical level of the slow-wave phase of sleep with the hypothalamic-pituitary mechanisms of growth hormone secretion. Thalamic neuronal lesions occurring in myotonic dystrophy could be responsible for such failure.

Adult↗
PubMed1976

Improvement of growth hormone response to stimulation in primary aldosteronism with correction of potassium deficiency.

Potassium depletion frequently occurs in primary aldosteronism and has been implicated as the cause of the impaired carbohydrate tolerance frequently associated with this syndrome. Glucose, insulin, and growth hormone regulation were studied in a 42-yr-old, male patient with an aldosterone-secreting adenoma when the patient was potassium-depleted and again after potassium repletion. Potassium repletion was documented by serial body potassium measurements, with an increase in body potassium from 2400 mEq to 2850 mEq after 400 mg spironolactone and 80 mEq supplemental potassium chloride were administered daily for 7 days. Potassium repletion resulted in improvement of the patient's glucose tolerance test, with a decrease in the peak glucose level from 184 mg/100ml to 130 mg/100ml and an increase in the peak insulin level from 46 muU/ml to 85 muU/ml. Intravenous administration of arginine resulted in a subnormal insulin response of 28 muU/ml in the base-line test and an increase to 59 muU/ml after potassium stores were repleted. Growth hormone response to arginine infusion was also initially minimal at 12.5 ng/ml, increasing markedly to 26 ng/ml after potassium replenishment. Insulin-induced hypoglycemia resulted in a depressed growth hormone response of 8 ng/ml when the patient was potassium-deficient, but a normal response of 30 ng/ml after potassium repletion. These observations demonstrate that impairment of both insulin and growth hormone responses to stimulation occur in primary aldosteronism with potassium depletion. These abnormalities may be reversed by potassium repletion.

Adenoma↗
PubMed1975

Age, smoking inhalation, and pulmonary function.

This study examined the relative effects of age and smoking on pulmonary function. Smoking was measured by six smoking variables, taken singly and as a composite. Subjects were 1,516 male participants in the Normative Aging Study. A stepwise multiple regression with vital capacity (VC) and forced expiratory volume at one second (FEV1.0) as the criteria accounted for 24.4% and 28.3% of the variance, respectively. Two-way analyses of variance showed that the age decline in pulmonary function was substantially greater for high inhalers than it was for low inhalers or nonsmokers. Age and the inhalation index were also noticeably and independently related to a decline in pulmonary function.

Age Factors↗
PubMed1975

Exaggerated growth hormone response to arginine infusion in Huntington's disease.

Growth hormone regulation was studied in 10 patients with Huntington's disease after intravenous administration of arginine. In 20 control subjects arginine infusion resulted in a rise of plasma growth hormone levels from a mean baseline value of 3.2+/-0.6 ng/ml to a peak level of 17.6+/-2.7 ng/ml at 60 min. Growth hormone rise in the majority of patients with Huntington's disease was clearly intact and significantly greater than normal in magnitude, increasing from the baseline level of 2.6+/-0.5 ng/ml to a peak level of 28.3+/-3.7 ng/ml at 60 min (P = less than 0.05). Carbohydrate tolerance of these patients was previously examined, and 4 with normal glucose tolerance and normal insulin responses to arginine infusion had growth hormone levels significantly higher than controls at 30 min. Six patients with impaired carbohydrate tolerance and exaggerated insulin responses to arginine had significantly higher growth hormone responses at 30 min and also at 60 min. Neuronal degeneration of several hypothalamic nuclei has been reported in Huntington's disease. The observations that growth hormone responds in an exaggerated fashion to stimulation by arginine infusion or falling glucose levels as previously described may be explained by intrahypothalamic dysfunction such as impairment of somatostatin secretion.

Adult↗