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Biomedical subjects

S Madsbad

Publications and source records attributed to S Madsbad.

At least 145 records · Page 8Linked to original sources
PubMed1982

Plasma testosterone and androstenedione in insulin dependent patients at time of diagnosis and during the first year of insulin treatment.

Ten male patients and 6 female patients with newly diagnosed insulin dependent diabetes mellitus and significant ketosis were studied before and during the first year of insulin treatment. At onset plasma concentrations of testosterone and androstenedione were significantly (P less than 0.02) decreased in female patients when compared to healthy sex- and age-matched controls. Plasma concentrations of testosterone and androstenedione increased significantly (P less than 0.001 and P less than 0.05) in both sexes during insulin therapy. Plasma concentrations of testosterone were not significantly different from controls in both sexes after 4 days of insulin treatment and remained so during the first year of insulin treatment. Plasma concentrations of androstendeione were not significantly different from controls in both sexes after 4 days of insulin treatment, but increased to levels significantly raised in both males (P less than 0.001) and females (P less than 0.05) after 7 days and during the first year of insulin treatment.

Adolescent↗
PubMed1982

Suppressor cell activity in patients with newly diagnosed insulin-dependent diabetes mellitus: a prospective study.

Suppressor cell activity (SCA) was investigated longitudinally, at the time of diagnosis and during the remission period, in 17 patients with insulin-dependent diabetes mellitus (IDDM). The suppressive effect of lymphocytes from patients was investigated after incubation with concanavalin A followed by inactivation. Suppression was measured as the ability of the lymphocytes to inhibit 3H-thymidine incorporation in concanavalin A stimulated normal donor lymphocytes. The main findings were: I. SCA was reduced, on the average, at diagnosis but normal during the remission period. II. Patients with the lowest SCA at diagnosis showed significantly lower C-peptide values during the remission period than other patients. III. No relationship was found between on the one side various tissue types and on the other SCA, C-peptide values, insulin dose, and degree of glucaemic control, neither at diagnosis nor during remission. Previous studies have pointed to the significance of immune reactions in diabetogenesis. The findings in the present study may associate SCA with the development of IDDM.

Adult↗
PubMed1982

Serum calcium fractions in diabetes mellitus.

Diabetes mellitus is associated with a decrease in bone mineral content and increased urinary excretion of calcium and phosphate. The purpose here was to elucidate the pathogenesis of these changes by comparing serum calcium fractions of diabetics and healthy controls. In a cross-sectional study, serum ionized calcium at pH 7.40, [Ca2+]7.4, of 46 insulin-treated diabetics was decreased in comparison with 44 healthy controls: mean 1.16 (SD 0.04) vs 1.21 (SD 0.03) mmol/L (p less than 0.001). The decreased [Ca2+]7.4 was associated with a higher concentration of complexed calcium in diabetic serum. The diabetics had higher concentrations of undetermined anions (p less tha 0.001) and this anion gap correlated negatively with [Ca2+]7.4 (r = -0.43, p less than 0.02). Serum [Mg2+] was decreased in the diabetics (p less than 0.001). Values for venous acid-base status, serum creatinine, total and ultrafiltrable calcium, parathyrin, and inorganic phosphate were the same in the two groups. [Ca2+]7.4, but not serum total calcium, had increased by 0.04 mmol/L (p less than 0.001) in the diabetics and by 0.02 mmol/L (p less than 0.01) in the controls by 90 min after breakfast, with and without subcutaneous insulin, respectively.

Adolescent↗
PubMed1982

Vitamin D metabolites in diabetic patients: decreased serum concentration of 24,25-dihydroxyvitamin D.

In order to elucidate if changes in vitamin D metabolism play a role for diabetic bone loss, the serum concentrations of the major vitamin D metabolites were studied in 26 adult male ambulatory insulin-treated diabetics, selected to have normal renal function and a duration of diabetes below 11 years. The patients were studied during usual metabolic control and exhibited wide ranges of hyperglycaemia and glycosuria. The serum concentrations of the major metabolites of vitamin D, 25-hydroxyvitamin D(2 + 3) (25OHD), 24,25-dihydroxyvitamin D(2 + 3) (24,25(OH)2D), and 1,25-dihydroxyvitamin D(2 + 3) (1,25(OH)2D), were measured in diabetics, and in age and sex matched controls. The diabetics had slightly decreased serum levels of 25OHD (42.0 nmol/l versus 55.5 nmol/l in normals, P less than 0.05), markedly decreased serum levels of 24,25(OH)2D (2.98 nmol/l versus 5.91 nmol/l, P less than 0.01), but serum levels of 1,25(OH)2D were virtually normal (64.2 pmol/l versus 68.3 pmol/l, ns). The close correlation between serum concentrations of 25OHD and 24,25(OH)2D observed in the normal subjects, was absent in the diabetics. There were no correlations between the serum levels of any of the vitamin D metabolites and the measured indices of glucose and calcium metabolism. It is concluded that insulin-dependent diabetic patients demonstrate definite alterations in serum levels of vitamin D metabolites, the significance of which remains unknown at present.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Effect of strict blood glucose control on residual B-cell function in insulin-dependent diabetics.

In 14 insulin dependent diabetics past their initial remission period B-cell function was evaluated using a test meal before and after 1 week of strict blood glucose control, and again 3 weeks later when the patients were outpatients on conventional therapy. Eight patients with fasting C-peptide above 0.07 nmol/l improved their B-cell function significantly (p Less Than 0.05) during the period of strict blood glucose control. However, the improvement was of short duration and was absent 3 weeks later in most patients. Six patients with fasting C-peptide below or equal to 0.07 nmol/l had no significant improvement in B-cell function during the period of strict control. The study shows that B-cell function and degree of blood glucose control are related in patients with fasting C-peptide above 0.07 nmol/l, and that B-cell function can change within days.

Adolescent↗
PubMed1981

Hyperzincuria in insulin treated diabetes mellitus--its relation to glucose homeostasis and insulin administration.

In order to elucidate some pathogenic factors of diabetic hyperzincuria we studied 60 adult insulin treated diabetic out-patients (40 males and 20 females), all with normal serum creatinine concentrations and absence of proteinuria during a 24-h period. Diabetic males and females both had significantly (p less than 0.01) increased zinc excretion rates (1.14 +/- 0.06 (S.E.M.) mumol/mmol creatinine and 1.37 +/- 0.10 mumol/mmol creatinine) compared with normal males and females (0.55 +/- 0.06 and 0.48 +/- 0.08, respectively). The urinary zinc excretion rate correlated positively with the degree of glycosuria (r = 0.36, p less than 0.01), but was not associated with the duration of the disease. However, serum zinc levels gave no evidence of a state of zinc depletion in these patients. It was calculated that zinc originating from a diabetic bone loss and the exogenous insulin administration accounted for only a small part of the hyperzincuria. Compensatory hyperabsorption and/or increased zinc content in the diabetic diet may therefore serve to explain the lack of zinc depletion in the presence of hyperzincuria.

Adult↗
PubMed1981

Practical clinical value of the C-peptide response to glucagon stimulation in the choice of treatment in diabetes mellitus.

In order to discriminate between insulin-dependent and non-insulin-dependent patients, serum C-peptide concentration was determined using antiserum M1230 in the fasting state and 6 min after an i.v. injection of 1 mg glucagon in 215 patients treated with insulin and 53 treated with diet and oral antidiabetics. A patient was considered well controlled without insulin when fasting blood glucose was below 8 mmol/l and when glucosuria was absent. After re-evaluation of therapy in hospital it was found that the majority of patients with a post-stimulatory serum C-peptide concentration above 0.60 pmol/ml appeared to have non-insulin-dependent diabetes mellitus. When fasting C-peptide was used, a great overlap was found between the two treatment groups. During evaluation of therapy in hospital, 6 previously insulin-treated patients could be well treated with diet and tablets and 6 diet- and tablet-treated patients required insulin. The glucagon test seems to be of value in the outpatient clinic to discriminate non-insulin-dependent from insulin-dependent patients.

Adult↗
PubMed1981

Very early changes in circulating T3 and rT3 during development of metabolic derangement in diabetic patients.

Alterations in circulating iodothyronines were studied in 15 juvenile type diabetic patients during the development of metabolic derangement after withdrawal of insulin. By means of measurements of circulating C peptide, one group of patients with and one without residual beta-cell function had been selected. In both groups there was a gradual decrease in serum T3 during the 12-hour period studied after withdrawal of insulin, while an increase in serum rT3 was observed after 4-6 hours. The alterations in serum T3 and the metabolic derangement were significantly more pronounced in patients without than with residual beta-cell function.

C-Peptide↗
PubMed1981

Development of bone mineral loss in insulin-treated diabetes: a 1 1/2 years follow-up study in sixty patients.

The change in bone mass during 1 1/2 years was determined in a longitudinal study of sixty adult insulin-treated diabetic out-patients. During the study period the mean bone mass decreased by 1.30 +/- 0.28 (SEM)% (P less than 0.001), to a mean value of 91.0 +/- 1.7% of normal (P less than 0.001). The rate of bone loss was significantly higher in patients with 1-6 years of diabetes (n = 29, bone loss: 1.96 +/- 0.32%/1 1/2 years) than in patients with longer duration of the disease (n = 31, bone loss: 0.61 +/- 0.44%/1 1/2 years, P less than 0.02). The endogenous insulin secretion estimated with the glucagon-stimulated serum C-peptide concentration decreased during the observation period in 58.6% of the patients with 1-6 years of diabetes compared to 16.1% among patients with 7-11 years of diabetes (P less than 0.002). The rate of bone mineral loss was almost 3 times higher in the twenty-two patients in whom endogenous insulin secretion had deteriorated (2.12 +/- 0.30%/1 1/2 years) than in the thirty-eight patients without as well as with unchanged or increased insulin secretion (0.78 +/- 0.39%/1 1/2 years, P less than 0.01). In twenty patients with an increased insulin dose during the study period the mean bone mineral loss was 2.05 +/- 0.36%/1 1/2 years compared to a mean bone mineral loss of 0.91 +/- 0.38%/1 1/2 years in the forty patients with unchanged or decreased insulin dosage (P less than 0.05). This longitudinal study further supports the hypothesis that the bone mineral loss in insulin-treated diabetic patients begins with the onset of clinical diabetes and that its development is associated with the deterioration of the beta-cell function and with the increment in insulin dosage. The rate of bone mineral loss is high during the first few years of clinical diabetes, but levels off with increasing duration of the disease.

Adult↗
PubMed1981

Decreased insulin removal contributes to hyperinsulinemia in obesity.

Peripheral plasma insulin and C-peptide concentrations during oral glucose tolerance tests were measured in 7 severely obese and 12 normal weight nondiabetic subjects. The insulin and C-peptide levels as well as incremental areas under the plasma curves were 2--5 times higher in the obese subjects (P less than 0.05). The C-peptide to insulin molar ratios as well as the relation between incremental areas under the plasma curves of the two peptides were used as relative measures of the hepatic insulin extraction. They were both reduced in the obese subjects, which suggests that decreased insulin removal may contribute to the hyperinsulinemia of obesity. Sixty minutes after the oral glucose load, all of the obese patients had higher peripheral venous insulin concentrations compared with those found in normal subjects with similar C-peptide levels. This suggests that the reduced insulin extraction is not entirely explained by increased beta-cell secretory activity, but is also a specific consequence of obesity.

Blood Glucose↗
PubMed1981

Hypoparathyroidism in diabetes mellitus.

Serum immunoreactive parathyroid hormone (iPTH) and indices of mineral and glucose metabolism were determined in 58 insulin treated diabetic patients (duration of disease 1-11 years). The mean serum iPTH level in all diabetic patients, measured simultaneously with sera from normal subjects, was 55% of normal mean (P < 0.01). The diabetic patients had hypomagnesaemia (P < 0.001), hypercalciuria (P < 0.001) and a 9.6% decrease in bone mass (P < 0.001). Low serum iPTH values were correlated with high glycosuria (R = -0.28, P < 0.05) and with long duration of diabetes (R = -0.31, P < 0.02). Patients with both high glycosuria and long diabetes duration had especially low iPTH values (mean 16 ng/l, n = 16) compared with patients with both low glycosuria and short diabetes duration (mean 32 ng/l, n = 15, P < 0.005) and with normal subjects (mean 37 ng/l, n = 28, P < 0.001). The 16 patients with low serum iPTH values also had higher urinary calcium excretion rate (P < 0.05) than the 15 patients with low glycosuria and short duration of diabetes. The diabetic hypoparathyroidism may be secondary to a primary disturbance of bone metabolism, with a negative net calcium balance.

Adult↗
PubMed1980

Islet-cell antibodies and beta-cell function in insulin-dependent diabetics.

Residual insulin secretion and islet-cell antibodies were studied in 399 insulin-dependent diabetics with age at onset of between 10--19.9 years (248 patients) or 30--39.9 years (151 patients). We found the prevalence of islet-cell antibodies to be independent of residual beta-cell function as measured by serum C-peptide and age at onset. The cause and role of the persistence of islet-cell antibodies in insulin-dependent diabetics remain obscure.

Adolescent↗
PubMed1980

Metabolic responses to hypoglycemia in juvenile diabetics.

Glucagon and metabolic responses to insulin-induced hypoglycemia were studied in seven juvenile diabetics, age 31 +/- 2 years (mean and S.E.M.), duration of diabetes 17 +/- 3 years, with diabetic autonomic neuropathy (decreased beat-to-beat variation in heart rate during hyperventilation and/or orthostatic hypotension) and in seven control patients of similar age and duration of diabetes with out neuropathy. Before the hypoglycaemic episode, normoglycemia had been maintained for at least 10 hours. Following hypoglycemia, a slight but significant and similar increase in plasma glucagon was found in both patient groups. Metabolic responses to hypoglycemia were also similar in the two patient groups. In conclusion, diabetic autonomic neuropathy has no effect on glucagon and metabolic responses to hypoglycemia in juvenile, insulin-treated diabetics.

Adult↗
PubMed1980

Impaired conversion of prednisone to prednisolone in patients with liver cirrhosis.

Fourteen patients with liver cirrhosis received oral prednisone or prednisolone (0.3 mg per kg) randomised on two consecutive days. Serum prednisone and prednisolone were measured over the following four hours. Mean serum prednisolone concentration after oral prednisone decreased with impaired liver function estimated by galactose elimination capacity (r = 0.64, P less than 0.03). Mean serum prednisolone concentration after oral prednisone in the seven patients with severely impaired liver function was only 53% (P less than 0.05) of that observed in the seven patients with slightly impaired liver function. Conversely, mean serum prednisone concentration after oral prednisone in the patients with severely impaired liver function was 74% higher (P = 0.05) than in patients with slightly impaired liver function. Mean serum prednisolone after oral prednisolone was independent of liver function. As only prednisolone exerts glucocorticoid activity, our results indicate that prednisolone should be preferred to prednisone in the treatment of patients with impaired liver function.

Administration, Oral↗