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Biomedical subjects

S Madsbad

Publications and source records attributed to S Madsbad.

At least 127 records · Page 7Linked to original sources
PubMed1983

Decreased serum concentration of ionized calcium in insulin-dependent human diabetes mellitus.

Low serum ionized calcium concentrations were observed in twenty-five insulin dependent diabetic outpatients compared with twenty-three age-matched normal subjects: mean 1.16 mmol/l (SEM 0.01) versus 1.20 mmol/l (0.01), P less than 0.002. Despite this, there was no compensatory increase in serum concentrations of immunoreactive parathyroid hormone, nor was serum total calcium decreased in the diabetic patients. Serum magnesium was significantly decreased in the diabetics compared with normals: mean 0.75 mmol/l versus 0.83 mmol/l, P less than 0.001. No significant correlation could be demonstrated between serum magnesium and serum ionized calcium or parathyroid hormone in the diabetic patients. Since no significant correlations were observable between serum ionized calcium and indices of diabetes control, the etiology and pathogenesis of decreased serum calcium ion in insulin-dependent human diabetes mellitus remain unknown.

Adolescent↗
PubMed1983

Whole body clearance of norepinephrine. The significance of arterial sampling and of surgical stress.

The whole body clearance of norepinephrine (NE) was measured in seven patients pre- and postoperatively. L[(3)H]NE was infused intravenously for 90 min and steady-state concentrations of L[(3)H]NE were measured at 75 and 90 min in both arterial and peripheral venous blood. Preoperatively, in the resting supine position, the clearance values based on arterial and venous sampling averaged 1.4 and 2.5 liter/min, respectively (P < 0.02). The difference in clearance values was due to a peripheral uptake of NE averaging 45%. The mean plasma NE increased from 1.70 nmol/liter preoperatively to 5.20 nmol/liter postoperatively (P < 0.02). The plasma appearance rate of NE averaged 2.4 nmol/min before surgery and it increased to 9.5 nmol/min postoperatively (P < 0.02). The plasma clearance of NE averaged 1.4 and 1.6 liter/min pre- and postoperatively, respectively (not significantly different). Our study demonstrates that the calculation of plasma NE clearance based on venous sampling results in values that are too high. Furthermore, such values may be influenced by individual variations in the peripheral uptake of NE, since we found no correlation between clearance values based on venous and arterial sampling. The increase in plasma NE postoperatively was due to an increase in the plasma appearance rate of NE because the clearance rate did not change.

Adult↗
PubMed1983

Diminished immunoreactive gastric inhibitory polypeptide response to a meal in newly diagnosed type I (insulin-dependent) diabetics.

The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. During all three tests, the diabetics had significantly lower plasma IR-GIP concentrations than the controls from 15-90 min after the standard meal. The IR-GIP response in the diabetics measured as the integrated area under the response curve corresponded to 70% of that of normal subjects. beta-cell function evaluated from the C-peptide response to the meal increased significantly from test I to test III whereas the IR-GIP response was similar during all three tests. As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia.

Adolescent↗
PubMed1983

Discrepancy between plasma C-peptide and insulin response to oral and intravenous glucose.

Plasma insulin, proinsulin, and C-peptide responses to 25 g glucose orally and intravenously administered were measured in 10 healthy males. Plasma insulin response was higher during the oral load in accordance with the "incretin" concept. However, the actual amount of insulin secreted, as measured by the plasma C-peptide response, was similar during the two glucose loads. The higher plasma insulin response after oral glucose was not due to crossreactivity with proinsulin in the insulin assay. These results suggest that the higher plasma insulin response during an oral glucose load is due at least partially to a lower hepatic extraction of insulin.

Administration, Oral↗
PubMed1983

Alterations of peripheral T-lymphocyte subpopulations in patients with insulin-dependent (type 1) diabetes mellitus.

Subpopulations of peripheral T-lymphocytes were studied in two groups of patients with insulin-dependent diabetes mellitus (IDDM): eleven newly diagnosed diabetics and twenty-one patients having diabetes of long duration (13 +/- 1 yr). Monoclonal antibodies to the surface antigens of helper (OKT 4) and suppressor (OKT 8) T-cell subsets and to a common T-cell antigen (OKT 3) were used. The percentage of suppressor T-lymphocytes were found reduced in both the newly diagnosed patients (p less than 0.001) and the patients with long-term IDDM (p less than 0.05) in comparison with 16 age-matched healthy control persons. Furthermore, the newly diagnosed diabetics showed a lower percentage of suppressor T-cells (p less than 0.05) and a higher amount of helper T-cells (p less than 0.01) than the patients with long-term diabetes. Concerning the percentage of the total number of T-cells and the absolute number of lymphocytes, there were no significant differences between the patient groups and the controls. As earlier studies have pointed to the significance of immune reactions in diabetogenesis, a pathogenetic importance of the observed imbalance of subpopulations of T-lymphocytes in IDDM should be considered.

Adult↗
PubMed1983

Plasma from insulin-dependent diabetics inhibits theophylline sensitive T-lymphocytes demonstrated in E-rosette assay.

This study concerns the effect of plasma from patients with insulin-dependent (type 1) diabetes mellitus (IDDM) on the capacity of normal donor lymphocytes to form rosettes with sheep erythrocytes. Parallel incubations were made of normal allogeneic peripheral lymphocytes with plasma from patients with IDDM and from normal donors. Lymphocytes incubated with plasma from 16 patients with newly diagnosed IDDM displayed a mean rosette formation percentage of 48 +/- 2, but 54 +/- 1 when incubated with control plasma (p less than 0.01). Repeated study in the same patients in the remission period gave similar findings; 46 +/- 2 and 53 +/- 2 (p less than 0.01) respectively. After fractionation of the donor lymphocytes, the reduced rosette formation percentage, after incubation with plasma from the diabetics, was found to be within the theophylline sensitive fraction of the lymphocytes, while the rosette formation percentage in the theophylline resistant fraction was normal. The reduction in rosette formation capacity at the time of diagnosis seemed to be independent of the tissue type of the patient. No relationships were apparent between rosette formation percentages and C-peptide, blood glucose values or glucosuria, neither at time of diagnosis nor in the remission period. The glycaemic control was found to be of no significance in rosette formation percentages in a triple study of 7 patients; first badly controlled, then very well controlled, and, finally again poorly controlled, though without severe ketoacidosis. The theophylline sensitive fraction of T-lymphocytes has been assumed to include suppressor T-cells. It is not known at present whether the described inhibition of these lymphocytes is of any pathogenetic significance.

Adult↗
PubMed1983

Lowered serum ionized calcium in insulin treated diabetic subjects.

The concentration of ionized calcium at pH 7.40, [Ca2+]7.4, in serum from 43 insulin dependent diabetic patients was lowered in comparison with 47 healthy controls (p less than 0.001), and the difference was biggest in children under sixteen. Serum total calcium, phosphate, and parathyroid hormone were normal, and it is inexplicable why the parathyroid glands did not react by raising serum total calcium. The lowered serum ionized calcium may contribute to the development of diabetic bone loss.

Adolescent↗
PubMed1982

Changes in platelet function, blood coagulation and fibrinolysis during insulin-induced hypoglycaemia in juvenile diabetics and normal subjects.

Haemostatic parameters were assessed before insulin induced hypoglycaemia and 0, 1 and 2 hr after discontinuation of insulin infusion in 7 non-diabetics, aged 28 (22-31) years (mean and range), and 8 juvenile diabetics, aged 31 (27-35) years, with a mean duration of diabetes of 4 years. The patients were normoglycaemic for at least 10 hr before the study. Platelet aggregation in vitro was induced by lower adenosine diphosphate (ADP) concentrations in the diabetics than in the controls before hypoglycaemia and 0 and 60 min after insulin infusion. Platelet counts decreased significantly in the diabetics after hypoglycaemia, whereas no changes were seen in the control group. The activated partial thromboplastin time (APTT) was reduced in both groups and significantly lower in the diabetics than in the controls 120 min after insulin infusion. Fibrinogen and factor VIII R:Ag increased after insulin infusion; highest values were seen in the diabetics. The euglobulin clot lysis time (ELT) was reduced in both groups during insulin infusion; 120 min after end of insulin infusion ELT was significantly longer in the diabetics than in the control group.

Adult↗
PubMed1982

Hyponatremia and hyperkalemia in relation to hyperglycemia in insulin-treated diabetic out-patients.

Interrelations between glucose and electrolyte homeostasis were evaluated in 193 insulin-treated diabetic out-patients. All had normal serum creatinine and were studied during their everyday metabolic control. Although the patients were selected to be without proteinuria and ketonuria, they exhibited wide ranges of blood glucose values (2.5-29.5 mmol/l) and urine glucose excretions (0-301 mmol/mmol creatinine). Patients with blood glucose values within 2.5-10 mmol/l (n = 80) had entirely normal levels of serum sodium (140.6 +/- 2.7 (SD) versus 141.0 +/- 2.6 mmol/l) and potassium (4.35 +/- 0.38 versus 4.40 +/- 0.38 mmol/l) as compared with normals (n = 371). In contrast, diabetics with higher blood glucose concentrations (n = 113) showed hyponatremia (137.7 +/- 2.6 mmol/l, p less than 0.001) and a moderate increase of serum potassium (4.60 +/- 0.39 mmol/l, p less than 0.001). On stratification into classes of blood glucose, serum sodium declined from 142 to 135 mmol/l (r = -0.61, p less than 0.001), whereas serum potassium rose from 4.33 to 4.87 mmol/l (r = 0.37, p less than 0.001). Despite these reciprocal changes the urinary excretion rates relative to creatinine of sodium potassium and water rose with rising degrees of glycosuria (r = 0.24, p less than 0.001; r = 0.28, p less than 0.001; and r = 0.63, p less than 0.001, respectively). The decline in serum sodium represents a well-known osmoregulatory response to hyperglycemia. However, the rising level of serum potassium in virtual absence of renal failure and ketonuria suggests an abnormality in potassium homeostasis. Diabetic dysregulation, or rather insulin deficiency may be its cause.

Cross-Sectional Studies↗
PubMed1982

The transient effect of strict glycaemic control on B cell function in newly diagnosed type 1 (insulin-dependent) diabetic patients.

Within 24h of diagnosis, 15 consecutive Type 1 (insulin-dependent) diabetic patients were allocated at random to one of two treatment groups: group A (n = 9, mean age: 28 years, range: 17-35 years) was treated conventionally with one or two daily doses of insulin; group B (n = 6, mean age: 27 years, range: 21-37 years) was treated with nine daily injections of fast-acting insulin for ten days and there-after conventionally as for group A. The mean diurnal blood glucose concentration during the initial ten days of insulin treatment was 11.7 +/- 0.5 mmol/l (mean +/- SEM) in group A and 6.4 +/- 0.3 mmol/l in group B (p less than 0.01). Pancreatic B cell function was evaluated 1, 7, 14, 90, and 180 days after the start of insulin treatment from the C-peptide response to a standard meal. At one and seven days after diagnosis, no difference was found in B cell function between the two groups. After 14 days, the amount of C-peptide secreted during the test meal was 18.0 +/- 2.6 nmol (mean +/- SEM) in group A compared with 29.0 +/- 3.6 nmol in group B (p less than 0.05). After 90 and 180 days, no difference was demonstrated in B cell function. The maximal B cell function observed was similar in the two groups, but occurred earlier in group B (at 14 days) than in group A (at 90 days) (p less than 0.05). This study indicates that strict initial glycaemic control may lead to an earlier improvement in B cell function, but that this improvement is of short duration.

Adolescent↗
PubMed1982

Hormonal, metabolic and cardiovascular responses to hypoglycaemia in Type 1 (insulin-dependent) diabetes with and without residual B cell function.

Hormonal, metabolic and cardiovascular responses to insulin induced hypoglycaemia were investigated in seven Type 1 (insulin-dependent) diabetic patients with residual B cell function, eight Type 1 diabetic patients without B cell function and six healthy subjects. No differences were found between the diabetic groups regarding nadir of glucose and rate of recovery to normoglycaemia. The patients with residual B cell function had a glucagon response to hypoglycaemia which was close to that of normal subjects. In patients without B cell function, the glucagon response to hypoglycaemia was present, albeit significantly smaller than in the patients with preserved B cell function (0.025 ng/ml, range 0.007-0.042 versus 0.054 ng/ml, range 0.029-0.087). The group without B cell function had signs of an exaggerated rate of lipolysis and ketogenesis compared with the patients with B cell function and the normal subjects.

Adult↗
PubMed1982

Renal hypomagnesaemia in human diabetes mellitus: its relation to glucose homeostasis.

Interrelations between magnesium and glucose metabolism were studied in 215 insulin-treated diabetic out-patients aged 7-70 years. All had normal serum creatinine concentrations (below 115 mumol/l) and none had other diseases or received drugs known to interfere with mineral metabolism. A definite hypomagnesaemia (less than normal mean - 2 SD) and hypermagnesiuria (greater than normal mean + 2 SD) occurred in 38.6% and 55% of the patients. In the presence of hypermagnesiuria the serum magnesium concentration was inversely correlated to the urinary magnesium excretion rate (R = -0.23, P less than 0.02). Serum magnesium correlated inversely with both fasting blood glucose (R = -0.32, P less than 0.001) and the urinary glucose excretion rate (R = -0.22, P less than 0.005). The urinary magnesium excretion rate correlated directly with the same variables (R = 0.27, P less than 0.001 and R = 0.58, P less than 0.001, respectively). These data indicate that the net tubular reabsorption of magnesium is decreased in diabetic patients in presence of hyperglycaemia, leading to hypermagnesiuria and hypomagnesaemia.

Adolescent↗
PubMed1982

Subcutaneous blood flow during insulin-induced hypoglycaemia: studies in juvenile diabetics with and without autonomic neuropathy and in normal subjects.

Subcutaneous blood flow was measured preceding insulin-induced hypoglycaemia, at the onset of hypoglycaemic symptoms and 2 h later in juvenile diabetics with and without autonomic neuropathy and in normal males. In all groups subcutaneous blood flow decreased at the onset of hypoglycaemic symptoms compared with pre-hypoglycaemic flow. Two hours after onset of hypoglycaemic symptoms, subcutaneous blood flow was still significantly decreased compared with pre-hypoglycaemic flow. In normal subjects local nerve blockade had no effect on blood flow changes during hypoglycaemia, whereas local alpha-receptor blockade abolished the vasoconstrictor response. We suggest that circulating catecholamines stimulating vascular alpha-receptors are probably responsible for flow reduction in the subcutaneous tissue during hypoglycaemia.

Adult↗
PubMed1982

Suppressor cell activity and beta-cell function in insulin-dependent diabetics.

Immunological mechanisms may play a role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM), and suppressor cell activity (SCA) has been found depressed at diagnosis. The aim of the present study was to elucidate whether patients with preserved beta-cell function display a different SCA than other patients. Sixteen patients without and 12 patients with beta-cell function after averagely 9 years' duration of IDDM were examined. The suppressive effect of lymphocytes 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: (1) No significant differences in SCA between patients with and without beta-cell function, and one of these patient groups had SCA significantly different from normal controls. (2) A correlation between SCA and administered dose of insulin among patients without beta-cell function. It is concluded that the actual SCA several years after diagnosis is not connected with the beta-cell function in patients with IDDM.

Adult↗
PubMed1982

No response of pancreatic hormones to hypoglycemia in diabetic autonomic neuropathy.

The responses of pancreatic hormones (i.e. glucagon, pancreatic polypeptide, and somatostatin) to insulin-induced hypoglycemia were investigated in 18 insulin-dependent diabetics without residual beta-cell function and in 6 normal subjects. Nine of the diabetics had autonomic neuropathy, and 9 had no neuropathy. After hypoglycemia, no significant increase in any of the 3 pancreatic hormones was found in the diabetics with autonomic neuropathy, whereas significant increments were found in the diabetics without neuropathy and in the normal subjects. These results suggest that autonomic nervous activity is of major importance for pancreatic hormone release during hypoglycemia in man.

Adult↗