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Biomedical subjects

S Madsbad

Publications and source records attributed to S Madsbad.

At least 163 records · Page 9Linked to original sources
PubMed1980

Beta-cell function and metabolic control in insulin treated diabetics.

In a random one day study beta-cell function was evaluated in 210 insulin treated diabetics by the serum C-peptide concentration 6 min after iv injection of 1 mg of glucagon. Sixty-five patients (31%) had residual beta-cell function. As a group these patients were characterized by having a higher age at onset of diabetes (P less than 0.01), a shorter duration of disease (P less than 0.01) and by receiving a smaller dose of insulin (P less than 0.01). However, their quality of metabolic control did not differ from the patients without beta-cell function. Although the concentrations of post-stimulatory C-peptide correlated inversely with both the 24-hour glycosuria (P less than 0.01) and the fasting blood glucose concentrations (P less than 0.02), only a subgroup with C-peptide concentrations exceeding 0.30 pmol/ml showed a definitely better degree of metabolic control than those without beta-cell function. As this subgroup also received the smallest dose of insulin these observations suggest that maintenance of beta-cell function above this level facilitates good metabolic control. Evidence is presented suggesting that measurements of the 24-hour glycosuria undertaken in a diabetes clinic create a too optimistic impression of the quality of metabolic control during every day life.

Adolescent↗
PubMed1980

Insulin secretory reserve in insulin dependent patients at time of diagnosis and the first 180 days of insulin treatment.

Eleven newly diagnosed insulin dependent patients were studied before and during the first 16 h after start of insulin treatment. All the patients were found to have significant amounts of C-peptide in plasma indicating residual insulin secretion. The fall in blood glucose after start of insulin therapy was followed by a parallel decrease in C-peptide (R = 0.99, P < 0.01) suggesting that the beta-cells may respond to variation in blood glucose. Eight of the patients were studied 1, 4, 7, 14, 90 and 180 days after start of insulin therapy. During the first 90 days of treatment an increasing maximal C-peptide concentration was found after a standard breakfast test meal. Two thirds of this improvement i beta-cell function was found after the initial 14 days with an average increase in maximal C-peptide of 260 per cent. The sensitivity to glucose improved.

Adolescent↗
PubMed1980

Depressed suppressor cell activity in patients with newly diagnosed insulin-dependent diabetes mellitus.

Suppressor cell activity (SCA) was studied in twenty-eight patients with insulin-dependent diabetes mellitus (IDDM), both newly diagnosed and of longer standing. Suppressive effect of peripheral blood lymphocytes from the patients was tested after 48 hr of 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. SCA was expressed in relation to the activity of peripheral blood lymphocytes from simultaneously investigated healthy control individuals. The main findings were: (1) SCA was significantly depressed in newly diagnosed diabetics and (2) newly diagnosed patients displayed significantly lower SCA than did patients with duration of disease between 2 and 8 months and between 5 and 8 years, who had suppressor cell activities not significantly different from healthy individuals. Earlier studies have pointed to the significance of immune reactions in diabetogenesis. On this basis, and on the strength of our present findings, it is suggested that an impaired SCA, causing a decreased inhibition of aggressive lymphocytes, may be implicated in the pathogenesis of insulin-dependent diabetes mellitus.

Adult↗
PubMed1979

Impaired response of pancreatic polypeptide to hypoglycaemia: an early sign of autonomic neuropathy in diabetics.

The pancreatic polypeptide (PP) response to insulin-induced hypoglycaemia was studied in 18 juvenile diabetics and was calculated as the difference between the prestimulatory PP concentration and the maximal concentration measured. The response was severely impaired in patients with autonomic neuropathy (mean +/- SE of mean 22 +/- 12 pmol/l) as compared with patients without neuropathy (252 +/- 51 pmol/l). Patients whose diabetes was of only a few years' duration showed a normal PP response to hypoglycaemia, and the response diminished significantly with increasing duration of diabetes. The decreased PP response to hypoglycaemia was significantly correlated with an increased threshold of the sense of vibration, (rs = 0.86). These results suggest that impaired, secretion of PP may serve as an early sign of autonomic neuropathy in diabetes.

Adult↗
PubMed1979

Role of residual insulin secretion in protecting against ketoacidosis in insulin-dependent diabetes.

The role of preserved beta-cell function in preventing ketoacidosis in type I insulin-dependent diabetes was assessed in eight patients with and seven patients without residual beta-cell function as determined from C-peptide concentrations. After 12 hours of insulin fatty-acid, and glycerol concentrations were all significantly higher in patients without beta-cell function than in those with residual secretion. Mean blood glucose concentrations reached 17.2 +/- SE of mean 1.3 mmol/l (310 +/- 23 mg/100 ml) in the first group compared with 8.8 +/- 1.4 mmol/l (159 +/- 25 mg/100 ml) in the second (P less than 0.01), while 3-hydroxybutyrate concentrations rose to 5.5 +/- mmol/l (57 +/- 5 mg/100 ml) and 1.4 +/- 0.3 mmol/l (15 +/- 3 mg/100 ml) in the two groups respectively (P less than 0.01). Individual mean C-peptide concentrations showed a significant inverse correlation with the final blood glucose values (r = -0.91; P less than 0.02). These findings strongly suggest that even minimal residual insulin secretion is important for metabolic wellbeing in diabetes and may prevent the development of severe ketoacidosis when insulin delivery is inadequate.

Adolescent↗
PubMed1979

Bone loss in diabetes: effects of metabolic state.

The significance of different risk factors for the development of bone loss in diabetes mellitus was evaluated in a cross sectional study of 215 insulin treated diabetic outpatients. Bone mineral content in the forearms was measured by photon absorptiometry and the metabolic status was evaluated by three indices: residual B-cell function, insulin dosage and fasting blood glucose. The mean bone mineral content was reduced to 90.2% of sex- and age-matched normal mean values (P less than 0.001). Stratification of the patients showed that bone mineral content was 99.3% of that found in sex- and age matched normal subjects in the group with residual B-cell function, low insulin dosage and low fasting blood glucose; it was only 79.3% of normal in the group with no detectable insulin secretion, high insulin dosage and more severe hyperglycaemia. Thus, residual insulin secretion and the quality of metabolic control are major factors in determining bone mineral content in insulin treated diabetic patients.

Blood Glucose↗
PubMed1979

Pancreatic beta cell secretion during oral and intravenous glucose administration.

The contribution of decreased hepatic insulin extraction to the relative hyperinsulinemia after oral glucose load as compared to intravenous glucose load was studied in 6 normal weight male volunteers by means of an analysis of the relationship between peripheral venous concentrations of insulin and C-peptide following similar glycemic stimuli after oral and intravenous glucose administration. The incremental areas under the insulin and C-peptide curves were higher during oral as compared to intravenous glucose administration, 436 (251--762) per cent and 267 (124-378) per cent respectively (mean and range). The ratio between corresponding incremental areas of insulin and C-peptide were 53 (17--103 per cent higher during oral glucose load. These findings suggest that the augmented peripheral insulin levels after oral glucose administration are caused by a combination of increased beta cell secretion and decreased hepatic insulin extraction.

Adult↗
PubMed1979

Bone mineral loss in insulin-treated diabetes mellitus: studies on pathogenesis.

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectionsl study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raising urinary calcium excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P less than 0.02), to glycosuria (P less than 0.02) and to insulin requirement (P less than 0.002), and positively to the glucagon-stimulated serum C-peptide levels (P less than 0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P less than 0.001) and glycosuria (P less than 0.001). The skeletal calcium loss corresponded to the excess of urinary excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.

Adolescent↗
PubMed1978

Passive transfer of diabetes mellitus from man to mouse.

Lymphocytes extracted from peripheral-blood samples from each of six patients with newly diagnosed insulin-dependent diabetes mellitus were transplanted into arthymic nude mice. At one or more sampling times (in the thirty-day study) blood sugar was higher in mice which had received lymphocytes from diabetic patients than in the control mice which had received lymphocytes from non-diabetic donors. Blood-sugar concentrations reached 260 mg/dl in some mice in the experimental group. This study demonstrates that lymphocytes may have an aggressive role in diabetogenesis. With this mouse experimental model mechanisms involved in diabetogenesis, and probably also in other disease in which lymphocytes are suspected of being involved in pathogenesis, could be investigated.

Adolescent↗
PubMed1978

Osteopenia in insulin treated diabetes mellitus. Its relation to age at onset, sex and duration of disease.

Bone mineral content was measured by photon absorptiometry in 215 insulin treated diabetic out-patients aged 7--70 years. As bone mass increases until the age of 20--25 years, patients were so selected that all remained within the same phase of bone mineral storage throughout the entire course of their diabetes. Other criteria for exclusion were diseases or drugs interfering with mineral metabolism and previous use of oral antidiabetic agents. As a group the patients demonstrated a bone mineral deficit of 9.8% compared with sex- and age-matched controls (P less than 0.001). Comparison between patients who had developed diabetes before the age of 20 years and after that of 25 years revealed deficits of 14% and 7%, respectively (P less than 0.001). Sex differences were not observed. The initiation of osteopenia seemed to coincide with the onset of clinical diabetes mellitus, and significantly reduced bone mineral content was observed after 2 years of diabetes (P less than 0.001). After 3--5 years the osteopenia appeared to attain a stable level.

Adolescent↗
PubMed1978

Hepatitis B virus infections among Danish dentists.

Since type B hepatitis is generally regarded as an occupational risk for dentists, the participants at the 1976 annual meeting of the Danish Dental Association were examined for hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs). A total of 1,338 dentists (89% of the dentists at the meeting and 29% of all Danish dentists) were included in the study by completion of a questionnaire and by radioimmunoassay of a blood sample for HGsAg and anti-HBs. None of the dentists was HBsAg-positive, but 110 (8.2%) had anti-HBs. An increasing frequency of anti-HBs was found with increasing age, but the figures were similar to the findings in a control population. Evidence is presented that hepatitis found before admittance to or during the time at dental school was predominantly not of type B. In contrast, type B hepatitis predominated during the professional activity of the dentists. On the basis of the serological findings in 29% of all Danish dentists, it is concluded that dentists cannot be regarded as a high-risk group for hepatitis B.

Aging↗
PubMed1978

Kinetics of human C-peptide in man.

A review of studies concerned with the metabolism of human C-peptide showed that the kidney is the major organ in C-peptide removal. The turnover rate of C-peptide was similar to that of proinsulin but considerably slower than that of insulin. An analysis of corresponding C-peptide and insulin concentrations in normal subjects after the administration of oral glucose or intravenous glucagon was used to define the relationships between the two peptides. These results show that different peripheral vein concentrations of insulin may correspond to identical C-peptide concentrations, depending on sampling conditions.

C-Peptide↗
PubMed1978

Prevalence of residual beta-cell function in insulin-dependent diabetics in relation to age at onset and duration of diabetes.

The influence of the age at onset as well as the duration of disease on the prevalence of residual beta-cell function was studied in insulin-dependent diabetic patients. Two hundred and sixty-seven patients presented at an early age (10-19.9 years) and 158 patients had a late onset (30-39.9 years of age). beta-cell function was evaluated by measuring serum C-peptide immunoreactivity. Fifty-six patients (21.0 per cent) in the early-onset group and 64 (40.5 per cent) in the late-onset group had residual beta-cell function. The prevalence of residual beta-cell function was almost 100 per cent during the first two years of disease and was lower thereafter in diabetics with early onset. About 15 per cent of all patients with a duration between 15 and 35 years had residual beta-cell secretory function.

Adolescent↗
PubMed1978

Hypomagnesemia, a risk factor in diabetic retinopathy.

The serum magnesium concentration was measured in 71 insulin-treated diabetic outpatients who had had the disease for 10 to 20 years. The patients were divided into two subgroups according to the severity of their retinopathy. As a whole the patients exhibited a definite hypomagnesemia (P less than 0.001) that was most pronounced in the subgroup having the severest degree of retinopathy (P less than 0.01). The subgroups were comparable regarding known risk factors implicated in diabetic retinopathy. Thus, hypomagnesemia appears to be an additional risk factor in the development and progress of this complication.

Adolescent↗