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Biomedical subjects

O K Faber

Publications and source records attributed to O K Faber.

At least 55 records · Page 3Linked 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↗
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

C-peptide response to glucagon in diabetics with and without complications.

Beta cell function has been studied by measurement of C-peptide responses to intravenous glucagon in 11 diabetics with advanced complications and compared with nine long-term diabetics without complications. The majority had no C-peptide responses, but there was evidence of beta cell function in one patient from each group. These observations suggest that some factor other than continuing beta cell function is involved in the complications of insulin-requiring diabetics.

Adult↗
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

Variation in 125I-insulin absorption and blood glucose concentration.

The absorption of monocomponent porcine 125I-insulin Monotard and Isophane was studied in six insulin dependent diabetic patients over a period of 12 days. The absorption of insulin was measured as the disappearance of radioactivity from sites of injection. The daily 125I-insulin doses ranged from 20 to 48 IU between patients. The insulin absorbed varied considerably within and between patients. The range of individual daily absorbed insulin varied from 19 to 104 per cent of the 125I-insulin dose. A significant correlation (p less than 0.05) was found between insulin absorption and blood glucose concentration. Insulin absorption rates were relatively high before all hypoglycaemic episodes and reactive hyperglycaemia was only observed when relatively low insulin absorption rates followed the hypoglycaemic attack. The results show that lability in some insulin dependent diabetics is explained by variation in insulin absorption.

Absorption↗
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

The effect of sulpiride induced hyperprolactinaemia on glucose tolerance and insulin secretion in normal subjects.

Blood glucose concentration and insulin secretion expressed by peripheral plasma insulin (IRI) and C-peptide levels were measured during saline and sulpiride infusion in five normal men. In another experiment the same variables were analysed in six normal males before and during oral sulpiride treatment for 5 days. The i.v. and oral administration of sulpiride resulted in a significant rise in serum prolactin levels. The stimulated serum prolactin concentrations were equivalent to those seen during stress. The sulpiride induced hyperprolactinaemia did not change blood-glucose, plasma IRI levels, hepatic insulin removal and glucose utilization during basal conditions or after i.v. glucose administration.

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↗
PubMed1979

Strategy in the diagnosis of insulinoma.

A simple diagnostic strategy in the diagnosis of insulinoma in adult subjects is proposed based upon the literature and own experiences. It comprises measurement of plasma proinsulin, insulin and C-peptide as well as blood glucose after an overnight fast. When a low or normal proinsulin concentration is found, organic hyperinsulinaemia is very unlikely, while elevated proinsulin, after exclusion of uremia, hepatic cirrhosis, thyreotoxicosis and surreptitious administration of insulin or sulfonylurea drugs, strongly indicates this condition.

Adenoma, Islet Cell↗
PubMed1979

Effects of spontaneous portal-systemic shunting on insulin metabolism.

Insulin degradation was measured by the C-peptide/insulin ratio in 19 patients with portal vein block with extensive spontaneous portal-systemic shunting but minimal liver cell damage: 13 patients with biopsy-proved cirrhosis and 12 controls. Blood obtained fasting and for 3 hr after oral glucose was assayed for glucose, insulin, and C-peptide. Fasting C-peptide and insulin levels in patients with portal vein block and those in controls did not differ. Eight of 13 cirrhotic patients had fasting hyperinsulinemia with a significantly reduced C-peptide/insulin ratio. After glucose administration, the C-peptide/insulin ratio in portal vein block patients with normal aspartate transaminase levels did not differ from control values. In portal vein block patients with elevated asparatate transaminase levels, the C-peptide/insulin ratio was significantly reduced only from 60 min onwards. All the cirrhotic patients showed a significantly reduced C-peptide/insulin ratio after glucose administration. It is suggested that portal-systemic shunting of blood in the presence of a normal liver does not influence hepatic insulin metabolism and that the hyperinsulinemia of cirrhosis is a feature of parenchymal liver damage. In addition, insulin degradation was abnormal in all cirrhotic patients at high insulin secretion rates, even when fasting insulin levels were normal.

Adolescent↗
PubMed1979

Diurnal profiles of serum insulin, C-peptide and blood intermediary metabolites in insulin treated diabetics, their relationship to the control of diabetes and the role of endogenous insulin secretion.

The 24-hour profiles of blood metabolites, serum free and total insulin, and C-peptide were measured in 16 insulin dependent diabetics, and then analysed in order to compare the effects of the presence or absence of residual endogenous insulin secretion and the presence of good or bad diabetic control as judged by the levels of blood glucose or total ketone bodies. Retention of endogenous insulin secretion, responsive to meals, and changes in the level of blood glucose and serum free insulin, were detected in nine patients, its presence having important effects in maintaining metabolic regulation closer towards normal. Despite the fact that apparently well controlled diabetics were selected for the study, the diurnal changes of the levels of blood metabolites, serum free and total insulin and their interrelationships were all grossly abnormal. The levels of both the blood total ketone bodies and the blood glucose were found to be a poor guide to the presence or absence of other metabolic abnormalities of diabetes. High levels of blood total ketone bodies appeared to have a protein sparing effect.

Adult↗
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

The effect of residual insulin secretion on exocrine pancreatic function in juvenile-onset diabetes mellitus.

Residual beta cell function was studied in 18 juvenile-onset diabetics by measuring serum C-peptide immunoreactivity (CPR) fasting, and after IV injection of glucagon (1 mg). This was compared with the exocrine pancreatic response to an IV infusion of secretin and cholecystokinin-pancreozymin. Outputs of pancreatic bicarbonate, amylase and trypsin were measured. Exocrine secretory pancreatic function was decreased in 14 patients. Fasting and maximal CPR showed that 9 patients had residual insulin secretion. For these 'CPR-secretors' there was a strong correlation between CPR and output of bicarbonate (r = 0.87, p less than 0.005) and amylase (r = 0.7, p less than 0.05), but not with trypsin. These results suggest the existence of an endocrine-exocrine relationship in the pancreas.

Adolescent↗
PubMed1978

Kinetics of human connecting peptide in normal and diabetic subjects.

The metabolic clearance rate (MCR) of synthetic human connecting peptide (C-peptide) was measured with a single-dose injection technique in six normal and seven diabetic subjects and with a constant infusion technique in one normal subject. The MCR of C-peptide did not differ in normal subjects (4.4 ml/min per kg; range, 3.7-4.9) and in diabetic subjects (4.7 ml/min per kg; range, 3.7-5.8). Employment of both techniques in one subject gave similar MCR. The average half-life of C-peptide in plasma calculated from the last 1-h period of the single-dose injection studies was longer in the insulin-dependent diabetics (42.5 min; range, 39.4-48.5) than in the normal subjects (33.5 min; range, 24.9-45.3). These results indicate that the beta-cell secretory capacity of normal and insulin-dependent diabetic subjects can be compared by measuring the C-peptide concentration in peripheral venous plasma. The difference in the half-life of C-peptide in plasma between diabetics and normals suggests an altered kinetics of the disappearance of the peptide, while the overall metabolism, as expressed by the MCR, is similar.

Adult↗
PubMed1978

HLA antigens in a family with maturity-onset type diabetes mellitus.

In a family with maturity-onset type of diabetes mellitus inherited as a dominant, autosomal trait (MODY), the HLA genotypes were compared with the glucose tolerance and the plasma insulin response to oral glucose. In the members with impaired glucose tolerance, the plasma insulin response was of the insulino-tardic type, while those with normal or borderline glucose tolerance had a normal plasma insulin response. HLA tissue typing for A, B, C and D series antigens carried out in 19 of the members showed no association between specific HLA antigens and imparied glucose tolerance. Moreover, when analysing the segregation of the disease and the HLA characters, several recombinants between MODY and HLA would have to be postulated if the gene(s) for this form of diabetes mellitus should be closely linked to the HLA locus.

Adolescent↗
PubMed1978

Characterization of seven C-peptide antisera.

The plasma C-peptide immunoreactivity (CPR) in 10 normal subjects varied considerably when measured with different antisera in parallel assays. The CPR level correlated with the blank "CPR" value measured in plasma devoid of C-peptide and to a lesser degree with the sensitivity of the standard curves obtained with the individual antisera. Storage of plasma samples at different temperatures and for different lengths of time before the analyses were carried out resulted in further variation in the CPR results. This was caused by a time- and temperature-dependent fall in CPR, which was more pronounced with some antisera than with others. This sensitivity to storage of plasma did not correlate with the antigenic characteristics of the antisera as determined by their reactivity with 11 specific fragments of the C-peptide molecule. The contribution of human proinsulin to the CPR concentration relative in normal subjects was considered to be negligible even though the relative immunoreactivity of human proinsulin and C-peptide ranged from 11 to 143 per cent among these antisera. These results suggest that differences in C-peptide antisera are a major reason for the variation in the concentration of circulating CPR as measured in different C-peptide immunoassays.

Animals↗