Treatment of hyperglycaemia in the elderly with diabetes mellitus.
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Aged↗
Biomedical subjects
S Madsbad
Publications and source records attributed to S Madsbad.
[Smoking and diabetes mellitus].
The prevalence of smokers among patients with diabetes is found to be lower than in the population as a whole. Diabetic patients have increased morbidity and mortality from cardiovascular diseases and, in the majority of investigations, smoking is found to be a risk factor in this relationship which does not differ quantitatively from that found in non-diabetics. On the basis of the literature, it has not proved possible to quantitate smoking as a risk factor for the development of peripheral arteriosclerotic vascular disease. Smoking involves hormonal and metabolic changes which are of particular interest in relation to diabetes mellitus. Thus, smoking stimulates the secretion of the antiinsulin hormones, particularly catecholamines, resulting in subcutaneous vasoconstriction which may be unfortunate as it influences insulin absorption. Patients who smoke do not, however, appear to present poorer glycaemic control than non-smokers. A few investigations have shown that smokers have greater insulin requirements than non-smokers. In type 1 (insulin-dependent) diabetes, there is evidence to suggest that diabetic nephropathy and proliferative retinopathy occur more frequently in smokers than in non-smokers. Smoking aggravates the pre-existing more pronounced osteoporosis which occurs in female insulin-dependent patients. It is therefore advantageous to advise diabetic patients against smoking from the point of view of diabetes as such.
Cardiovascular Diseases↗
[Conventional insulin treatment and treatment using multiple injections in diabetes mellitus].
The relationship between development of late diabetic complications and the degree of diabetic control is discussed and thus also the indications for intensive insulin treatment. To promote improved understanding of the basis for treatment with multiple insulin injections, regulation of glucose metabolism in normal individuals is reviewed. The practical management in different insulin regimes and the advantages and disadvantages of these are mentioned. In particular, problems in connection with the "early morning phenomenon", postprandial hyperglycaemia and day-to-day variations in insulin absorption are emphasized.
Blood Glucose↗
Different percentages of CD8+ lymphocytes in long-term type 1 diabetics with and without residual beta cell function.
About 15% of Type 1 diabetics display residual beta cell function after more than 10 yr duration of diabetes, indicating that the disease mechanisms have stopped before all beta cells are destroyed. Peripheral blood lymphocytes were studied from such patients, 11 females and 12 males, 29 +/- 1 yr old, who had had diabetes for 14 +/- 1 yr. A completely matched group of 23 Type 1 diabetics with the same disease duration, but without residual beta cells, were also studied together with a healthy control group. Lymphocytes were marked with monoclonal OKT antibodies and examined by flow cytometry (FACS). There was no difference between the three groups in the absolute number of lymphocytes and helper T-cells (CD4+:40.2 +/- 1.3 vs. 40.4 +/- 1.3 vs. 41.1 +/- 1.8%). In respect of CD8+ (suppressor/cytotoxic) T-cells, the diabetics without beta cells showed 25.9 +/- 1.0%, significantly less than both the patients with preserved beta cell function (29.0 +/- 0.9%, p less than 0.02) and the controls (29.5 +/- 1.3%, p less than 0.02). CD3+ (pan) T-cells showed parallel changes (67.8 +/- 1.5 vs. 71.0 +/- 1.4 vs. 72.2 +/- 1.4%, p less than 0.05). The metabolic state was similar in the two patient groups, and there was no correlation between metabolic and immunological parameters. It is unknown whether the normalization of the T-cell subpopulation, especially the CD8+ lymphocytes, in patients with residual beta cell function at a point when the disease process is apparently at rest, is of causal significance, or of only marker significance.
Adult↗
Gastric inhibitory polypeptide in newly diagnosed ketotic type I (insulin-dependent) diabetics.
Plasma concentrations of 5,000 daltons (5 kDa) immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured before and up to 16 hours after the start of low-dose insulin treatment in newly diagnosed ketotic type I (insulin-dependent) diabetics. Nine patients were non-fasting. Before insulin treatment mean IR-GIP was 31 +/- 6 pmol/l (range 9-65 pmol/l). Four patients had IR-GIP concentrations in the normal fasting range (10-25 pmol/l), and nine patients had concentrations below 35 pmol/l. The remaining patients had IR-GIP concentrations in the normal postprandial range. A meal eaten after the start of insulin treatment caused an increase in IR-GIP in all patients. All patients had beta-cell function as estimated by plasma C-peptide. Individual changes in C-peptide were significantly correlated to changes in blood glucose both after the meal (r = 0.80, p less than 0.01) and during insulin treatment (r = 0.85 +/- 0.04). No correlation could be found between IR-GIP and blood glucose, C-peptide or insulin concentrations. Newly diagnosed ketotic type I diabetics have IR-GIP concentrations within the normal postprandial level. Hypoinsulinaemia, hyperglycaemia, and hyperketonaemia do not by themselves increase 5 kDa IR-GIP markedly above normal fasting levels.
Adolescent↗
Metabolic state does not influence lymphocyte subsets in type 1 diabetic patients.
In most studies the distribution of peripheral lymphocyte subsets at diagnosis of type 1 diabetes has been found to be altered. Lymphocyte subpopulations were therefore studied during longitudinal changes in the glycaemic control of 11 type 1 diabetics to investigate whether poor metabolic status affects these results. To avoid any influence of the etiopathogenetic mechanisms, the patients studied had a disease duration of 10 +/- 2 (SEM) years and all but one had no residual beta-cell function. The patients were selected randomly amongst those with a long record of poor glycaemic control and at the first examination they had a mean fasting blood glucose of 15 +/- 1 mmol/l and a mean glucosuria of 67 +/- 11 g/24 h. They were then hospitalized and strictly regulated using pump treatment, resulting in a massive reduction in glucosuria (0 +/- 0 g/24 h) and fasting blood glucose (6 +/- 1 mmol/l) at a second examination a week later. Five of the patients were tested for a third time 35 +/- 4 days later and were still in very good glycaemic control. Peripheral lymphocytes were labelled with monoclonal antibodies and examined by flow cytometry (FACS). Neither CD3+ (pan) T-lymphocytes, CD4+ (helper) T-cells, CD8+ (suppressor/cytotoxic) T-cells, the relation between CD4+ and CD8+ T-cells, nor the total amount of lymphocytes, changed significantly between the first, second, and third examination. None of the results were significantly different from those of healthy controls. There was no correlation between any of the immunological and metabolic parameters. It is concluded that metabolic influence on the distribution of lymphocyte subsets is unlikely.
Adult↗
Metabolic and cardiovascular responses to epinephrine in diabetic autonomic neuropathy.
Norepinephrine-induced vasoconstriction, which is mediated by alpha-adrenergic receptors, is accentuated in patients with autonomic neuropathy. In contrast, responses mediated by beta-adrenergic receptors, including vasodilatation and metabolic changes, have not been evaluated in these patients. To study these responses, we administered epinephrine in a graded intravenous infusion (0.5 to 5 micrograms per minute) to seven diabetic patients without neuropathy, seven diabetic patients with autonomic neuropathy, and seven normal subjects. Mean arterial pressure decreased significantly in the patients with autonomic neuropathy (P less than 0.01) but was unchanged in the other groups. Since cardiac output increased to a similar extent in the three groups, the decrease in blood pressure was due to a significantly larger decrease (P less than 0.01) in total peripheral vascular resistance in the patients with autonomic neuropathy. The heart rate increased significantly more during the infusions in the patients with neuropathy than in those without neuropathy. Epinephrine produced a greater increase in blood glucose, the glucose-appearance rate, lactate, glycerol, and free fatty acids in the patients with autonomic neuropathy than in the other groups (P less than 0.05). These findings indicate that several beta-receptor-mediated responses to epinephrine are enhanced in patients with diabetic autonomic neuropathy. The underlying mechanism remains to be elucidated.
Adult↗
[Diabetes mellitus and surgery].
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Anesthesia↗
Effect of porcine gastric inhibitory polypeptide on beta-cell function in type I and type II diabetes mellitus.
The effect of highly purified natural porcine GIP on C-peptide release was examined in six type I (insulin-dependent) diabetics (IDD) with residual beta-cell function, six type II non-insulin-dependent) diabetics (NIDD), and six normal subjects. All subjects were normal weight. From -120 minutes to 180 minutes glucose or insulin was infused IV to achieve a constant plasma glucose level of 8 mmol/L. On two separate days GIP (2 pmol/kg/min) or isotonic NaCl at random were infused from 0 to 30 minutes. After 10 minutes of GIP infusion plasma IR-GIP concentrations were in the physiologic postprandial range. At 30 minutes a further increase in IR-GIP to supraphysiologic levels occurred. In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all). The responses of the diabetics were significantly lower than that of the normal subjects (P less than .001 for both groups). No further increase in C-peptide occurred during the remaining 20 minutes of the GIP infusion in the diabetic subjects (IDD, 0.49 +/- 0.05; NIDD, 0.83 +/- 0.10 nmol/L). In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients.
Adult↗
Outcome of the glucagon test depends upon the prevailing blood glucose concentration in type I (insulin-dependent) diabetic patients.
The outcome of 97 paired glucagon and meal tests was related to the prevailing fasting blood glucose concentrations on the two test days. At blood glucose concentration less than 7 mmol/l both the C-peptide responses and the maximal (6 min) C-peptide concentrations during the glucagon tests were significantly lower than the corresponding values found during the meal tests. During the glucagon tests, a direct relationship was found between the responsiveness of the pancreatic beta-cells and fasting blood glucose values when these were between 3 and 7 mmol/l. No significant difference was found between the outcome of the two tests when the fasting blood glucose concentration was greater than 7 mmol/l. The results indicate that the outcome of the glucagon test in Type I patients depends upon the prevailing fasting blood glucose concentration and that the predictive value of the glucagon test as to how the beta-cells will respond to a meal during everyday life is low when fasting blood glucose is less than 7 mmol/l.
Adult↗
Heterogeneity of immunoreactive gastric inhibitory polypeptide in the plasma of newly diagnosed type 1 (insulin-dependent) diabetics.
The aim was to compare the three molecular forms of plasma immunoreactive gastric inhibitory polypeptide (IR-GIP) i.e. void volume (Vo), 8 and 5 kDa IR-GIP, found in type 1 diabetics with those found in normal subjects. Plasma from 6 non-fasting newly diagnosed ketotic type 1 diabetics obtained before and 1 h after a test meal given at start of insulin treatment, and before and 1 h after a test meal given after one and seven days of insulin treatment, respectively, was gel filtered and so was plasma from 6 normal subjects. The immunoreactivity in the effluents was measured with five different antisera. The elution positions of the three peaks were similar in controls and diabetics. With any given antiserum none of the components differed significantly as to amount of immunoreactivity between diabetics and controls, neither after the meals nor in the fasting state. The amount of Vo did not change in response to the meal, whereas the 8 and 5 kDa forms in the diabetics increased similarly to the increase in normals, also during ketosis. The Vo component did not differ significantly between diabetic and normal subjects, but it decreased significantly after start of insulin treatment. In the non-fasting, ketotic state before start of insulin treatment, no IR-GIP form was elevated significantly above normal postprandial levels. We conclude that the molecular forms of IR-GIP are similar in type 1 diabetics and normal subjects, but the molecular forms measured and their relative amounts vary according to which antiserum is used. The present study does not support that lack of insulin and ketosis markedly influence IR-GIP in plasma.
Adult↗
Effect of sham-feeding on glucose tolerance and insulin secretion.
Glucose, 25 g, was infused iv with or without sham-feeding in seven normal males. Sham-feeding improved glucose tolerance, incremental area of blood glucose being 63% (P less than 0.05) of that during iv glucose without sham-feeding. The actual insulin secretion evaluated from the total area under the C-peptide and insulin curves did not differ during iv glucose with or without sham-feeding. These results suggest that the cephalic-vagal reflex improves glucose tolerance during iv glucose, independent of changes in beta-cell function.
Adult↗
Lack of influence of residual beta-cell function on the glucagon and pancreatic polypeptide secretion in type I (insulin-dependent) diabetic patients.
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Adolescent↗
Rapid changes in plasma androgens during insulin withdrawal in male type 1 (insulin-dependent) diabetics.
Plasma concentrations of testosterone, androstenedione and dihydrotestosterone were measured in 15 Type 1 (insulin-dependent) diabetics with (n = 8) and without (n = 7) B-cell function during 12 h of insulin withdrawal and compared with those of 8 normal subjects. Before insulin withdrawal no significant difference was found in androgen concentrations between the diabetic and the normal subjects. The normal diurnal profiles, with highest androgen concentrations in the morning before insulin withdrawal (08:00) and lowest concentrations at 20:00 h were maintained in the diabetics. However, testosterone and dihydrotestosterone concentrations were lower in the diabetics after 4 h of insulin withdrawal and remained so throughout the study. The concentrations of androstenedione were not significantly different between diabetics and normal subjects except after 4 h of insulin withdrawal. Despite the patients without B-cell function were more metabolically decompensated from after 4 h of insulin withdrawal compared with patients with B-cell function, no significant differences were found in androgen concentrations between the two groups although a tendency to lower concentrations were seen in the group without B-cell function.
Adolescent↗
The effect of residual beta-cell function on the development of diabetic retinopathy.
The effect of residual B-cell function on retinopathy was evaluated in a cross-sectional study of 533 insulin-dependent diabetic patients (disease duration 0 to 45 years). One hundred and fifty-three patients with residual B-cell function, as evaluated by stimulated plasma C-peptide concentration, had lower prevalence of retinopathy than patients without B-cell function. The patients with B-cell function had a shorter duration of diabetes and were older at onset, but there was no difference in age at the time of the study. When patients with similar duration of diabetes were compared, no differences in the degrees of retinopathy could be demonstrated between patients with and without B-cell function. These results indicate that residual B-cell function does not protect against or delay the development of diabetic microvascular lesions.
Adolescent↗
Changes in T-lymphocyte subsets after elective surgery.
In seven patients undergoing elective cholecystectomy or vagotomy, helper and suppressor/cytotoxic T-cells were quantified by use of monoclonal antibodies (OKT) preoperatively and on postoperative days 2 and 7. The total number and percentage distribution of T-cells (OKT 3) did not change significantly in the study period and the total number of helper T-cells (OKT 4) was similar in the three tests, but the number of suppressor/cytotoxic T-cells (OKT 8) on postoperative days 2 and 7 showed significant rise from the preoperative value. Consequently, significant decrease in OKT 4/8 ratio was found 2 days (1.47 +/- 0.23) and 7 days (1.80 +/- 0.28) postoperatively, as compared with the preoperative ratio (2.85 +/- 0.44). Since reduced ratio of OKT 4/8 has been shown in disorders associated with diminished immunocompetence, our findings may be related to the increased susceptibility to bacterial infections seen in post-surgery patients.
Aged↗
Effect of two periods with intensified insulin treatment on B-cell function during the first 18 months of type 1 (insulin-dependent) diabetes mellitus.
Fifteen consecutive type 1 (insulin-dependent) diabetics were randomized within 24 hrs of diagnosis of the disease into two groups for treatment: group A (N = 9) was treated conventionally with one or two daily doses of insulin, group B (N = 6) was treated with nine daily injections of fast-acting insulin for ten days after diagnosis and for 7 days after 15 months duration of diabetes. For remaining time group B was treated conventionally like 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) and 6.0 +/- 0.3 mmol/l in group B during the 7 days with intensified treatment 15 months later. B-cell function was assessed from the C-peptide response to a standard meal 17 and 14 days and 3, 6, 9, 12, 15 and 18 months after start of insulin treatment. After 14 days the C-peptide response was significantly higher (60%) in group B than in group A (P less than 0.05). The second period with strict control improved B-cell function in 4 out of 5 patients with B-cell function. At no test other than after 14 days was there any difference in B-cell function between the groups. Short-term improvement of glycaemic control at onset of disease and after the remission period seem without effect on the long-term outcome of B-cell function in type 1 (insulin-dependent) diabetics.
Adolescent↗