[Insulin pump therapy].
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Diabetes Mellitus↗
Biomedical subjects
E Helve
Publications and source records attributed to E Helve.
High density lipoprotein subfractions during continuous insulin infusion therapy.
This study compared the effects of continuous subcutaneous insulin infusion (CSII) and conventional insulin therapy (CIT) on serum lipid and lipoprotein levels in type I diabetic patients during 1 year cross-over study (6 months on CSII and 6 months on CIT). The study group consisted of 28 normolipidemic and nonobese diabetic patients (14 males and 14 females) aged 31 +/- 2 yr. The glycemic control was moderate (HbA1 10.2 +/- 0.3%) before starting the study. During the first 6 months, the HbA1 level fell significantly in the CSII group (from 10.4 +/- 0.5% to 9.8 +/- 0.4%, P less than 0.05), but remained unchanged in patients on CIT. During the second 6 months after cross-over no significant alterations in HbA1 levels were observed in either group. HDL-cholesterol (HDL-chol) rose by 38% during the first 6 months in the patients using CSII (P less than 0.001) and by 18% in the CIT group (P less than 0.005). The rise in HDL-chol was accounted for by an increase in both HDL2-chol and HDL3-chol subfractions. Following the shift from CIT to CSII, HDL2-chol rose further (P less than 0.05), whereas HDL3-chol remained unchanged. When CSII was changed to CIT, the HDL3-chol level decreased (P less than 0.02), but HDL2-chol remained constant. There was no correlation between HDL-cholesterol and HbA1 levels or between the changes in either variable. HDL2-chol was 35% higher in females when compared to males at entry, and it rose in both sexes during CSII. HDL3-chol elevated during CSII only in females. CSII or CIT treatments did not cause significant changes in cholesterol or triglyceride levels of VLDL or LDL lipids during the study. Thus, even a mild improvement in glycemic control during CSII is associated with a rise in HDL-chol, particularly the HDL2 subfraction.
Adult↗
Treatment of familial and non-familial hypercholesterolaemia: a review of HMG-CoA reductase inhibitors and probucol.
Hypocholesterolaemic agents are powerful modifiers of the plasma lipoprotein pattern. In addition to lowering plasma low density lipoprotein (LDL) cholesterol, such drugs may elevate, decrease or have no effect on high density lipoprotein (HDL) cholesterol. Bile acid binding resins and 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase inhibitors cause a reduction in hepatic cholesterol content resulting in stimulation of LDL receptor activity. This decreases the plasma LDL level, while HDL cholesterol levels remain unchanged or increase. Probucol, on the other hand, lowers both LDL and HDL cholesterol. It does not act by stimulating LDL receptor activity and is effective in some patients with homozygous familial hypercholesterolaemia who virtually lack LDL receptors. Despite their different lipoprotein-modifying effects, both HMG-CoA reductase inhibitors and probucol are regarded useful in the prevention and retardation of atherosclerosis.
Arteriosclerosis↗
A crossover comparison of continuous insulin infusion and conventional injection treatment of type I diabetes.
We evaluated the feasibility and effectiveness of continuous subcutaneous insulin infusion therapy (CSII) as compared to conventional injection treatment (CIT) in an ordinary diabetic clinic in a one-year randomized crossover study of 65 type I diabetic patients. Home blood glucose levels were lower during CSII (8.6 +/- 0.2 mmol/l, mean +/- SEM) than during CIT (9.1 +/- 0.3 mmol/l, p less than 0.05). During the first six months, HbA1 fell on CSII therapy (from 10.6 +/- 0.4 to 9.7 +/- 0.3%, p less than 0.001), whereas no change occurred during CIT. After the crossover, HbA1 decreased again on CSII (p less than 0.05), but rose in patients shifted from CSII to CIT (p less than 0.05). The fall in glycosylated haemoglobin during CSII correlated with the initial HbA1 level (r = 0.54, p less than 0.001). Ketoacidosis was more common during CSII (16 vs. 2 verified episodes). Hypoglycaemia occurred infrequently, without difference between CSII and CIT. Fifty-six per cent of the patients preferred CSII after the study. In conclusion, while CSII slightly improves the metabolic control, the improvement in the unselected study population is less than previously reported among highly selected patients.
Adolescent↗
Continuous insulin infusion therapy and retinopathy in patients with type I diabetes.
The effect of continuous subcutaneous insulin infusion (CSII) and conventional injection therapy (CIT) on retinopathy was evaluated in a 1-year crossover study (6 + 6 months) with 54 type I diabetic patients. The glycaemic control improved significantly but did not reach euglycaemic levels during CSII (P less than 0.01-0.001), whereas no change was observed during CIT. At baseline, 50% of the patients had no retinopathy, 20% had only minimal changes, 26% had moderate background retinopathy, and 2 patients had proliferative changes. During CSII, the retinopathy grade impaired in 7 patients, whereas no deterioration occurred during CIT. Improvement of retinopathy grading was observed in 2 patients during CSII and in 5 during CIT, respectively. Individual retinal lesions also progressed more and improved less during CSII (12:3) as compared with CIT (10:9). The net impairment in both retinopathy grading and individual lesions was significant during CSII as compared with CIT (P less than 0.05). There was no difference in the baseline characteristics (severity of retinopathy, age, sex, duration of diabetes, insulin dose, blood pressure, serum creatinine), in the fall of glycosylated haemoglobin or number of hypoglycaemic episodes between the patients with and without worsening of retinopathy during CSII. The present study suggests that even a moderate improvement in metabolic control induced by CSII may be associated with a risk of progression of retinopathy during the first months of therapy.
Adolescent↗
Hyperglycemia decreases glucose uptake in type I diabetes.
It has recently been postulated that hyperglycemia per se may contribute to insulin resistance in diabetes. To examine this possibility directly, we measured glucose uptake after 24 h of hyperglycemia (281 +/- 16 mg/dl) and normoglycemia (99 +/- 6 mg/dl) in 10 type I (insulin-dependent) diabetic patients (age 33 +/- 3 yr, relative body wt 102 +/- 3%) treated with continuous subcutaneous insulin infusion. Hyperglycemia was induced by an intravenous glucose infusion, whereas saline was administered during the control day. During both studies the patient received a similar diet and insulin dose. After hyper- and normoglycemia, a primed continuous infusion of insulin (40 mU X m-2 X min-1) was started, and plasma glucose was adjusted to and maintained at 142 +/- 2 and 140 +/- 2 mg/dl, respectively, during 60-160 min of insulin infusion. The rate of glucose uptake after hyperglycemia averaged 8.3 +/- 1.1 mg X kg-1 X min-1, which was lower than the rate after the normoglycemic period (10.1 +/- 1.2 mg X kg-1 X min-1, P less than .001). In conclusion, short-term hyperglycemia reduces glucose uptake in type I diabetic patients. Thus, part of the glucose or insulin resistance in these patients may be caused by hyperglycemia per se.
Adult↗
Improvement of diabetic control by continuous subcutaneous insulin infusion therapy changes fatty acid composition of serum lipids and erythrocytes in type 1 (insulin-dependent) diabetes.
The influence of improved diabetic control on the fatty composition of serum lipids, erythrocytes and platelets was investigated in 24 patients with Type 1 (insulin-dependent) diabetes treated for 6 months with either continuous subcutaneous insulin infusion (n = 14) or conventional insulin therapy (n = 10). The groups were matched for age, sex, body mass index, serum lipids, duration of diabetes, glycosylated haemoglobin and insulin dose. Glycaemic control improved, and the contents of dihomogammalinolenic acid and arachidonic acid but not linoleic acid rose significantly (p less than 0.05), in serum lipids of patients treated with continuous infusion. No changes were observed in the group treated with insulin injections. Both in serum and erythrocytes the n-6 polyunsaturated fatty acid ratios rose consistently in the patients, with improvement of control regardless of the mode of treatment. Furthermore, the change of HbA1 was negatively correlated with that of arachidonic acid in erythrocytes. No changes were found in the platelet fatty acid compositions. The findings suggest that improved diabetic control enhances the conversion of linoleic acid to arachidonic acid, probably by activating enzymes needed for chain elongation and desaturation.
Adult↗
Smoking and insulin sensitivity in type I diabetic patients.
Smoking increases counterregulatory hormone secretion and reduces capillary flow, both of which could reduce insulin mediated glucose disposal. To evaluate whether smoking has any effect on body sensitivity to insulin, we measured insulin-mediated glucose disposal (1 mU euglycemic insulin clamp) during acute smoking in seven male type I diabetic patients. In addition, we performed a cross-sectional study to compare insulin sensitivity in 12 habitually smoking and 22 nonsmoking diabetic patients matched for age, relative body weight, sex, diabetes duration, HbA1, C-peptide, and insulin dose. In the acute study, baseline counterregulatory hormone levels were comparable in the smoking and control experiment. During smoking (9 to 12 cigarettes), carboxyhemoglobin level rose by 57% (P less than 0.01). Circulating adrenaline, cortisol, growth hormone, and glucagon levels were 40% to 100% higher during smoking than during the control clamp study (P less than 0.05-0.01). During acute smoking the rate of insulin-mediated glucose uptake (7.3 +/- 1.0 mg/kg/min) was not significantly different from that without cigarettes (6.8 +/- 0.7 mg/kg/min). In the cross-sectional study, the rate of glucose uptake was comparable in habitually smoking (5.0 +/- 0.5 mg/kg/min) and nonsmoking patients (4.8 +/- 0.3 mg/kg/min). Thus, inspite of a significant rise in counterregulatory hormones, neither acute nor habitual smoking causes substantial changes in insulin sensitivity in type I diabetics.
Adult↗
No association between retinopathy and insulin resistance in type 1 diabetes.
Intact endothelial cell function has been suggested to be important for insulin action. An association between retinopathy and insulin resistance has been found in type 2 diabetes. To evaluate, whether insulin resistance is related to retinopathy in insulin dependent diabetes, we examined 36 type 1 diabetic patients with various degrees of retinopathy: 7 patients had proliferative, 15 had background and 14 patients had no retinopathy. The three groups were matched for age, sex, body weight and insulin dose. Compared with patients with no retinopathy, those with proliferative retinopathy had a longer (P less than 0.05) duration of diabetes (13 +/- 3 vs 22 +/- 3 years for no vs proliferative retinopathy), and higher (P less than 0.05) serum creatinine (74 +/- 4 vs 97 +/- 8 mumol/l), triglyceride (0.69 +/- 0.04 vs 1.02 +/- 0.17 mmol/l) and diastolic blood pressure (77 +/- 3 vs 90 +/- 10 mmHg) levels. The rate of insulin-mediated glucose metabolism (1 mU euglycaemic insulin clamp) was virtually identical in each diabetic group (4.80 +/- 0.42, 4.90 +/- 0.36 and 4.98 +/- 0.74 mg/kg/min) and 40% below that in 8 matched normal subjects (7.53 +/- 0.53 mg/kg/min, P less than 0.001). In conclusion, proliferative retinopathy is related to long duration of diabetes, incipient nephropathy and hypertension. Insulin resistance characterizes the majority of patients with type 1 diabetes but is unrelated to retinopathy.
Adult↗
Relationship between oral glucose tolerance and insulin sensitivity in healthy man and type 1 diabetic patients.
The relationship between insulin sensitivity and oral glucose tolerance was studied in 8 conventionally treated type 1 diabetic patients (age 34 +/- 4 years, relative body weight (RBW) 113 +/- 5%) and in 11 healthy subjects (age 35 +/- 3 years, RBW 114 +/- 2%). In each subject and patient, oral glucose tolerance (75 g glucose) and in vivo sensitivity to insulin (euglycaemic clamp technique, 1 mU/kg/min insulin) were measured. The response to oral glucose in the diabetic patients was measured during maintenance of similar peripheral plasma free insulin levels as in the normal subjects during the oral glucose tolerance test (OGTT). During the OGTT, the post-glucose plasma glucose values in the diabetic patients were markedly higher (P less than 0.001) than in the normal subjects. During the clamp study, the rate of glucose metabolism in the diabetic patients (4.53 +/- 0.58 mg/kg/min) was 37% lower than in the normal subjects (7.19 +/- 0.67 mg/kg/min, P less than 0.02). The area under the glucose curve was inversely related to the rate of glucose metabolism in both the diabetic (r = -0.72, P less than 0.02) and the normal (r = -0.69, P less than 0.02) subjects. The slope of the curve was substantially steeper in the diabetic than the control subjects. Thus, peripheral insulin sensitivity contributes to oral glucose tolerance both in healthy man, and even to a greater extent, in type 1 diabetic patients.
Adult↗
Pathogenesis and prevention of the dawn phenomenon in diabetic patients treated with CSII.
The mechanism of the dawn phenomenon was studied in 12 C-peptide-negative type I diabetic patients (age 30 +/- 2 yr) treated with continuous subcutaneous insulin infusion. During constant basal infusion, nocturnal glycemia remained constant until 4 a.m., but began to rise thereafter in 10/12 patients, with the mean rise from 4.6 +/- 0.4 mmol/L to 6.1 +/- 0.7 mmol/L (P less than 0.01) by 8 a.m. In these patients the rate of glucose production (Ra, 2.14 +/- 0.04 mg/kg/min, 3-H3-glucose infusion) exceeded the rate of utilization (Rd, 1.89 +/- 0.03 mg/kg/min, P less than 0.02). When the patients were restudied after the infusion rate was increased by 49 +/- 7%, Ra fell to 1.75 +/- 0.03 mg/kg/min (P less than 0.01) and the dawn phenomenon was abolished. However, both Ra and Rd remained higher in the diabetic subjects (P less than 0.05) than in eight healthy control subjects, in whom Ra (1.66 +/- 0.02 mg/kg/min) was equal to Rd with glycemia remaining unchanged. Peripheral free insulin levels in the diabetic patients were similar during constant (12.3 +/- 0.5 mU/L) and increased infusion rate (11.3 +/- 0.4 mU/L), and higher than those of the control subjects (5.2 +/- 0.2 mU/L, P less than 0.05). A diurnal rise in serum cortisol levels occurred 1 h earlier in the diabetic than in the control subjects, and Ra was directly proportional to serum cortisol concentration (r = 0.61, P less than 0.01). Serum growth hormone levels were also slightly higher in the diabetic than the control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Insulin resistance in type I diabetes].
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Diabetes Mellitus, Type 1↗
Site of insulin resistance in type 1 diabetes: insulin-mediated glucose disposal in vivo in relation to insulin binding and action in adipocytes in vitro.
To evaluate the mechanism of insulin resistance in type 1 diabetes mellitus, we measured insulin sensitivity in vivo and insulin action in adipocytes in vitro. The study groups consisted of 18 insulin-treated type 1 diabetic patients and 14 matched normal subjects. In each subject, insulin-mediated glucose disposal in vivo was measured by the euglycemic clamp technique. An open surgical biopsy was performed in 9 diabetic and 7 healthy subjects to obtain abdominal sc adipose tissue for the measurement of [125I]insulin binding, D-[14C]-glucose transport, oxidation, and lipogenesis. During the euglycemic clamp studies, similar steady state plasma glucose (4.8 mmol/liter) and insulin (80 mU/liter = 700 pM) levels were maintained in both groups. The rate of glucose metabolism (M) was 43% lower in the diabetic patients (4.75 +/- 0.34 mg/kg X min) than in the normal subjects (8.27 +/- 0.43 mg/kg X min; P less than 0.001). [125I]Insulin binding to adipocytes was reduced in the diabetic patients (26% reduction in tracer binding; P less than 0.05) due to a reduction in receptor number. Insulin binding was not related to the M value at any insulin concentration. Basal and insulin-stimulated rates of glucose transport were not significantly different in diabetic and normal subjects. The basal glucose oxidation rate was reduced by 50% (P less than 0.02), and maximal glucose oxidation was reduced by 49% (P less than 0.03) in the diabetic patients (237 +/- 30 vs. 359 +/- 49 pmol/30,000 cells X 90 min, basal vs. maximal glucose oxidation, respectively) compared to those in normal subjects (513 +/- 101 vs. 700 +/- 133 pmol/30,000 cells X 90 min). The percentage responses of glucose oxidation and glucose transport to insulin were similar in both groups. Glucose oxidation rates at basal (r = 0.68; P less than 0.01), half-maximally (ED50; r = 0.70; P less than 0.01), and maximally (r = 0.64; P less than 0.05) effective insulin concentrations were positively related to the M value. Basal and insulin-stimulated rates of lipogenesis were comparable between the diabetic and normal subjects. In conclusion, insulin-mediated glucose disposal in vivo is reduced in conventionally treated type 1 diabetic patients. In vitro, adipocytes from diabetes bound slightly less insulin at tracer insulin concentrations, but the magnitude of this reduction was not related to impairment of glucose metabolism in vivo. Of the pathways of glucose metabolism studied, the rate of glucose oxidation was most affected. A significant relationship was found between the M value and the rate of in vitro glucose oxidation.(ABSTRACT TRUNCATED AT 400 WORDS)
Adipose Tissue↗
Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes.
To study the effects of rigorous insulin therapy on serum lipoproteins in patients with noninsulin-dependent diabetes not controlled with oral agents only, we measured serum lipoproteins, apoproteins, lipolytic enzymes, and glucose disposal using an insulin clamp technique before and after 4 weeks of insulin therapy. Lipoproteins were isolated by ultracentrifugation and high density lipoprotein (HDL) subfractions, by rate-zonal density gradient ultracentrifugation. The group included 11 women and eight men (age 58 +/- 1 years and RBW 125 +/- 4%). Body weight, glycosylated hemoglobin, mean diurnal glucose, plasma free insulin, and glucose uptake (M-value) were 75 vs. 76 kg; 11.9 vs. 8.9%; 234 vs. 124 mg/dl; 12 vs. 27 microU/ml; and 5.0 +/- 0.4 vs. 7.1 +/- 0.6 mg/kg/min before and after insulin therapy, respectively. After insulin therapy there was a decrease of very low density lipoprotein (VLDL) triglyceride (-60%, p less than 0.001) but an increase of HDL2 cholesterol (+21%, p less than 0.001); HDL2 phospholipids (+38%, p less than 0.001); HDL2 proteins (+23%, p less than 0.01); and HDL2 mass (127 +/- 11 vs. 158 +/- 12 mg/dl, p less than 0.001). There was a decrease of HDL3 cholesterol (-13%, p less than 0.05); HDL3 phospholipids (-16%, p less than 0.05); HDL3 proteins (-18%, p less than 0.001); and HDL3 mass (179 +/- 6 vs. 146 +/- 6, p less than 0.01). Zonal profiles showed a redistribution of particles from HDL3 to HDL2. Serum apo A-I increased (p less than 0.05), apo A-II remained constant, but apo B decreased (-29%, p less than 0.001). The most marked change during insulin therapy was a 2.3-fold increase in adipose tissue lipoprotein lipase (LPL) activity (p less than 0.001). The changes of VLDL and HDL subfractions were not explained by respective changes of the blood glucose, free insulin, or M-value. The data indicate that intensive insulin therapy induces antiatherogenic changes in serum lipids and lipoproteins and suggest that the induction of LPL by insulin is the major factor responsible for redistribution of HDL particles from HDL3 to HDL2.
Adult↗
Overnight interruption of wearing insulin pump: substitution dose and injection site of insulin.
Discontinuing wear of the insulin pump for short periods enhances the feasibility of continuous subcutaneous insulin infusion (CSII) therapy. Because insulin requirements differ during pump and injection therapy, we studied the optimal substitution dose and injection site in seven type I diabetic patients to compensate for the overnight (2100-0730 h) interruption of CSII. The missed basal continuous infusion dose was replaced by injecting intermediate-acting insulin subcutaneously in three different ways: 1.5 times the dose in the abdomen, twice the dose in the abdomen, and twice the dose in the buttock. During CSII, glycemia remained unchanged throughout the night. Both 1.5 times and twice the replacement doses injected in the abdomen resulted in an initial decline in blood glucose with hypoglycemia in two patients followed by a rebound rise. When the replacement dose of 1.5 times was used, blood glucose rose by 4.9 +/- 1.2 mM overnight (P less than .02). These changes after abdominal injection were associated with a rapid early absorption of injected insulin with hypoinsulinemia in the morning. With twice the replacement dose injected in the buttock, insulin absorption was slower, fluctuations in nocturnal glycemia were minor, and the blood glucose level at 0730 h was similar to that of the previous night. There was a significant inverse correlation between blood glucose and serum free-insulin levels in the early morning (r = - .60, P less than .01). In conclusion, a substitution dose of 1.5 times to twice the missed basal infusion rate injected in the buttock compensates for the overnight interruption of CSII without risk of major fluctuations in blood glucose levels or nocturnal hypoglycemia.
Abdomen↗