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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the influence of a program of exercise training consisting of three weekly sessions, each 45 min long, for 12 wk, on indices of physical fitness, glycemic control, and insulin sensitivity in nine adolescents with type I diabetes; six age-matched adolescents with diabetes of equivalent duration served as nonexercised controls. All subjects were instructed not to change dialy insulin dose or caloric intake. In the exercised group, maximal oxygen uptake during graded cycle ergometry to volitional exhaustion increased by 9 +/- 2.7% (P less than 0.01) and lean body mass increased by 4 +/- 1.8% (P less than 0.05). Insulin sensitivity, assessed via the euglycemic clamp technique at insulin infusion rates of 100 mU/M2/min, showed an increase of insulin-mediated glucose disposal from 274 +/- 33 to 338 +/- 28 mg/M2/min, representing an increase in insulin sensitivity of 23 +/- 5% (P less than 0.01). None of these indices changed in the control group. Despite increased insulin sensitivity, glycohemoglobin levels remained at 12 +/- 1% before and after the 12 wk of exercise training, indicating no improvement in overall glycemic control. No increase in hypoglycemic reactions was reported in either group. We conclude that exercise training may be a valuable adjunct in managing type I diabetes providing there is concomitant attention to diet and insulin. Exercise training alone, however, does not improve glycemic control, although it improves physical fitness and insulin sensitivity.
Diabetes Care
PMID:Effects of exercise training on insulin sensitivity in adolescents with type I diabetes. 405 32

Urinary N-acetyl-beta-D-glucosaminidase (NAG), a proximal tubule lysosomal enzyme, has been used as an indicator of subtle renal injury. Since it has been positively and significantly correlated with hemoglobin A1c and microalbuminuria, it has been suggested that this enzyme may also reflect metabolic control. Albumin excretion is exacerbated in adult diabetic individuals during exercise; such exercise-induced albuminuria may be a forerunner of diabetic nephropathy. Metabolic control, degree of exertion, and duration of diabetes have been suggested to influence this increase in albuminuria during exercise. Studies of children are few and have produced inconsistent results. Thus we studied 28 insulin-dependent diabetic children ranging in age from 5 yr to 16 yr and 27 age-matched controls using treadmill exercise; two exercise periods consisting of (1) graded increases in speed and grade at 3-min intervals until exhaustion and (2) a constant speed and grade necessary to produce 2/3-3/4 maximal heart rate for 30 min were performed. Capillary blood glucose, urinary NAG/creatinine (cr) ratios (UNAG/Ucr) and urinary albumin/creatinine ratio (Ualb/Ucr) were measured before and after each exercise period; hemoglobin A1c was also measured. The latter averaged 11.8 +/- 0.6% (mean +/- SEM); contrary to previous studies, this was not correlated with pre- or postexercise UNAG/Ucr. During both exercise periods, blood glucose dropped 271 +/- 19 mg/dl to 213 +/- 21 mg/dl (period 1) and 230 +/- 22 mg/dl to 157 +/- 21 mg/dl (period 2).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care
PMID:Effect of exercise on urinary N-acetyl-beta-D-glucosaminidase activity and albumin excretion in children with type I diabetes mellitus. 405 33

Via the artificial endocrine pancreas--apparatus "BIOSTATOR" 100 patients were studied and treated, namely: 90 with diabetes mellitus, 7 with hyperinsulinism and 3 with obesity. The 24-h insulin needs of the diabetics with insulin-dependent and non-insulin dependent with secondary exhaustion type of diabetes, were determined. The following subcutaneous insulin dosage was determined, depending on the insulin amount spent during the 24-h biostator control. It was established that the necessary reduction of the intravenously administered insulin is 30% on the average with the passing over to subcutaneous regime. The indices of lipid metabolism were also studied as well as numerous hormones with which the carbohydrate compensation leads to a change. The problem of the "morning" phenomenon is discussed.
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PMID:[Use of the artificial endocrine pancreas in the clinic]. 409 82

Plasma beta-thromboglobulin concentration was measured in ten uncomplicated insulin-dependent diabetic subjects, in ten insulin-dependent patients with retinopathy and in ten age- and sex-matched healthy controls, both at rest and after cycloergometric exercise to exhaustion. Resting plasma beta-thromboglobulin was similar in the two patient groups and significantly higher than the control group. After exercising, plasma beta-thromboglobulin rose significantly only in the control group. Platelet hyperactivity is therefore present even in uncomplicated diabetes mellitus and is not influenced by the presence of complications. A chronic overstimulation of platelets could be responsible for the high basal plasma beta-thromboglobulin concentration in diabetes mellitus and for its abnormal behaviour after physical exercise.
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PMID:Plasma beta-thromboglobulin concentration at rest and after physical exercise in complicated and uncomplicated diabetes mellitus. 621 Feb 18

Residual B-cell function was studied by measuring 24-hour C-peptide excretion in the urine of 73 Type 1 and 63 Type 2 (28 orally-controlled and 35 insulin-treated) diabetics. Urine C-peptide excretion correlated highly significantly with serum C-peptide concentrations in both the control (r = 0.74, P less than 0.01) and the three diabetic groups (r = 0.89, r = 0.74 and r = 0.89 respectively, P less than 0.001 for all). C-peptide in urine was measurable in 31 of 73 Type 1 diabetics (42%). The earlier the onset and the longer the duration of diabetes, the lower was the proportion of patients with detectable B-cell rest secretion. Preserved residual B-cell function was inversely correlated with the degree of metabolic lability. A significant inverse correlation was also found in this group between 24-hour C-peptide excretion and daily insulin demand (r = 0.78, P less than 0.001). Twenty-nine of the 35 insulin-treated Type 2 diabetics had secondary failure to sulfonylureas and were treated with insulin at the time of the study. Although their daily C-peptide excretion (6.11 +/- 3.71 nmol/24 h) was significantly lower than either the control value (11.30 +/- 0.94 nmol/1, P less than 0.001) or that of orally controlled patients (9.28 +/- 6.16 nmol/l, P less than 0.05) all patients had urine C-peptide concentration in the measurable range. The development of secondary failure to sulfonylureas does not therefore imply complete exhaustion of pancreatic B-cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Residual B-cell function in insulin dependent (Type 1) and non insulin-dependent (Type 2) diabetics (relationship between 24-hour C-peptide excretion and the clinical features of diabetes). 636 Jul 42

In order to evaluate factors influencing the duration of residual B-cell function in maturity-onset diabetics we investigated 104 patients (age 60 +/- 11 years) with a mean duration of disease of 11.3 +/- 8.7 years by measuring fasting C-peptide (FCP) and fasting blood glucose levels (FBG), C-peptide increment after a standardized breakfast and both mean diurnal plasma glucose (MBG) and mean diurnal C-peptide levels (MCP). C-peptide levels were found to be reciprocally dependent on both the age at onset (positively) and, conversely, on the duration of diabetes (y = 0.75 + 0.026x1-0.049x2; R = 0.52, t1 = 2.76, t2 = -4.08). In particular, the present B-cell secretory capacity appears to be lower the younger the patients were at onset, thus suggesting that inherent impairment of B-cell capacity may play a crucial role in determining age at onset of type II diabetes and thus the duration of their residual B-cell function. Moreover, by analyzing separately the data from patients treated with insulin and oral agents respectively, we found that the influence of the duration of the disease on the rate on B-cell exhaustion is unrelated to the mode of treatment even though B-cell capacity at onset appears to be more severely reduced in insulin-treated subjects who, apart from anything else, were younger at onset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Duration of residual B-cell function in maturity-onset diabetes. 638 92

To assess the effects of metabolic control upon beta cell function in diabetes, pro-insulin and insulin were determined following gel-filtration of plasma at two time points in each three diabetic patients, once when the metabolic state was severely deranged and again after the metabolic state had improved after therapy. Before therapy, proinsulin concentration were 30 pM (as IRI), both fasting and at 2 hours after an oral glucose load. These values did not change with treatment. Insulin concentrations were 22 pM at both time points before therapy. With treatment, plasma insulin increased 2-fold at fasting and 7-fold at 2 hours after oral glucose. These results suggest an exhaustion of the insulin pool in beta cells during severe metabolic decompensation of diabetes, a condition which may be reversed by correction of the metabolic states of the patients with proper therapy.
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PMID:Alteration of beta-cell function in different diabetic states. 639

B-cell function was studied in 20 diabetic children, with an age at onset of diabetes between 1.16 years (8.8 +/- 4.0). Serum samples were taken before the first insulin injection and after 1, 3, 6, 9 and in a few patients after 18 months. At 3, 9, and 18 months the patients were also given a standardized breakfast load. Serum proinsulin, C-peptide, IRI and insulin antibodies (IgG) were determined. At onset 19 patients had measurable C-peptide (0.22 +/- 0.17 pmol/ml; range 0.05-0.58). Proinsulin varied between 0.000-0.25 pmol/ml (0.069 +/- 0.071) and at onset amounted to 31.3 +/- 29.4 (0.100)% of C-peptide as compared to 3.3 +/- 1.1 (1.7-6.6) in non-diabetics. A long partial remission was significantly correlated to a low proinsulin/C-peptide ratio at onset. In patients with low fasting proinsulin and no insulin antibodies, breakfast stimulation was accompanied by an increased proinsulin release at 3 and 9 months. The results suggest that abnormal proinsulin secretion is a feature of the 'B-cell exhaustion' complex in juvenile-onset diabetes.
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PMID:Abnormal proinsulin/C-peptide ratio in juvenile diabetes. 675 59

Insulin binding to monocytes was assessed before and after plasma insulin suppression by diazoxide in 14 obesity-related diabetic subjects. Four of the five patients with mild carbohydrate intolerance (FBS less than 150 mg%) and hyperinsulinism exhibited low monocyte insulin binding. Despite an increase in insulin binding after 7 days of diazoxide therapy, no improvement in carbohydrate tolerance could be demonstrated. Lack of improvement may have been related to persistent diazoxide effect. An additional group of 4 patients with low plasma insulin values and more severe carbohydrate intolerance (FBS greater than 150 mg%) had high monocyte insulin binding. This group, as well as a group of patients with intermediate insulin responses, tolerated diazoxide poorly and developed moderate ketonuria or severe hyperglycemia (plasma glucose greater than 350 mg%) necessitating discontinuation of the drug after 3-6 days. The studies in these patients suggest that obesity-related diabetes may be characterized early by mild elevation of plasma glucose, hyperinsulinism and impaired monocyte insulin binding. As beta cell exhaustion occurs, more severe hyperglycemia intervenes and insulin binding to monocytes increases.
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PMID:Role of insulin receptors in obesity-related diabetes. 675 56

Diabetes mellitus predisposition is observed in the increased insulin activity of the pancreatic islet, followed by its exhaustion, and in its congenital or postnatal decreased activity. The former is seen in obese subjects, in large-born children and their mothers or in the children, whose mothers suffered from diabetes mellitus during pregnancy. The latter is discovered in hereditary diabetes mellitus, in hypertension and angiosclerosis. To avert diabetes mellitus in predisposed subjects a fixed-calory diet should be recommended for the pancreatic islet protection. Systematic blood and urine examinations are to be performed for revealing the initial pancreatic islet damage. Prophylactic treatment of these patients is realized by endocrinologists and the selection for therapy is carried out by special physicians.
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PMID:[Prediabetic states and the prevention of diabetes mellitus]. 676 Jan 78


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