Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured circulating levels of C-peptide, pancreatic glucagon, cortisol, growth hormone and metabolites (glucose, non-esterified fatty acids, glycerol and 3-hydroxybutyrate) in fibro-calculous-pancreatic diabetic (FCPD, n = 28), insulin-dependent diabetic (IDDM, n = 28) and non-diabetic control (n = 27) subjects during an oral glucose tolerance test. There was no difference in the two diabetic groups in age (FCPD 24 +/- 2, IDDM 21 +/- 2 years, mean +/- SEM), BMI (FCPD 16.0 +/- 0.6, IDDM 15.7 +/- 0.4 kg/m2), triceps skinfold thickness (FCPD 8 +/- 1, IDDM 7 +/- 1 mm), glycaemic status (fasting plasma glucose, FCPD 12.5 +/- 1.5, IDDM 14.5 +/- 1.2 mmol/l), fasting plasma C-peptide (FCPD 0.13 +/- 0.03, IDDM 0.08 +/- 0.01 nmol/l), peak plasma C-peptide during OGTT (FCPD 0.36 +/- 0.10, IDDM 0.08 +/- 0.03 nmol/l) and fasting plasma glucagon (FCPD 35 +/- 4, IDDM 37 +/- 4 ng/l). FCPD patients, however, showed lower circulating concentrations of non-esterified fatty acids (0.73 +/- 0.11 mmol/l), glycerol (0.11 +/- 0.02 mmol/l) and 3-hydroxybutyrate (0.15 +/- 0.03 mmol/l) compared to IDDM patients (1.13 +/- 0.14, 0.25 +/- 0.05 and 0.29 +/- 0.08 mmol/l, respectively). This could be due to enhanced sensitivity of adipose tissue lipolysis to the suppressive action of circulating insulin and possibly also to insensitivity of hepatic ketogenesis to glucagon. Our results also demonstrate preservation of alpha-cell function in FCPD patients when beta-cell function is severely diminished, suggesting a more selective beta-cell dysfunction or destruction than hitherto believed.
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PMID:The ketosis-resistance in fibro-calculous-pancreatic-diabetes. 1. Clinical observations and endocrine-metabolic measurements during oral glucose tolerance test. 156 31

The prevalence of DM is about 0.4/1000 children with a lower incidence in the rural areas. Children comprise 3-5% of the total diabetics. A study of 55 pediatric cases of DM (1980-84) showed that only 22 (40%) had ketoacidosis on admission. Ten (18.2%) had onset of illness before 4 years of age. HLA antigen studies in childhood IDDM have shown a positive linkage disequilibrium with Bw21 (RR-12.7), and DR3 (RR = 16.6). Prevalence of islet cell antibodies (ICA) was 30.9% (n = 110) as compared with 0.8% in controls. Antibodies against Coxsackie B2 virus were increased (75.5% vs 46.4% in controls). The C-peptide content was substantially low. Malnutrition related DM occurs in adolescents in some parts of India. It is characterized by moderate hyperglycemia, low serum glycerol, relative insulin insensitivity, and pancreatic malformation/calcification in about 1/4 of subjects. There is no association with HLA antigens or ICA, and the precise etiology is unclear. Mortality was 3.6% in patients admitted in our hospital but is higher in other regions due to poverty and relative lack of health care facilities.
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PMID:The challenge of childhood diabetes mellitus in India. 263 90

Resistance to the metabolic effects of insulin has been reported with regard to glucose disposal in type I diabetic patients (IDDM) even when they were euglycemic. Our aim was to study glucose, lipid, and amino acid metabolism during glucose clamping at multiple levels of insulin in 10 normal (N) and 6 IDDM patients. Blood glucose was maintained constant (4.7 mmol/liter) at three insulin plateaus (160 min each) [42 +/- 6 (SD) 89 +/- 11, and 1255 +/- 185 microU/ml in N and 36 +/- 4, 80 +/- 13, and 1249 +/- 107 microU/liter in IDDM]. Mean glucose disposal was 34 +/- 11, 69 +/- 10, and 84 +/- 22 mumol kg-1 min-1 in N and 16 +/- 5, 40 +/- 18, and 65 +/- 27 in IDDM, respectively. Baseline concentrations of blood lactate, pyruvate, alanine, and branched chain amino acids were 560 +/- 130, 36 +/- 9, 212 +/- 44, and 451 +/- 19 mumol/liter, in N and 793 +/- 179 (P less than 0.05), 45 +/- 14, 195 +/- 50, and 439 +/- 33 in IDDM, respectively. The maximum percent change of lactate during the euglycemic clamp was +147 +/- 23% in N and +75 +/- 15% (P less than 0.05) in IDDM; that of branched chain amino acids was -61 +/- 5% in N and -48 +/- 7% (P less than 0.01) in IDDM. Baseline concentrations of glycerol, FFA, and adipate were 44 +/- 15, 449 +/- 152, and 8 - 8 mumol/liter in N and 39 +/- 14, 473 +/- 44, and 41 +/- 14 (P less than 0.01) in IDDM. The maximum percent change of glycerol during the euglycemic clamp was -50 +/- 8% in N and -16 +/- 8% (P less than 0.01) in IDDM, that of FFA -98 +/- 3% in N and -70 +/- 4% in IDDM (P less than 0.05). No significant differences were found between N and IDDM with regard to blood concentrations of ketone bodies, citrate, ketoglutarate, and hydroxymethylglutaryl coenzyme A both before and during the euglycemic clamp. The lactate percent increase was significantly correlated to glucose disposal rate (P less than 0.001). The lactate turnover rate increased during the euglycemic clamp and was lower in IDDM than in N. We conclude that during euglycemic-multiple insulin clamp studies the greater lactate increase suggests that the flux of glycolysis is higher in N than in IDDM, tricarboxylic acid concentrations are comparable in N and IDDM, and FFA, glycerol, and branched chain amino acid decreases were less in IDDM than in N, suggesting that IDDM patients are resistant to insulin with regard to lipid and protein metabolism. The higher adipate basal values demonstrate enhanced omega-oxidation in IDDM.
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PMID:Type I diabetes is characterized by insulin resistance not only with regard to glucose, but also to lipid and amino acid metabolism. 351 29

The effect of restoration of euglycemia with the artificial beta-cell (Biostator GCIIS) on triglyceride metabolism was studied in seven normolipidemic patients with type I diabetes mellitus. Very-low-density lipoprotein triglyceride (VLDL-TG) transport was determined with [3H]glycerol as an endogenous precursor of VLDL-TG; the resultant kinetic data were evaluated by multicompartmental analysis. Studies of triglyceride metabolism were performed in diabetic patients taking their usual dose of subcutaneous insulin (control study) and after 72 h of euglycemia with the artificial beta-cell (Biostator study). Treatment with the artificial beta-cell resulted in a decrease in mean (+/- SE) 24-h plasma glucose levels from 199 +/- 9 to 123 +/- 7 mg/dl and an increase in mean plasma free-insulin levels from 12.3 +/- 1.9 to 27.6 +/- 4.2 microU/ml (P less than .05). These changes were accompanied by a decrease in mean plasma TG levels from 134 +/- 29 to 88 +/- 15 mg/dl (P less than .05). Kinetic studies demonstrated that the change in plasma triglyceride levels was primarily due to a decrease in VLDL-TG transport (i.e., synthesis), which fell from 11.7 +/- 2.5 mg X h-1 X kg-1 ideal wt during the control study to 7.5 +/- 2.0 mg X h-1 X kg-1 ideal wt during the Biostator study (P less than .05). There was no significant change in fractional catabolic rates of VLDL-TG between the two studies (0.35 +/- .05 vs. 0.38 +/- .07 h-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment with artificial beta-cell decreases very-low-density lipoprotein triglyceride synthesis in type I diabetes. 355 99

Glucose and intermediary metabolite responses during incremental insulin infusion (basal, 0.005, 0.01, and 0.05 U X kg-1 X h-1) were examined in IDDM subjects with duration of diabetes of greater than 5 yr (group D5: n = 8, duration 13.5 +/- 3.9 yr, mean +/- SD) and less than 1 yr (group D1: n = 8, duration 0.3 +/- 0.1 yr) from diagnosis. Group D5 had significantly elevated basal plasma free-insulin levels (D5 27.4 +/- 9.6, D1 15.5 +/- 9.4 mU/L; P less than .05). Nonetheless, basal blood glucose (D5 13.8 +/- 4.8, D1 7.1 +/- 1.5 mM; P less than .01), plasma nonesterified fatty acid (NEFA) (D5 1.26 +/- 0.12, D1 0.89 +/- 0.10 mM; P less than .01), blood glycerol (D5 0.12 +/- 0.05, D1 0.07 +/- 0.02 mM; P less than .05), and blood ketones (D5 1.25 +/- 0.91, D1 0.26 +/- 0.20 mM; P less than .01) were higher in group D5. During insulin infusion, group D5 had significantly elevated plasma free-insulin (P less than .05) and blood glucose (P less than .01) levels. Isotopically determined glucose turnover showed metabolic clearance rates were significantly diminished in group D5 during all insulin infusions, indicating a marked impairment of peripheral glucose metabolism. In individual subjects the relationship of blood glucose, plasma NEFA, and blood total ketones (log scale) with the simultaneously occurring plasma insulin level (log scale) was linear for each metabolite.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple aspects of insulin resistance. Comparison of glucose and intermediary metabolite response to incremental insulin infusion in IDDM subjects of short and long duration. 355 3

In order to investigate the causes underlying metabolic instability in type I diabetes mellitus, we studied 8 unstable (group 1) and 4 well-controlled (group 2) diabetic patients, matched for age and duration of diabetes. Subjects were connected overnight to an artificial pancreas and brought to normoglycemia. On the following morning, insulin administration was discontinued for 6 hours and both metabolic and hormonal studies were carried out during this period. After insulin withdrawal, group 1 showed a faster rise of blood glucose (peak: 324.63 +/- 24.93 vs 175.25 +/- 42.63 mg/dl, p less than 0.01), beta-OH-butyrate (peak: 2,273.25 +/- 415.78 vs 550.50 +/- 158.17 mumol/l, p less than 0.01), and glycerol (164.10 +/- 38.90 vs 28.25 +/- 10.6 mumol/l, p less than 0.01). C-peptide secretion increased in group 2 from 0.09 +/- 0.052 to 0.22 +/- 0.099 pmol/ml whereas it remained almost undetectable in group 1 (p less than 0.01, group 1 vs group 2). Growth hormone, cortisol and immunoreactive glucagon were not significantly different in the two groups at any time after insulin withdrawal. Free insulin, after repeated s.c. or i.m. injection of porcine monocomponent insulin (10 IU), was not different in the two groups. We concluded that type I diabetic patients showing severe metabolic instability produced more glucose, ketone bodies and glycerol after insulin withdrawal than control 'stable' patients. This difference could not be accounted for by an excessive secretion of counterregulatory hormones or by an erratic insulin absorption from the injection sites and may have been related to the degree of B-cell failure, as measured by the absence of C-peptide and/or to the degree of insulin resistance.
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PMID:Metabolic instability in type I diabetic patients. Studies on insulin absorption, hepatic production of metabolites and glucose counterregulation. 390 36

Metabolic rhythms were studied over 24 hours in eight adolescents with insulin dependent diabetes before and two months after attempting to improve diabetic control with home blood glucose monitoring. A significant improvement in blood glucose concentration was observed, although 24 hour mean concentrations remained grossly abnormal. This improvement was accompanied by significant falls in blood glycerol and total ketone bodies concentrations and a significant rise in blood lactate concentration. Without attention to other factors affecting diabetic control, the introduction of home blood glucose monitoring produces only a small improvement in control.
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PMID:Metabolic rhythms in adolescents with diabetes. 395 37

In order to evaluate the effects of moderate alcohol intake on intermediate metabolites, five normal subjects and five euglycemic insulin-dependent diabetics (IDDM) were administered two different isocaloric diets; in one diet 35% of the caloric intake consisted of red wine. The insulin-dependent diabetics were connected to an artificial endocrine pancreas (AEP), and glucose levels were continuously monitored. Blood lactate, pyruvate, acetoacetate (AcAc), 3-hydroxybutyrate (3-OHB), glycerol, free fatty acids (FFA), and alanine levels were measured over a 15-hour period from 9 AM to 12 PM. The results showed that alcohol intake did not significantly influence the glucose profiles in either group (111 +/- 4 mg/100 ml versus 110 +/- 4 mg/100 ml for IDDM; 72 +/- 2 mg/100 ml versus 82 +/- 3 mg/100 ml for controls, 15-hour mean +/- SEM), but in both groups it induced a marked increased in the levels of lactate (1.115 +/- 0.067 mM/liter with alcohol versus 0.706 +/- 0.031 mM/liter without alcohol for IDDM; 0.847 +/- 0.052 mM/liter with alcohol versus 0.666 +/- 0.035 mM/liter without alcohol for controls), in the lactate/pyruvate ratio (24.04 +/- 2.12 with alcohol versus 11.42 +/- 0.20 without alcohol for IDDM; 20.84 +/- 2.16 with alcohol versus 11.62 +/- 0.27 without alcohol for controls), in the levels of 3-OHB (0.081 +/- 0.007 mM/liter with alcohol versus 0.046 +/- 0.003 mM/liter without alcohol for IDDM; 0.067 +/- 0.007 mM/liter with alcohol versus 0.025 +/- 0.002 mM/liter without alcohol for controls) and in the 3-OHB/AcAc ratio (1.452 +/- 0.153 with alcohol versus 0.599 +/- 0.036 without alcohol for IDDM; 1.723 +/- 0.198 with alcohol versus 0.439 +/- 0.040 without alcohol for controls) because of a more reduced redox state. Alcohol intake during meals depressed alanine concentration, while glycerol levels showed a transient increase. Reduced blood FFA concentrations after alcohol intake were observed only in controls. This study demonstrates that moderate alcohol intake with meals also affects intermediate metabolites despite euglycemia. These effects were similar both in normal subjects and in IDDM, even if the harmful effects of alcohol may be enhanced by poor metabolic control in the latter.
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PMID:Metabolic effects of moderate alcohol intake with meals in insulin-dependent diabetics controlled by artificial endocrine pancreas (AEP) and in normal subjects. 634 61

Complete acquired lipoatrophic diabetes (LD) is characterized by nonketotic insulin-resistant diabetes, elevated very low-density lipoprotein (VLDL) triglyceride (TG) levels, and absent subcutaneous fat. We studied a young child in whom LD atypically developed after the onset of type 1 diabetes mellitus. On uncontrolled home diet the patient had triglyceride levels over 1,000 mg/dL on multiple occasions. In order to demonstrate the effects of caloric and dietary-fat restriction on VLDL metabolism, 3H-glycerol and autologous 125I-VLDL were used to quantitate the turnover of VLDL-TG and VLDL-apolipoprotein B (apo B) during two periods of caloric restriction. Consumption of a 900-kcal 40-g fat diet resulted in a plasma triglyceride level of 1383 mg/dL (ten-fold elevation). This hypertriglyceridemia was associated with markedly increased production rates of both VLDL-TG (73.7 mg/kg/h) and VLDL-apo B (126.9 mg/kg/d). Consumption of a 900-kcal 25-g fat diet resulted in a plasma TG level of 663 mg/dL. This reduction in plasma TG was associated with a 40% decrease in VLDL-TG production rate (PR) (45.1 mg/kg/h). There was no change in the production rate (PR) of VLDL-apo B. The hypertriglyceridemia in this patient was due to marked over production of VLDL. Furthermore, the studies demonstrate: (1) the independent benefits of caloric and dietary-fat restriction in the treatment of LD, and (2) that fat restriction lowered plasma triglyceride by its effect on the VLDL-TG production rate.
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PMID:Very low-density lipoprotein metabolism in an unusual case of lipoatrophic diabetes. 638 60

Insulin-dependent diabetes mellitus (IDDM) is characterized by a metabolic and hormonal disarray that may be more evident during exercise. However, the metabolic response to exercise of different intensities has not been evaluated in IDDM. We therefore used stable isotope techniques and indirect calorimetry to quantify substrate kinetics and oxidation during 30 min of exercise at 45 and 75% of maximal oxygen uptake (Vo2max) in seven men with IDDM (D group) infused with insulin at a constant basal rate. Normal control subjects (C group) matched for age, weight, and Vo2max were also studied. During moderate exercise, glucose uptake (Rd) was lower in the D than in the C group (15.3 +/- 1.0 vs. 20.8 +/- 1.6 mumol.min-1.kg-1; P < 0.05). Carbohydrate oxidation also tended to be lower in the D group (71.0 +/- 7.2 vs. 87.5 +/- 10.6 mumol.min-1.kg-1; P = 0.08). The D group relied on fat oxidation to a greater extent than did the C group (16.9 +/- 1.1 vs. 10.4 +/- 1.6 mumol.min-1.kg-1; P < 0.05). The enhanced fat oxidation was not due to increased lipolysis because no differences occurred in glycerol release (Ra) or in plasma free fatty acid Ra or concentration, and the source of the extra lipid appeared to be intramuscular fat stores. These differences in substrate metabolism were not evident during exercise at 75% of Vo2max. The lower glucose uptake and oxidation in the diabetic subjects during moderate, but not intense, exercise suggest that glucose metabolism is regulated differently depending on exercise intensity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipid and carbohydrate metabolism in IDDM during moderate and intense exercise. 765 30


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