Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The primary purpose of the present study was to evaluate the role of lipid and glucose metabolism in vasospastic angina. A group of 93 patients in whom the presence of ischemic heart disease was suggested, were classified into the control (C) group, consisting of 30 patients; the coronary artery disease (CAD) group, consisting of 47 patients; and the vasospastic angina (VSA) group, consisting of 16 patients. Among these three groups, age, total cholesterol (TC), triglyceride (TG), HDL-cholesterol (HDL-C), atherogenic index (AI), apolipoproteins and the prevalence of diabetes mellitus were compared. No age difference was seen among the three groups. The TC was the highest in the CAD group, followed by the VSA and C groups. A significant difference in TC was noted between the C and CAD groups and the C and VSA groups. TG levels were higher in the CAD group than in the C and VSA groups, without a significant difference among the three groups. The AI was significantly higher in the CAD group than in the C and VSA groups. No significant difference was noted in the prevalence of diabetes mellitus among the three groups. Apolipoprotein A-I (apo A-I) levels were higher in the VSA group than in the C and CAD groups, and the difference between the VSA and CAD groups was significant. Apolipoprotein A-II (apo A-II) levels were significantly higher in the VSA group than in the C and CAD groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Study on lipid and glucose metabolism in patients with vasospastic angina. 266 90

In 21 non-insulin-dependent diabetic patients with secondary drug failure, once-daily long-acting insulin lead to a moderately improved metabolic control. At the conclusion of the study (eight months) the fasting blood glucose and HbA1c concentrations were significantly decreased, but the postprandial blood glucose concentrations in the afternoon were unaltered. The peripheral insulin sensitivity, as measured by the intravenous insulin tolerance test, and the lipoprotein lipase activity in adipose and skeletal muscle tissue had increased. After initiation of insulin therapy there was a transient decrease of the fasting and glucagon-stimulated C-peptide concentrations. The very low density lipoprotein lipids and apolipoprotein B, A-I and A-II were also reduced transiently. The only significant difference in lipoprotein composition at eight months compared with on admission, was an increased cholesterol and decreased triglyceride concentration in the high density lipoproteins. There were significant relationships between the C-peptide, but not the peripheral insulin, concentrations and the serum lipid concentrations. This may indicate that high peripheral insulin concentrations after administration of exogenous insulin may affect the hepatic lipoprotein production less than the portal insulin concentrations mainly derived from endogenous production.
Diabetes Res 1989 Nov
PMID:C-peptide but not insulin concentrations are related to the serum lipoprotein levels during insulin treatment of non-insulin-dependent diabetes mellitus (NIDDM) patients. 269 85

Arginase activity is elevated in livers of diabetic animals compared to controls and there is evidence that this is due in part to increased specific activity (activity/mg arginase protein). To investigate the molecular basis of this increased activity, the physicochemical and kinetic properties of hepatic arginase from diabetic and control mice were compared. Two types of arginase subunits with molecular weights of 35,000 and 38,000 were found in both the diabetic and control animals and the subunits in these animals had similar, multiple ionic forms. Kinetic parameters of purified preparations of arginase for arginine (apparent Km and Vmax values) and the thermal stability of these preparations from diabetics and controls were also similar. Furthermore, no difference was found in the distribution of arginase activity among different subcellular liver fractions. Separation of basic and acidic oligomeric forms of arginase by fast-protein liquid chromatography resulted in a slightly different distribution of activity among the forms in the normal and diabetic group. The apparent Km values for Mn2+ of the basic form of the enzyme were 25 and 33 microM for the enzyme from normal and diabetic animals, respectively; for acidic forms, for which two apparent Km values were measured, the values were 8 and 197 microM for arginase from controls and 35 and 537 microM from diabetics. These results indicate that in diabetes, while no marked changes in the physicochemical characteristics of arginase are obvious, some changes are found in the interaction of arginase with its cofactor Mn.
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PMID:Comparison of biochemical properties of liver arginase from streptozocin-induced diabetic and control mice. 280 20

To determine whether alterations in lipoprotein phospholipid composition might be an unrecognized factor that contributes to the unexplained acceleration of atherogenesis and the loss of sex-related protection from the development of coronary heart disease in women with insulin-dependent diabetes mellitus, we have estimated levels of neutral lipids, apolipoproteins (A-I, A-II, B), and free cholesterol (FC) in plasma and the four major phospholipid constituents of the very low-density lipoprotein + low-density lipoprotein and high-density lipoprotein (HDL) fractions in 12 ambulatory female patients with varying degrees of diabetic control. Although levels of triglyceride, cholesterol, HDL-cholesterol, and lipoprotein phospholipids in whole plasma of the patients with diabetes were similar to those in controls, their FC levels and FC/lecithin ratio, a recently described index of cardiovascular risk, both were abnormally increased (p less than 0.01). In the HDL-containing plasma fraction, concentrations of sphingomyelin, lecithin, and lysolecithin all were significantly reduced (p less than 0.05; p less than 0.01, and p less than 0.02, respectively). These compositional changes may be potentially atherogenic, because a reduction in the phospholipid content of HDL may impair its capacity to promote the efflux of cholesterol from cells, and the transfer of cholesterol ester from HDL to the larger apo-B-containing lipoproteins is inhibited when their content of FC is increased relative to phospholipid. These previously unrecognized qualitative defects, which are inapparent in the routine estimation of plasma lipids, may compromise reverse cholesterol transport and thereby promote atherogenesis in women with insulin-dependent diabetes mellitus.
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PMID:Abnormal high-density lipoprotein composition in women with insulin-dependent diabetes. 291 87

Serum and lipoprotein lipids were examined in 133 newly diagnosed (type II) diabetic patients (70 men, 63 women), aged 45-64 yr, and in 144 randomly selected nondiabetic control subjects of similar age (62 men, 82 women). The serum total cholesterol levels in diabetic and nondiabetic subjects were similar, but the HDL-cholesterol levels were lower and the serum total triglyceride levels higher in the diabetic than in nondiabetic subjects. No significant differences were found in apoprotein A-I and A-II levels between the diabetic and nondiabetic subjects. After adjustment for age, alcohol intake, obesity, 2-h postglucose serum insulin, and serum triglycerides, male diabetic subjects still had lower HDL-cholesterol levels than corresponding nondiabetic subjects. On the other hand, female diabetic subjects had higher serum triglycerides than their nondiabetic counterparts, even after adjustment for age, alcohol intake, 2-h postglucose serum insulin, and obesity.
Diabetes Care
PMID:Serum lipids and lipoproteins in newly diagnosed non-insulin-dependent (type II) diabetic patients, with special reference to factors influencing HDL-cholesterol and triglyceride levels. 308 7

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.
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PMID:Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth. 308 29

High density lipoprotein (HDL) kinetics were studied by injecting [3H]apoprotein A-I (apoA-I)/HDL into 12 subjects with normal glucose tolerance and 12 patients with noninsulin-dependent diabetes mellitus (NIDDM). The results indicate that the mean fractional catabolic rate (FCR) of apoA-I/HDL was significantly faster [0.63 +/- 0.07 (+/- SEM) vs. 0.39 +/- 0.02 1/day; P less than 0.001] and the apoA-I/HDL synthetic rate greater (29.4 +/- 2.9 vs. 22.9 +/- 1.3 mg/kg X day; P less than 0.02) in patients with NIDDM than in normal subjects. Furthermore, there were statistically significant inverse relationships between apoA-I/HDL FCR and plasma levels of both HDL cholesterol (r = -0.71; P less than 0.001) and apoA-I (r = -0.63; P less than 0.001). In addition, the increase in apoA-I/HDL FCR was directly related to fasting plasma glucose (r = 0.78; P less than 0.001) and insulin (r = 0.76; P less than 0.001) concentrations. These data support the view that the decrease in plasma HDL cholesterol and apoA-I levels commonly found in patients with noninsulin-dependent diabetes is due to an increase in the catabolic rate of apoA-I/HDL secondary to the defects in carbohydrate metabolism present in these patients.
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PMID:High density lipoprotein (HDL) metabolism in noninsulin-dependent diabetes mellitus: measurement of HDL turnover using tritiated HDL. 311 4

The serum concentrations of apolipoproteins C-III, B, and A-I were determined in children with type I diabetes mellitus to establish whether they correlated with the level of glycosylated hemoglobin (Hb A1) and to determine whether these values differ between diabetic children and a population of normal children. Triglyceride (TG), total cholesterol (TC), and apolipoprotein (Apo) levels were studied in 95 children with type I diabetes; 51 of the children were attending a diabetes clinic and 44 were attending a diabetes summer camp. The level of Hb A1 correlated with Apo C-III (P less than .001) and TC (P less than .001) values in the clinic group, but not with Apo A-I or TG levels in either group. The Apo C-III level was higher in both groups of diabetic children (8.0 +/- 0.5 and 9.5 +/- 0.4 mg/dl) (P less than .01) than in normal subjects (6.1 +/- 0.2 mg/dl). We conclude that the Apo C-III level tends to be higher in diabetics than in normal subjects, even in the normotriglyceridemic camp group. The Apo C-III level correlated with both the TC level and Hb A1, suggesting that Apo C-III determinations in type I diabetic patients may permit early identification of atherosclerotic risk.
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PMID:Plasma apolipoprotein C-III levels in children with type I diabetes. 312 78

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.
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PMID:Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes. 327 41

Serum lipoproteins and apolipoproteins were studied at diagnosis and 6, 12 and 24 months later in 30 consecutive children aged 3-15 years with newly detected Type 1 (insulin-dependent) diabetes mellitus (December 1982-October 1984) and in 44 healthy control children. Serum triglycerides at diagnosis were significantly higher than after 6-24 months and also higher than in the control group (p less than 0.001). At follow-up, triglycerides in the very low density lipoproteins and low density lipoproteins were restored to normal, while high density lipoprotein triglycerides remained high. Serum cholesterol at onset of diabetes was significantly higher than in the control children (p less than 0.01), mainly because of increased very low density lipoprotein cholesterol (p less than 0.001). Cholesterol in serum and in the serum lipoprotein fractions was similar to that in the control children at follow-up, except that high density lipoprotein cholesterol was higher in the diabetic children after 6 months. The concentrations of the serum apolipoproteins A-I, A-II and B were higher at onset of diabetes than in the control children (p less than 0.001, p less than 0.01, p less than 0.05 respectively), with a significantly increased ratio of apolipoprotein A-I to A-II in the diabetic children (p less than 0.001). The serum apolipoprotein concentrations were normalised during treatment. The ratio of apolipoprotein A-I to B did not differ from that in control children. On admission, there were strong positive correlations between HbA1c and the concentrations of the very low density lipoproteins and the low density and high density lipoprotein triglycerides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum lipids and apolipoproteins in children with type 1 (insulin-dependent) diabetes during the first two years of the disease. 338 18


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