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

Lipids are transported in the blood in four major classes of lipoproteins. The triacylglycerol-rich lipoproteins are chylomicrons and very-low-density lipoproteins (VLDL) which are produced by the small intestine and liver, respectively. These lipoproteins mainly carry fatty acids to adipose tissue and muscle where the triacylglycerol is hydrolysed by lipoprotein lipase. The resulting particles that remain in the blood are chylomicron remnants and low-density lipoprotein (LDL), respectively. The remnant is taken up by the liver via endocytosis which is mediated by a specific receptor for apolipoprotein E (apoE). LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. 'Nascent' high-density lipoprotein (HDL) particles are secreted by the liver and intestine and then undergo modification to become HDL3 and then HDL2 as they acquire cholesterol ester. They facilitate the reverse transport of cholesterol back to the liver. Little is known of the hormonal regulation of lipoprotein uptake by the liver. Recently, we have shown that insulin and tri-iodothyronine (T3) increase the specific binding of LDL to cultured hepatocytes whereas dexamethasone (a synthetic glucocorticoid) has the opposite effect. The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. These findings may in part explain the hypercholesterolaemia and increased risk of premature atherosclerosis that can be associated with poorly controlled diabetes or hypothyroidism.
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PMID:The biochemistry of lipoproteins. 314 85

Coronary heart disease in insulin-dependent (IDDM) and in non-insulin-dependent diabetes (NIDDM) is associated with lipid and lipoprotein changes favouring atherosclerosis. Whether lipid and lipoprotein abnormalities are associated also with peripheral vascular disease in both types of diabetes is largely unknown. Therefore, we studied lipid and lipoprotein levels and their association with claudication in a representative sample of diabetic and non-diabetic subjects in East Finland. Altogether 87 subjects had IDDM (43 men, 44 women), 264 subjects NIDDM (126 men, 138 women) and 120 subjects were non-diabetic controls (63 men, 57 women). Patients with IDDM had an increased level of HDL and HDL2-cholesterol and patients with NIDDM a decreased level of HDL and HDL2-cholesterol and an increased level of total, LDL and VLDL triglycerides than did non-diabetic subjects. Analyses in both types of diabetes by claudication status revealed that total and LDL-cholesterol and total and VLDL triglycerides tended to be higher and HDL and HDL2-cholesterol lower in those having claudication as compared to those without a claudication symptom. Similarly, total cholesterol/HDL-cholesterol ratio and LDL-cholesterol/HDL-cholesterol ratio were also more atherogenic in patients with claudication than in those without claudication. In conclusion, our results indicate that in both types of diabetes peripheral vascular disease is associated with lipid and lipoprotein abnormalities favouring atherosclerosis.
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PMID:Lipid and lipoprotein abnormalities in diabetic patients with peripheral vascular disease. 321 81

Lipid peroxide levels and plasma lipids were studied in plasma lipoprotein fractions of streptozotocin diabetic rats, spontaneous hypertensive rats (SHR) + diabetes, and in myocardial infarction rats (MIR) + diabetes. The duration of diabetes in all experimental groups was 2.5 months. We found a tendency of elevation of cholesterol in VLDL and fall in HDL2 but the differences were not significant. Total plasma triglycerides were increased in the three diabetic groups, and the increase was due to LDL fraction but again the differences were not significant. The lipid peroxide (LP) level in total plasma showed a significant increase in the three diabetic groups: in Wistar diabetic rats LP increased 3 times, in MIR + diabetes 3.5 times, and in SHR + diabetes 5 times. The increase of LP in the three diabetic groups was due to LDL with good correlation (r = 0.60) between LP and triglycerides in LDL of the three diabetic groups. The results are in agreement with the concept of the importance of lipoprotein fraction changes: increased cholesterol, triglycerides and lipid peroxides in atherogenic (VLDL and LDL) fractions, and decreased levels in antiatherogenic (HDL, HDL2) fractions in diabetes mellitus.
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PMID:Streptozotocin-induced diabetes in rat. II. Lipid and lipid peroxide changes of lipoprotein fractions in diabetes complicated by hypertension and myocardial infarction. 323 44

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

Previous studies have suggested that hyperinsulinemia and upper body adiposity are each separately associated with elevated BP and triglyceride (TG) levels, and with lower high density lipoprotein (HDL) cholesterol levels. The joint effect of hyperinsulinemia and upper body adiposity on lipids, lipoproteins, and BP, however, has not been previously studied. We hypothesized that the effect of body fat distribution on cardiovascular risk factors might be mediated through hyperinsulinemia. We measured BP, lipids and lipoproteins, HDL subfractions, and insulin and glucose concentrations as part of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Insulinemia and glycemia were assessed as the sum of the fasting, half-hour, one-hour, and two-hour insulin and glucose levels, respectively, measured during a standardized oral glucose tolerance test. Individuals who had diabetes according to National Diabetes Data Group criteria were excluded from the analyses. In univariate analyses, both hyperinsulinemia and waist-to-hip ratio (WHR), a measure of upper body adiposity, were positively associated with TG and negatively associated with total HDL and HDL2 cholesterol levels. However, when the effects of glycemia and insulinemia were controlled for by analysis of variance, WHR was no longer significantly related to TG levels. By contrast, WHR continued to be inversely related to total HDL and HDL2 cholesterol even after adjustment for glycemia and insulinemia. Hyperinsulinemia was only weakly related to HDL cholesterol. These results suggest that insulinemia and glycemia might mediate the effects of upper body adiposity on TG, although not on HDL and HDL2 cholesterol. Hyperinsulinemia was also positively associated with diastolic and systolic BP in men.
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PMID:Hyperinsulinemia, upper body adiposity, and cardiovascular risk factors in non-diabetics. 328 48

A summary of the lipoprotein and carbohydrate risk factors for coronary heart disease associated with use of oral contraceptives is followed by a discussion of the methodological difficulties in measuring them, and then by a description of the properties of commonly used oral steroids. Impaired glucose tolerance, high insulin levels, reduced HDL cholesterol and increased LDL cholesterol and VLDL triglycerides are features of coronary heart disease, diabetes, obesity and use of oral contraceptives. A more accurate assessment of glucose tolerance may be measurement of the plasma C-peptide of insulin. Lipid risk factors are subject to wide individual variation as well as special difficulties for pill users. For example, the convenient dextran sulfate method of precipitating HDL, from which the LDL value is calculated, may not be accurate for pill takers because of elevated triglycerides. Even assay of apolipoprotein B is subject to this distortion. If apolipoprotein methods can be standardized, assay of apolipoprotein A1, corresponding to the HDL2 subclass, may be appropriate. Progestins of the gonane class, such as levonorgestrel, because of their androgenic activity, induce changes in lipid risk factors in women similar to those of men. The net effect of the combination of estrogen and progestin is what matters, however. Although progestin-only pills have no effect on carbohydrate metabolism, combined pills decrease glucose tolerance with time, induce hypertriglyceridemia, and oppose the tendency of the estrogen to increase HDL. Norethindrone or other estrane compounds have less impact. Data on triphasics are sparse, but suggest a lesser effect also. New progestins with lower androgenic effects are being developed, although they may confer the added risk of increased triglycerides. Parenteral steroid administration or use of natural hormones are potential solutions.
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PMID:Oral contraceptives and coronary heart disease: modulation of glucose tolerance and plasma lipid risk factors by progestins. 328 33

A random sample of men (319) aged 20 to 59 was examined in one of the administrative districts in Moscow. A study was made of the blood plasma content of HDL2 and HDL3 cholesterol, triglycerides with relation to insulinemia and glycemia both on an empty stomach and during the GTT. An analysis of the data obtained led to a conclusion that the level of insulinemia was a factor influencing the level of HDL2 and HDL3. Derangements in the metabolism of the above lipoproteins were likely to be associated with a high risk of CHD development especially among patients with diabetes mellitus. Therapeutic measures aimed at insulin secretion reduction were recommended for the normalization of lipid metabolism including the content of HDL2 and HDL3.
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PMID:[Indices of carbohydrate metabolism and levels of HDL2 and HDL3 cholesterol in the blood plasma of males]. 332 Oct 31

The aim of the present study concerning patients with long-term insulin-dependent diabetes mellitus was to determine whether the serum lipid and lipoprotein concentrations differ in subjects with and without residual insulin secretion. We also investigated whether factors such as sex, smoking, physical activity and microvascular lesions were associated with particular lipoprotein profiles. C-peptide excretion (greater than or equal to 0.2 nmol) in 24-hour urine samples was used as an indicator of residual insulin secretion. Twenty-two pairs of patients with and without residual insulin secretion matched for age at onset and disease duration were participating in the investigations of glycaemic control and microvascular lesions. The HbA1c was significantly lower in C-peptide excretors than in the non-excretors (6.9 +/- 0.3 vs. 7.9 +/- 0.3%, p less than 0.025). The lipids and lipoprotein fractions were all within normal limits. The HDL2/3 ratio was significantly higher in C-peptide excretors than in non-excretors (1.72 +/- 0.28 vs. 1.10 +/- 0.09, p less than 0.05). Multiple regression analysis showed that factors, such as physical activity, body mass index and glycaemic control could explain more of the variation in the different lipid and lipoprotein fractions than residual C-peptide excretion alone. The only fraction correlating with C-peptide excretion was HDL3 cholesterol. It is concluded that minute residual insulin secretion per se is of minor importance for the regulation of lipids and lipoproteins. Glucose control and residual insulin secretion together with environmental factors seem to be of great importance for the regulation of the lipid and lipoprotein levels in insulin-dependent diabetes mellitus.
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PMID:Serum lipid and lipoprotein levels in long-term insulin-dependent diabetes mellitus. Relation to residual insulin secretion, microvascular lesions and environmental factors. 332 27

The effects of four months' physical exercise on serum lipids, lipoproteins and lipid metabolizing enzymes were studied in 25 non-insulin-dependent diabetic patients divided randomly into exercise (n = 13) and control (n = 12) groups. Exercise induced a significant decrease in serum LDL-cholesterol and an increase in serum HDL-cholesterol and HDL2-cholesterol. Triglycerides showed a temporary decrease. Apoproteins A1 and B were virtually unchanged. Postheparin plasma lipoprotein lipase increased markedly during the exercise period while no change occurred in adipose tissue lipoprotein lipase, hepatic lipase or lecithin:cholesterol acyltransferase. In the control group no significant changes occurred in any of the lipid variables. In the light of the knowledge of LDL-cholesterol as a causative and HDL-cholesterol as a protective factor in atherogenesis in non-diabetics the changes caused by exercise in non-insulin-dependent diabetics can be considered favourable.
Diabetes Res 1988 Feb
PMID:Effects of long-term physical exercise on serum lipids, lipoproteins and lipid metabolizing enzymes in type 2 (non-insulin-dependent) diabetic patients. 339 67

Out of a total of 170 patients with a first myocardial infarction, aged below 65 years, consecutively admitted to the Coronary Care Unit of a large urban hospital, only 14 did not present with any risk factor(s) for atherosclerosis (smoking, hypertension, diabetes and obesity). None of these 14 patients showed significant hyperlipidemia. Compared to a control series of normal individuals of the same age (50.0 +/- 5.8 years for males and 61.6 +/- 3.0 years for females), they showed a significant reduction of high-density lipoprotein (HDL)-cholesterol and of apolipoprotein A-I (respectively -18.2 and -9.5%). However, the most striking abnormality was a 30% decrease of the HDL2 mass and of HDL2 cholesterol; both HDL2 and HDL3 had a reduced cholesteryl ester content in the patients. Reduced HDL2 mass and cholesterol levels in plasma, accompanied by significant alterations in HDL subfraction composition, are consistent with a defective cholesterol esterification in HDL. HDL2 deficiency may be a primary alteration in myocardial infarction patients without other significant risk factors.
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PMID:Reduced HDL2 levels in myocardial infarction patients without risk factors for atherosclerosis. 342 54


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