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

During the period January 1979-March 1983, we have conducted in Jerusalem a case control study of all patients under the age of 65 surviving their first diagnosed myocardial infarction, in order to evaluate the importance of the conventional risk factors and to detect additional factors through quantifying plasma apolipoprotein concentrations. As a control group, we have chosen a sample from a previously studied Jewish population (LRC study), representative of the adult Jerusalemite population, parents of children born during 1958-1961. To complete the younger age group missing in the LRC population, we added a population studied in the Kiryat Yovel district of Jerusalem. We report here the results obtained from interviews and analysis of 532 cases (448 males and 84 females), and 869 controls (457 males and 412 females). In order to overcome the effects of age and ethnic origin on the risk factors, we have divided our populations according to age and country of origin of their fathers. Age, sex, smoking, history of high blood pressure, diabetes, elevated plasma triglycerides and/or cholesterol, and decrease in plasma HDL cholesterol, emerged as the most powerful and significant risk factors in this study. Other putative risk factors such as socioeconomic status, dietary habits, physical activity and obesity index were not found to be significantly different between cases and controls. It is noteworthy that smoking was more important as a risk factor in the younger age groups, whereas hypertension and diabetes were more important in the older age groups, particularly in females. The differences in lipid levels were considerably more prominent in the young age groups in both sexes. Myocardial infarction was observed more frequently in patients of European or American extractions. Apolipoproteins A-I, A-II, E and B determined in this study were shown to be affected partly by age and country of origin. Apo E and apo B levels were significantly higher and Apo A-I significantly lower in patients with myocardial infarction when compared to controls.
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PMID:Analysis of risk factors in 532 survivors of first myocardial infarction hospitalized in Jerusalem. 345 28

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. 352 12

This review discusses the genetic factors in the development of arteriosclerosis and coronary heart disease (CHD). In several studies, multivariate analysis of prospective mortality/morbidity data and angiographic findings have indicated that a family history of CHD contributed to CHD risk independently of the established risk factors. In addition, ethnic groups that differ in the prevalence and incidence of CHD also markedly differ in blood groups and protein-enzymatic markers. These or other genetic differences may affect CHD rates. Data from fraternal and identical twins, the source of some early genetic CHD findings, are reviewed. Genetic disorders of lipoprotein metabolism and transport, such as familial hypercholesterolemia, as well as other monogenic disorders are discussed. The role of apoprotein E polymorphism i other monogenic disorders are discussed. The role of apoprotein E polymorphism in determining plasma LDL variability among individuals is considered. Recombinant DNA technology, molecular cloning, and the identification of restriction fragment length polymorphisms are new tools for investigators who assess DNA polymorphism. Recent advances in that domain include: DNA polymorphisms affecting blood levels of apo A-I and A-II, association of a DNA insertion on chromosome 19 with severe premature atherosclerosis, and information concerning linkage of the genes for various apolipoproteins. In addition, the evidence for a major genetic component in diabetes mellitus and research into the genetic aspects of hypertension are reviewed. The male/female ratio in pathologically and epidemiologically assessed atherosclerosis may provide clues to the role of genetics. Early structural changes in the coronary artery intima are compatible with the ethnic and gender predilection. A key question in understanding underlying mechanisms in atherosclerosis is why coronary arteries are occluded in individuals whose other arterial systems are largely unaffected. The review concludes with a discussion of the directions and implications of future genetic research in arteriosclerosis with an emphasis on uncovering genetically determined differences in arterial wall response to blood flow. Subpopulations with different genetic risks may be identified, in which case universal preventive strategies might be replaced with specific ones.
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PMID:Genetic aspects of arteriosclerosis. 352 20

There is a very high probability that lipoprotein metabolism plays a central role in the etiology of coronary heart disease. In sedentary persons one way to favorably alter lipoprotein metabolism and possibly delay the progression of coronary atherosclerosis is by an increase in their habitual physical activity. More physically active persons tend to have lower plasma triglycerides and very low density lipoprotein concentrations, and a greater high-density lipoprotein mass due to higher concentrations of the subfraction HDL2 and apoprotein A-I. Plasma low-density lipoprotein concentrations usually are not significantly reduced by exercise unless accompanied by weight loss, but there may be important changes in the distribution among the low-density subfractions. These exercise effects are most likely mediated by alterations in the activity of enzymes involved in the synthesis, transport and catabolism of the various lipoproteins including lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase. In healthy persons as well as in patients with ischemic heart disease, diabetes and renal failure, an increase in moderate-intensity, endurance-type activity requiring an expenditure of approximately 4 MJ (1,000 kcal) per week usually produce favorable lipoprotein changes. Above this level a dose-response relationship exists, with greater changes occurring up to energy expenditures of 19 MJ (4,500 kcal) per week.
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PMID:The influence of exercise training on plasma lipids and lipoproteins in health and disease. 353 12

The objective of this paper is to review the extent and mechanisms of lipoprotein alterations in pregnancy, present new data relating to placental lipid transport in normal humans and diabetic animals and consider possible effects on fetal growth and development in normal and diabetic pregnancy. The concentration of all lipoprotein fractions increases during pregnancy. VLDL cholesterol and triglyceride increase 2.5-fold over prepregnancy levels and LDL cholesterol increases 1.6-fold, all with peak levels at term. HDL cholesterol is maximally increased in midgestation by 1.45-fold and subsequently declines to 1.15-fold at term. The mechanisms of these lipoprotein changes have not been studied in humans but the hypertriglyceridemia in animal models is related to enhanced VLDL entry into the circulation. In addition, diminished adipose tissue lipoprotein lipase (LPL) activity in late gestation may cause a rerouting of triglyceride fatty acids to other tissues such as muscle and uterus for oxidation, rather than storage, since triglyceride transport is not reduced in pregnancy. All of these changes appear to be sex hormone mediated. In diabetic pregnancies, the available data indicate that triglyceride concentrations are increased and HDL cholesterol concentrations are decreased with reference to lipoproteins in nondiabetic pregnant women. Previously unpublished data show that a transplacental FFA gradient exists across the umbilical circulation in the direction of the fetus and is proportional to the maternal FFA concentration. No gradient is seen for triglyceride or total plasma cholesterol. However, transport of unmeasured amounts of triglyceride fatty acids may still occur via placental LPL and be exaggerated in diabetes where LPL declines in adipose tissue but not in placenta. The mechanism of transplacental cholesterol transport remains to be defined. Preliminary studies suggest that it depends on HDL as well as LDL since both can provide cholesterol for placental progesterone synthesis. In addition, fetal weight and length are associated with maternal apoproteins A-I and A-II, both major apoproteins of HDL. By lowering HDL in pregnancy, diabetes mellitus could negatively affect these relationships. In conclusion, sex hormone mediated modifications of lipoprotein physiology are described in pregnancy which may enhance triglyceride fatty acid transport to muscle for oxidation and LDL and HDL cholesterol delivery to growing maternal and fetal tissues, a process that diabetes could globally disrupt.
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PMID:Lipoprotein metabolism in pregnancy, fat transport to the fetus, and the effects of diabetes. 354 67

Different types of diabetes mellitus have different effects on high density lipoprotein (HDL) metabolism. Impaired glucose tolerance may be associated with no change or a slight decrease in HDL cholesterol. Type I diabetes may have normal or elevated HDL cholesterol levels. This HDL elevation may be due to an increase in HDL2 or HDL3. Apo A-I/Apo A-II ratio is also higher in these diabetics. Type II diabetics may have normal or low HDL cholesterol levels as well as normal or decreased Apo A-I levels. In gestational diabetics, the mean HDL cholesterol is lower than controls. Dietary therapy resulting in greater than 10% weight loss in obese diabetics leads to an increase in their HDL-cholesterol levels, although the effect on the latter is controversial. Intensive insulin therapy (for 2-3 weeks) increases serum apo A-I and HDL-cholesterol levels. End-stage renal disease also affects HDL metabolism. In general, patients with this disorder have a decrease of cholesterol and an increase in triglyceride in their HDL. There is an increase in apo E and a decrease in apo CII in their HDL. Apo A-I levels are unaffected whereas apo A-II levels are decreased. Renal transplant patients may have low, normal or high HDL cholesterol and normal or high apo-I levels. In non-diabetic, normotriglyceridemic patients peritoneal dialysis increases their HDL-cholesterol. In non-diabetic hypertriglyceridemic and diabetic patients, peritoneal dialysis causes no change in their HDL-cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of diabetes mellitus and end-stage renal disease on HDL metabolism. 379 61

Lipoproteins were isolated by sequential ultracentrifugation, and the concentrations and compositions were determined in nondiabetic (ND), borderline diabetic (BD), and diabetic (D) Macaca nigra males consuming a chow ration. The total concentrations and components of the VLDL and IDL increased significantly with metabolic deterioration (P less than 0.01). Concentrations and components of LDL increased in the BD and D monkeys, but changes were not statistically significant. The HDL2 and HDL3 particles were virtually unchanged among the three different metabolic groups. The VLDL was the major carrier of the triglycerides, especially in D monkeys. Cholesterol was present predominantly in the LDL. The LDL-cholesterol to HDL-cholesterol ratio increased in the BD and D monkeys, owing mainly to increases in the LDL-cholesterol content. Apoprotein antisera showed apoprotein B in the VLDL, IDL, and LDL, apoprotein E in the VLDL and IDL, and apoprotein A-I in the HDL2 and HDL3 fractions. Because Macaca nigra consume a nonatherogenic, low-cholesterol, low-fat ration, the changes in lipoproteins, particularly in VLDL and IDL, are attributable to metabolic alterations associated with diabetes.
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PMID:Lipoprotein patterns in nondiabetic, borderline diabetic, and diabetic Macaca nigra. 382 73

It has been hypothesized that plasma triglyceride fatty acids may traverse the placenta and contribute to infant adiposity particularly in GDM pregnancy. It has also been hypothesized that high-density lipoproteins (HDL) can both deliver cholesterol to and remove cholesterol from the placenta. To determine if these maternal parameters are related to fetal growth in normal pregnancy, we have examined relationships of lipoprotein lipids, apoproteins, hormones, fuels, clinical chemistries, and maternal weight at 36 wk gestation to infant birth weight, birth weight ratio (birth weight corrected for gestational age), birth length, and head circumference in a cohort of pregnant women attending a prepaid health plan, Group Health Cooperative of Puget Sound. Associations were examined using a multivariate regression analysis of several groups of related variables. Results show that the birth weight and/or birth weight ratio are weakly positively associated with maternal very-low-density lipoprotein (VLDL) triglyceride and statistically significantly positively associated with apoprotein A-I, placental lactogen, estradiol, bilirubin, and maternal prepregnancy weight and pregnancy weight gain. Glucose and insulin predict birth weight only in pairwise analysis. Significant negative predictors of birth weight or birth weight ratio include VLDL cholesterol, apoprotein A-II, SGOT, and creatinine. Significant positive predictors of birth length include apoproteins A-I, placental lactogen, and maternal weight. Apoprotein A-II negatively predicts birth length. Only maternal prepregnancy weight predicts head circumference.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Jun
PMID:Relationships of infant birth size to maternal lipoproteins, apoproteins, fuels, hormones, clinical chemistries, and body weight at 36 weeks gestation. 392 27

Plasma triglycerides, total cholesterol, phospholipids, HDL-cholesterol, HDL-phospholipids, apolipoproteins A-I and B, haemoglobin AIc and C-peptide were measured in 113 children and adolescents (49 males and 64 females) with insulin-dependent diabetes. These patients were divided into four groups according to sex and age (more or less than 12 years old) and into three subgroups according to metabolic control. In female adolescents with poor control, triglycerides and apolipoprotein B were increased whereas HDL-cholesterol, HDL-phospholipids and (HDL/LDL + VLDL)-cholesterol were significantly decreased. In poorly-controlled male adolescents, similar changes were observed except for HDL-cholesterol and HDL-phospholipids which were not significantly decreased. In adolescents, haemoglobin AIc correlated directly with triglycerides, total cholesterol, phospholipids, apolipoprotein B and inversely with HDL-cholesterol, HDL-phospholipids and (HDL/LDL + VLDL)-cholesterol. In children aged less than 12 years, no significant change of HDL-cholesterol or apolipoprotein B was observed even in the poorly-controlled group.
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PMID:[Effect of metabolic control on plasma lipids and lipoproteins in insulin-dependent diabetes in children and adolescents]. 392 11

A polymorphic DNA sequence of the apolipoprotein (apo) A-I gene region was studied in relation to non-insulin-dependent diabetes mellitus (NIDDM). We have examined 100 patients with NIDDM and 100 control subjects as well. The presence of a unique 2.5-kilobase (kb) EcoRI fragment was found in 13 diabetic patients and two control subjects with family history of diabetes. There were six homozygotes and nine heterozygotes among them. The analysis of clinical data did not confirm any linkage between the presence of a 2.5-kb fragment and atherosclerosis. These findings suggest that the observed defect in the apo A-I gene region may confer susceptibility to NIDDM.
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PMID:Apolipoprotein A-I gene polymorphism and susceptibility of non-insulin-dependent diabetes mellitus. 393 51


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