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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The insulin response to an oral glucose load (100 gm.) in 127 patients with a previous myocardial infarction (MI) (six months to one year) and in 65 patients with surgically treated or arteriographically identified peripheral vascular disease (PVD) was compared with that of 89 controls after matching the three collectives for age, glucose tolerance, and per cent ideal body weight (% IBW). The insulin response was of greater magnitude in MI and PVD groups than in respective control groups also in the absence of hyperglycemia, hypertriglyceridemia, and obesity. This finding suggests that hyperinsulinism may represent an early metabolic alteration associated with the development of MI and PVD. The insulin secretion pattern was prevalently of the delayed type in association with impaired glucose tolerance and with hypertriglyceridemia but not with overweight. Correlations between serum insulin, triglyceride (TG) levels, and % IBW were also investigated. We found a strong correlation (p less than 0.001) between stimulated insulin levels and % IBW in MI patients and none in PVD patients; conversely, the correlation between serum insulin and TG levels was very high (p less than 0.001) in PVD patients and only weak (p less than 0.05) in MI patients. No correlation was found between cholesterol (CH) levels and any of the other parameters studied. According to these results, it seems likely that hyperinsulinism plays a major role as a closely associated factor to obesity in those subjects who develop an MI, whereas in PVD patients the raised insulin levels may favor lipid accumulation in the arterial intima and accelerate the progress of atherosclerosis.
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PMID:Insulin response to oral glucose in patients with a previous myocardial infarction and in patients with peripheral vascular disease. Hyperinsulinism and its relationships to hypertriglyceridemia and overweight. 127 7

Long term complications continue to be the major source of morbidity and mortality in patients with diabetes. Acarbose could potentially help to reduce diabetic complications if it improved glucose control, reduced lipid levels and hyperinsulinaemia. Acarbose has been shown to effectively reduce postprandial hyperglycaemia and haemoglobin A1c. This effect might be helpful in patients with insulin-dependent diabetes mellitus, as insulin injections do not provide complete control of rises in postprandial glucose levels, and in patients with non-insulin-dependent diabetes mellitus, because it simplifies the treatment programme. If improved control is shown to reduce complications, acarbose may be helpful. Although acarbose does not reduce hyperinsulinaemia, it reduces lipid levels and thus could reduce the risk of atherosclerosis.
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PMID:Preventing long term complications. Implications for combination therapy with acarbose. 128 May 78

Insulin resistance is a frequent phenomenon and a marker of increased risk for non-insulin-dependent diabetes mellitus (NIDDM) and atherosclerosis. According to recent estimations, not only individuals with obesity, NIDDM, and impaired glucose tolerance (IGT) but also one fourth of the "healthy" glucose tolerant and the majority of the hypertensive population are insulin resistant. Insulin resistance describes a tissue- and pathway-specific defect of glucose metabolism that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. The initial defect can be directly measured by glucose clamp and other sophisticated techniques; the clinical syndrome may be derived from a network of related variables known to be associated with reduced insulin action. Because neither clamps nor serum insulin screenings will be available on a widespread basis, early diagnosis based on clinical criteria is crucial. A new interpretation of the "thrifty" genotype hypothesis may explain why insulin resistance, which formerly apparently represented an advantage in the evolutionary selection process, is such a frequent phenomenon. Improvement of impaired insulin action as a therapeutic principle may play a future central role in an integrated lifestyle approach of primary prevention of noncommunicable diseases such as NIDDM, hypertension, and atherosclerosis.
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PMID:What is the clinical significance of insulin resistance? 128 40

The monosaccharide content was examined in apoprotein B and lipids of total low density lipoprotein (LDL) preparations isolated from the blood of healthy individuals and patients with coronary atherosclerosis, as well as in desialylated and sialylated LDL obtained by affinity chromatography on Ricinus Communis Agglutinin-agarose. The glycoconjugates of total apoprotein-B of healthy subjects' LDL were found to consist of N-acetylglycosamine, galactose, mannose and sialic acid in a molar ratio of 2:1:2.5:1. The content of protein-bound neutral sugars was the same in healthy subjects and patients, while there was a lower sialic acid amount in the patients. The level of protein-bound sialic acid in patients' desialylated LDL was 2- to 3-fold lower than that in sialylated LDL. In contrast to apoprotein-B glycoconjugated, the lipid-bound carbohydrate chains of total LDL preparations had N-acetylgalactosamine and glucose, but not mannose. In total LDL from patients, the content of all lipid-bound carbohydrates was 1.5- to 4-fold lower than that in LDL from healthy subjects. In healthy subjects and in patients alike, the neutral sugar content of a lipid subfraction of desialylated LDL was lower than in those of sialylated LDL. It is concluded that atherogenic desialylated LDL differ from non-atherogenic sialylated LDL in neutral sugar levels.
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PMID:[Carbohydrate composition of native and desialylated low density lipoproteins in the plasma of patients with coronary atherosclerosis]. 128 15

Insulin resistance (IR), probably a common pathway of atherosclerosis development in various diseases, was suggested to be related to magnesium (Mg) deficiency. The in vivo observations required an in vitro extension. The study was performed on isolated rat soleus muscle incubated in Ringer bicarbonate with/without Mg. Mg deficiency inhibited basal, insulin- and tolbutamide-stimulated glucose utilization. Insulin-stimulated glucose utilization was inhibited even in the case that insulin was given to rats before sacrifice. Similar inhibition of glucose utilization was found in Ca deficiency and the simultaneous lack of Mg had no additive effect. It is concluded that Mg deficiency inhibits glucose utilization at the level of Ca mediation of glucose transport regulation.
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PMID:Magnesium deficiency impairs rat soleus muscle glucose utilization and insulin sensitivity. 130 45

Atherosclerosis is probably caused by multiple interacting factors such as disturbed lipid metabolism; endothelial cell damage, leading to platelet aggregation and monocyte invasion with the release of mitogenic factors; and disorders of fibrin balance, leading to persisting fibrin deposits. Deficient fibrinolysis may (1) predispose to fibrin deposition and contribute to the pathogenesis of atherosclerosis and (2) contribute to occlusive thrombus formation on fissured plaque, provoking atherothrombosis. Prospective epidemiologic studies have so far not provided definitive evidence that deficient fibrinolysis constitutes a significant risk factor for the development of atherosclerosis. Two recent findings, however, strongly suggest a contribution: (1) Increased lipoprotein(a) levels that reduce tissue-type plasminogen activator (t-PA)-mediated clot lysis are a clear risk factor for atherosclerosis; and (2) increased plasminogen activator inhibitor-1 (PAI-1) levels in patients with disturbed glucose tolerance predispose to an accelerated development of atherosclerotic disease. However, deficient fibrinolysis constitutes a risk factor for the development of thrombotic complications (acute myocardial infarction) in patients with coronary artery disease. The potential role of deficient fibrinolysis in the pathogenesis of atherosclerosis and of atherothrombosis suggests that drugs normalizing deficient endogenous fibrinolysis by either reducing PAI-1 synthesis or by stimulating endogenous t-PA synthesis may be of clinical value. Although regulation of the gene expression of PAI-1 and t-PA is presently under active investigation, no potent specific and safe agents to downregulate PAI-1 or to upregulate t-PA have as yet been identified. Retinoic acid appears to be a specific inducer of t-PA synthesis in human endothelial cells in culture and may constitute a model for the development of drugs that stimulate endogenous t-PA synthesis.
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PMID:On the role of coagulation and fibrinolysis in atherosclerosis. 134 93

There were examined 222 men and 253 women over 18 years of age, selected at random from among country people living in the area of the nascent Coal Basin of Lublin district. There was determined their height and body weight, degree of overweight, general fat content in the body, arterial systolic and diastolic blood pressure as well as blood serum cholesterol concentration, concentration of triglicerides, glucose and uric acid in the blood. It was found out that the level of studied vascular atherosclerosis risk factors in the population under study was lower than the level found by the Polish Experiment in other populations.
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PMID:Atherosclerosis risk factors in the inhabitants of the nascent Coal Basin of Lublin region. 134 29

Untreated hypertension in age groups below 60 years has been shown to be associated with significant elevations in serum cholesterol and triglyceride levels. Drug therapy of hypertension has also been shown to have adverse effects on lipoproteins. We have investigated lipid and lipoprotein levels in a community-based sample of men and women 60 years and older belonging to one of the following groupings: (a) normal blood pressure (n = 1075); (b) untreated hypertension (n = 329); (c) drug-treated hypertension (n = 880). Serum lipid, lipoprotein, apolipoprotein or plasma glucose levels did not vary significantly between untreated hypertensives and normotensives of either sex. In a multiple regression model controlling for possible influences of age, overweight, alcohol and tobacco usage, and presence of coronary heart disease, anti-hypertensive drug therapy significantly predicted increased serum triglycerides (P less than 0.001) and reduced high density lipoprotein (HDL) cholesterol levels (P less than 0.01) in both sexes, reduced apolipoprotein A-I levels in males (P less than 0.001), and increased apolipoprotein B (P less than 0.01) and plasma glucose levels (P less than 0.001) in females. Adjusted triglycerides were 20% higher and HDL cholesterol was 7% lower in the presence of anti-hypertensive drug therapy. These effects were partially consistent with the known actions of thiazide diuretics and beta-blockers which were used by more than 50% and 40% of subjects, respectively.
Atherosclerosis 1992 Jan
PMID:Dubbo Study of the elderly: hypertension and lipid levels. 134 82

Advanced glycosylation end products (AGEs) form spontaneously from glucose-derived Amadori products and accumulate on long-lived tissue proteins. AGEs have been implicated in the pathogenesis of several of the complications of aging and diabetes, including atherosclerosis and renal disease. With the use of recently developed AGE-specific antibodies, an AGE-modified form of human hemoglobin has been identified. Termed hemoglobin-AGE (Hb-AGE), this modified species accounts for 0.42 percent of circulating hemoglobin in normal individuals but increases to 0.75 percent in patients with diabetes-induced hyperglycemia. In a group of diabetic patients treated with the advanced glycosylation inhibitor aminoguanidine, Hb-AGE levels decreased significantly over a 1-month period. Hemoglobin-AGE measurements may provide an index of long-term tissue modification by AGEs and prove useful in assessing the contribution of advanced glycosylation to a variety of diabetic and age-related complications.
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PMID:Hemoglobin-AGE: a circulating marker of advanced glycosylation. 141 74

Recent epidemiological studies have shown some beneficial health effects of the long chain (n-3) polyunsaturated fatty acids found in fatty fish. Although the results of these studies are often ambiguous and inconclusive, they have prompted many intervention trials to study the effects of n-3 fatty acids (FA) on the cardiovascular risk profile. However screening of the literature revealed that many of the beneficial effects of fish (oil) were obtained in intervention studies which had several serious shortcomings in their design. Therefore we started a placebo controlled randomised trial with increasing doses of n-3FA (respectively 0; 1.12; 2.24 and 3.37 g n-3 FA/day) and in order to have a maximum compliance this study was done in healthy monks. Fifty eight subjects took the fish oil capsules during 12 months and were thereafter followed for another 6 months. We couldn't detect any effect of n-3 FA supplementation on total cholesterol, HDL cholesterol, LDL cholesterol, apo A1, Lp(a), HbA1C, glucose, fibrinogen, factor VIII, antithrombin III, plasminogen activator inhibitor, tissue plasminogen activator and von Willebrand factor concentration, on bleeding time or on systolic or diastolic blood pressure. A pronounced significant dose dependent decrease of triglyceride levels was seen, while a slight but statistical significant decrease of apo B levels was observed in the highest fish oil dose. As the importance of triglycerides in the pathogenesis of atherosclerosis is still under discussion, the clinical relevance of these finding is not clear at the moment. It seems therefore improbable that the anti-atherosclerotic action of n-3 FA is due to an effect on the lipid, apoprotein, coagulation or fibrinolysis parameters as measured in our study. Hence further research must be focused on other parameters (prostaglandins) which can be influenced by n-3 FA and which probably play an equally important role in the atherosclerotic process.
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PMID:Influence of supplementation with N-3 fatty acids on different coronary risk factors in men--a placebo controlled study. 141 84


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