Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arteries are not simply conduits for the transport of blood, but consist of metabolically active tissue which has the capacity to synthesize all the components of the atherosclerotic lesion. The smooth muscle cell appears to be the most important metabolically active cell in the arterial wall. There is little information on arterial metabolism in human diabetes. Experimental diabetes depressed all aspects of arterial lipid metabolism and this effect is reversed by insulin. Insulin promotes changes in arterial metabolism which are similar to those an atherosclerosis. Thus the relationship of human diabetes to the metabolism of the arterial wall is complex and little understood.
Acta Diabetol Lat
PMID:The lipid metabolism of the arterial wall and its abnormalities in diabetes. 79 61

The inotropic action of tolbutamide previously demonstrated in vitro was evaluated in 15 nondiabetic subjects during diagnostic cardiac catheterization. Following bolus injection of 250 mg of tolbutamide intravenously, a rise of serum insulin and a slight fall of serum potassium were observed. Inotropic response was determined from significant fall in PEP/LVET ratio, significant fall of left ventricular end-diastolic pressure, shift to an augmented function curve in work-pressure relationships, and prominent rise of dP/dt values at comparable heart rates. The inotropic effect was greatest at 5-15 min with return to near control values at 30 min. An unusually marked inotropic response was observed in one subject. While the measurable net hemodynamic effect of tolbutamide in the human heart is small, its effect on ischemic and normal areas within the heart of a diabetic patient with atherosclerosis may be different. Thus, its ultimate effect on the diseased heart may be significant.
 ...
PMID:Inotropic action of tolbutamide on human myocardium. 122 7

The present study, concerning 145 insulin-dependent diabetics showed positive relationships between the severity of retinal disease on the one hand, and body weight, blood pressure, and serum cholesterol level on the other. These relationships remain significant when the duration of the clinical diabetes and the age of the patient are taken into account. Two interpretations are suggested. They are not incompatible. In diabetic subjects, either the increase in blood pressure and serum cholesterol level causes an aggravation of diabetic retinopathy or there exists a common factor at the origin of retinal lesions and of an increase in risk of cardiovascular disease through atherosclerosis.
Acta Diabetol Lat
PMID:Diabetic retinopathy, duration of diabetes and risk factors of atherosclerotic cardiovascular disease. 122 3

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.
 ...
PMID:Magnesium deficiency impairs rat soleus muscle glucose utilization and insulin sensitivity. 130 45

To elucidate the potential association of diabetic autonomic neuropathy with increased prevalence of silent coronary artery disease (CAD), 138 asymptomatic diabetic subjects were screened using exercise ECG. 24-h ambulatory ECG and dynamic thallium scintigraphy. Fourteen patients with exercise-induced myocardial ischaemia and angiographically confirmed CAD (greater than or equal to 50% coronary artery narrowing) were found using this protocol. Their autonomic nervous function was assessed using standard cardiovascular tests and compared with that of 23 consecutive diabetic patients catheterised because of symptomatic CAD (mean New York Heart Association class 3.0). The diabetic patients with symptomatic CAD had more severe coronary atherosclerosis than the diabetic patients with asymptomatic CAD assessed by jeopardy score (P less than 0.01). The groups did not, however, differ with respect to autonomic function tests. Five patients (22%) with symptomatic CAD and 3 patients (21%) with asymptomatic CAD had definite autonomic dysfunction, i.e. two or more abnormal tests. Thus, our results suggest that the frequency of autonomic neuropathy is not increased in diabetic patients with asymptomatic CAD. The contribution of diabetic autonomic neuropathy to the absence of cardiac pain needs further clinical and pathological studies.
Acta Diabetol 1992
PMID:Asymptomatic coronary artery disease in diabetes: associated with autonomic neuropathy? 157 55

The excess risk of atherosclerosis that is associated with diabetes mellitus cannot be completely accounted for by other known risk factors. Recent studies have suggested that increased glycation of high density lipoproteins (HDL) at high glucose concentrations causes functional abnormalities that might contribute to accelerated atherosclerosis. Other investigators also have shown that elevated glucose concentrations can stimulate the activity of protein kinase C in cultured cells. Because protein kinase C appears to be involved in HDL receptor-mediated efflux, the hypothesis that a high glucose concentration in vitro might modulate HDL-mediated efflux of cholesterol from human fibroblasts was tested. These studies indicate that a high glucose level alone does not affect the interaction of normal HDL3 with cultured human skin fibroblasts.
Acta Diabetol 1991
PMID:High glucose levels do not directly impair cellular binding of HDL3 or HDL-mediated efflux of cholesterol from human skin fibroblasts. 166 7

Plasma lipids, lipoproteins and apolipoproteins (apo) were analysed in 30 young Arab IDDM and 50 young insulin-requiring NIDDM women. The mean age of IDDM and NIDDM groups was 20.2 and 34.5 years, and mean duration of diabetes was 5.7 and 4.6 years, respectively. Two groups of 40 and 60 healthy women (matched for age and BMI) provided corresponding control groups. In comparison with control subjects, diabetics showed marked increases in the following parameters: total cholesterol (TC), low density lipoprotein (LDL) cholesterol, total triglycerides (TG), very low density lipoprotein (VLDL) triglycerides, phospholipids, apoB, LDL apoB, glucose and glycosylated hemoglobin (HbA1c) as well as the ratios of total cholesterol/high density lipoprotein (HDL) cholesterol, LDL-cholesterol/HDL-cholesterol, LDL cholesterol/high density lipoprotein (HDL) cholesterol, LDL-cholesterol/HDL-cholesterol, LDL cholesterol/high density lipoprotein 2 (HDL2) cholesterol and apoB/apoAI. Plasma LCAT activity, concentrations of HDL3 apoAI and apoAII in plasma and lipoprotein fractions were normal in both the diabetic groups. Levels of C-peptide, HDL, HDL2 and HDL3 cholesterol, plasma apoAI, HDL apoAI and HDL2 apoAI were markedly decreased in the diabetic groups as compared to their corresponding controls. There was no significant correlation between fasting glucose or HbA1c and any of the above parameters. Despite insulin therapy in both the diabetic groups studied, abnormalities in lipids, apoB and apoAI still persisted. Our data suggest a possible higher risk of atherosclerosis in these patients.
Acta Diabetol Lat
PMID:Plasma lipoproteins and apolipoproteins in insulin-dependent and young non-insulin-dependent Arab women. 186 93

The effects of first generation sulphonylurea compounds carbutamide, gliclazide and tolbutamide as well as second generation compounds glibenclamide and glipizide on the cardiovascular system were investigated in dogs. Six dogs received each compound intravenously at cumulative dose levels of 74, 296, 1184 mumol/kg of carbutamide and tolbutamide, 0.4, 2.0, 10.0 mumol/kg of glibenclamide and glipizide, and 16, 48 and 144 mumol/kg of gliclazide. Mean arterial blood pressure, myocardial contractile force, cardiac output and heart rate were measured. The rate of change of myocardial contractile force development (positive dF/dt), as well as of myocardial relaxation (negative dF/dt) were measured. The first generation sulphonylureas were found, in dogs, to exert a positive inotropic effect in contrast to second generation compounds. The clinical importance of our findings may be in the potential for the malfunction of the cardiovascular system (based on cardiopathy, neuropathy, atherosclerosis, and obesity), developing in diabetes, to be further impaired by the first generation sulphonylureas. Therefore, second generation sulphonylureas should be preferred in the therapy of type 2 diabetics, if satisfactory metabolic control cannot be achieved by dietary management alone and sulphonylurea treatment becomes necessary.
 ...
PMID:Direct effect of hypoglycemic sulphonylureas on the cardiovascular system of dogs. 201 35

In a group of 19 patients selected at random, suffering from hypertension and signs of atherosclerosis of the coronary vessels glucose intolerance was revealed in 10 patients. Comparisons disclosed: a) Levels of immunoreactive insulin (IRI) rose more and declined more slowly in patients with glucose intolerance than in patients with glucose tolerance. b) The ratio IRI/glucose in plasma of patients with glucose intolerance increased less than in patients with satisfactory tolerance. c) 500 mg tolbutamide by the oral route reduced the blood sugar level during the first and second hour following administration of 75 mg glucose substantially more in patients with glucose intolerance. d) Tolbutamide reduced at the same time intervals also the rise of IRI levels, approximately equally in both groups of patients. e) Tolbutamide increased the IRI/glucose ratio during the investigated intervals. The authors conclude that a direct influence on glucose utilization in peripheral tissues is involved and an increased insulin sensitivity of skeletal muscles and other tissues after tolbutamide.
 ...
PMID:[Improvement in glucose tolerance and insulin sensitivity after a single administration of tolbutamide in hypertensive patients]. 203 14

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
Acta Diabetol Lat
PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90


1 2 3 4 5 6 7 8 9 10 Next >>