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)

Hypertension, dyslipidemia, and glucose intolerance cocluster in the population and act synergistically in increasing coronary artery disease risk. The mechanisms by which these risk factors interact in atherosclerosis are complex. First, hypertension, dyslipidemia, and altered insulin sensitivity may have a common pathophysiological basis. Activation of neurohormonal mechanisms may be implicated in many or all of these processes. In addition, underlying these processes may be common genetic and environmental influences. Second, these risk factors ultimately act on the blood vessel, thereby leading to atherosclerosis. Elevated serum lipids lead to vessel wall responses, including endothelial dysfunction, smooth muscle cell proliferation, lipid accumulation, foam cell formation, and, eventually, necrosis and plaque development. Hypertension may induce shear-related injury to the vessel. Endothelial injury (caused by hypertension) and vascular cell proliferation (induced by increased pressure and/or vasoactive substances) are effects that amplify the atherosclerotic process. In addition, diabetes and hyperinsulinemia can increase vascular tone, impair endothelial function, and stimulate vascular smooth muscle cell proliferation. Control of these risk factors should prevent or attenuate the vessel wall responses. Emphasis is now being placed on pharmacological therapeutic modalities that decrease blood pressure and improve insulin sensitivity and lipid metabolism. Identification of common links between risk factors, such as neurohormonal mechanisms (e.g., angiotensin), should lead to better therapeutic strategies.
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PMID:Atherosclerosis and hypertension: mechanisms and interrelationships. 169 33

To assess whether different electrophysiological characteristics could account for the heterogeneous secretion of individual beta-cells in vitro, we used patch-clamp configurations to study currents in plaque-forming (insulin-secreting) and non-plaque-forming rat pancreatic beta-cells that were distinguished in a reverse hemolytic plaque assay (RHPA) after a 30-min stimulation by 16.7 mM glucose. RHPA showed that the population of single beta-cells under study was stimulated (P less than 0.01-0.001) to secrete insulin by 16.7 mM glucose, 100 microM tolbutamide, 20 microM glyburide, or 30 mM KCl but, under these conditions, also comprised beta-cells that did not secrete detectable amounts of insulin. Under current clamp conditions, secreting and nonsecreting beta-cells showed analogous resting membrane potentials (approximately 60 mV) and were similarly depolarized by 30 mm KCl and 100 microM tolbutamide. Under voltage-clamp conditions, total membrane conductance (approximately 6 nS) was also similar in the glucose-responsive and -unresponsive beta-cells, which, when monitored in the whole-cell configuration after RHPA, showed the following currents: a voltage-dependent Na+ current, a voltage-activated Ba2+ current, a voltage-dependent K+ delayed-rectifier current, a voltage-dependent Ca(2+)-activated K+ current, and a voltage-independent and tolbutamide-sensitive K+ current. In the cell-attached configuration and the presence of 2.8 mM glucose, secreting and nonsecreting beta-cells displayed a similar single-channel activity that was abolished when glucose concentration was raised to 16.7 mM. We conclude that beta-cells studied after RHPA have an electrically normal membrane whether they release insulin in response to 16.7 mM glucose or not.
Diabetes 1991 Aug
PMID:Ion channels of glucose-responsive and -unresponsive beta-cells. 171 62

In the present investigation, the frequency and severity of periodontal disease was assessed in a group of 71 patients with a mean duration of 16.5 years of insulin-dependent diabetes mellitus (IDD). The diabetics, aged 17-63 years, were under treatment at the diabetic outpatient clinic of the III Department of Medicine, University Central Hospital of Helsinki and at two clinics of the Helsinki Health Centre. Based upon their long-term medical records, 44 individuals were assessed to have a poorly controlled insulin-dependent diabetes mellitus (PIDD). At baseline of the present study, the PIDD group had a mean blood glucose level of 11.8 mmol/l and a mean glycosylated hemoglobin (HBA1) level of 10.7%. 27 subjects were classified as having a controlled insulin-dependent diabetes mellitus (CIDD). For each individual, site-specific recordings were made for the plaque index, gingival index, pocket depth, loss of attachment, bleeding after probing, gingival recession and radiographic loss of alveolar bone. Under similar plaque conditions, adult subjects with a long-term PIDD were found to have lost more approximal attachment and bone than subjects with a CIDD (P = 0.046, P = 0.019). These differences were not equally obvious when the subjects were classified according to the history of medical complications, such as retinopathies, neuropathies and nephropathies.
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PMID:Periodontal conditions in insulin-dependent diabetes mellitus. 173 6

Macroangiopathy (or atherosclerosis) is a common and chronic complication in diabetic patients. Unlike other diabetic complications, atherosclerosis is not unique to diabetes, confounding analysis of its relationship with the diabetic condition. Evidence of an independent role for diabetes in the development of atherosclerosis remains equivocal. The main determinant of macrovascular disease may be an interaction between diabetes and the aging process. Similarly the question of a relationship between macrovascular disease and good metabolic control remains unanswered. Macroangiopathy in diabetic populations seems to be related to similar predictors and pathological mechanisms operating in the general population. However, after analysis of these common risk factors for macroangiopathy, a diabetes-specific risk remains. Low-density lipoprotein metabolism is markedly disturbed in poorly controlled diabetic patients. This is manifest as a concert of actions which increase formation of foam cells and fatty streaks. The next step in the atherosclerotic process, the formation of fibrous plaques, may be associated with the platelet hyperactivity seen in diabetes. This may promote overshooting of repair mechanisms at the vessel wall. Release of a specific diabetic serum growth factor from the platelets may be responsible for the later stages of fibrous plaque development and the increased atherosclerotic risk in diabetes.
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PMID:Diabetes and arterial disease. 182 66

Results show that diabetes, which is a major risk factor for arterio-atherosclerosis, mimicks an accelerated aging, at least as far as the thickening of basement membranes and fibronectin and collagen biosynthesis are concerned. A similar sequence of events could be demonstrated in human atherosclerotic plaque formation. In conclusion, we could demonstrate a disregulation of extracellular matrix components biosynthesis (type-III collagen and fibronectin) in diabetes and atherosclerosis.
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PMID:Modifications of the biosynthesis of type-I and type-III collagens and fibronectin during diabetes and atherosclerosis. 187 89

Dislodgement of atheromatous plaque from the ascending aorta following manipulation is one of the principal causes of stroke following cardiac surgery. To define clinical correlates that predict the presence of severe atherosclerosis, we performed ultrasonographic evaluation of the ascending aorta at the time of cardiac surgery in 100 consecutive patients. The ascending aorta was divided into three equal segments for analysis, and the severity of atherosclerosis was determined as mild when intimal thickening (less than 3 mm) was localized to one segment, moderate when intimal thickening (greater than 3 mm) was present in one or two segments, and severe when intimal thickening (greater than 3 mm) was present throughout the entire circumference in all three segments. Thirty-eight percent of the studies were normal, mild atherosclerosis was present in 33%, moderate atherosclerosis in 19%, and severe atherosclerosis in 10% of the patients. Palpation of the ascending aorta to detect atherosclerosis significantly underestimated the presence (p less than 0.001) and severity (p less than 0.001) of atherosclerosis when compared with ultrasonography. Age, carotid artery disease, diabetes, gender, smoking, and hypertension were evaluated for their ability to discriminate between normal and severely atherosclerotic aortas. Stepwise logistic regression analysis showed age (p less than 0.02) and diabetes (p less than 0.04) to be significant independent predictors of the presence of severe atherosclerosis in the ascending aorta. Based on the ultrasonographic findings, the operative procedure was altered to reduce the risk of embolization in 17% of the patients. We conclude that high-resolution images of the ascending aorta for identification of atherosclerosis can be obtained by ultrasonography.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intraoperative ultrasonographic evaluation of the ascending aorta in 100 consecutive patients undergoing cardiac surgery. 193 41

Using serum from a prediabetic patient as a probe, we screened 0.5 x 10(6) recombinants from a rat islet lambda gt11 expression library. One plaque-producing antigen reactive with this prediabetic serum was identified, subcloned, and sequenced. Analysis of the sequence reveals that the clone encodes a 136-amino acid fragment of carboxypeptidase-H (enkephalin convertase). Carboxypeptidase-H is a molecule expressed within islet secretory granules and neurendocrine cells. The patient whose antibodies recognize this recombinant molecule (termed DG-1) was negative for anti-DG-1 antibodies in 1984, developed the antibodies by 1986, and remained positive until the development of diabetes in 1988. To date, serum from 5 of 20 cytoplasmic islet cell antibody-positive relatives reacted with the expressed protein, while none of 14 control sera reacted. On Western blotting, the initial patient's serum used for the screening reacts with a 52-kDa antigen corresponding to the mol wt of the membrane form of carboxypeptidase-N. The current study has identified carboxypeptidase-H as an autoantigen recognized by serum of pretype I diabetes, and the methodology used should aid in identification of additional autoantigens associated with type I diabetes.
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PMID:Identification and cloning of a granule autoantigen (carboxypeptidase-H) associated with type I diabetes. 195 1

The periodontal condition of patients with insulin-dependent diabetes mellitus was evaluated in terms of plaque, gingival indices, pocket depth, and alveolar bone loss. Thirty male and female diabetic patients aged 5 to 18 years were compared with 30 non-diabetic subjects and correlated with sex and age. Statistical analyses of the data showed that the mean plaque index was significantly higher (P less than 0.01) among the diabetic patients (1.23) than among the control subjects (0.81). The plaque index was significantly higher (P less than 0.01) among diabetic females (1.34) than among diabetic males (1.10), whereas no sex differences were observed in the control group. The arithmetic means obtained for gingival index were statistically higher (P less than 0.01) for the diabetics (0.58) when compared with the controls (0.15), but no significant differences were obtained when the values were correlated with sex and age. Pocket depth did not differ statistically between groups. When pocket depth was correlated with sex, a statistically significant difference (P less than 0.05) was observed only for the palatal region, with a depth of 2.1 mm in female patients and 1.92 mm in male patients. When pocket depth was correlated with age, a positive correlation (P less than 0.01) was detected in the diabetic group for all regions investigated, whereas the correlation was not significant in the control group. Mean alveolar bone loss was higher in the anterior upper (1.94 mm) and anterior lower (1.87 mm) regions of the diabetic group when compared to the controls (1.52 and 1.37 mm respectively), the difference being significant at the 5% level of probability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Manifestations of insulin-dependent diabetes mellitus in the periodontium of young Brazilian patients. 202 65

Mode of death, frequency of a healed or an acute myocardial infarct, or both, number of major epicardial coronary arteries severely narrowed by atherosclerotic plaque, and heart weight were studied at necropsy in 889 patients 30 years of age or older with fatal atherosclerotic coronary artery disease. No patient had had a coronary bypass operation or coronary angioplasty. The 889 patients were classified into four major groups and each major group was classified into two subgroups: 1) acute myocardial infarct without (306 patients) or with (119 patients) a healed myocardial infarct; 2) sudden out of hospital death without (121 patients) or with (118 patients) a healed myocardial infarct; 3) chronic congestive heart failure with a healed myocardial infarct without (137 patients) or with (33 patients) a left ventricular aneurysm; and 4) sudden in-hospital death without (20 patients) or with (35 patients) unstable angina pectoris. The mean age of the 687 men (77%) was 60 +/- 11 years, and of the 202 women (23%), 68 +/- 13 years (p = 0.0001). Although men included 77% of all patients, they made up approximately 90% of the out of hospital (nonangina) sudden death group. The frequency of systemic hypertension and angina pectoris was similar in each of the four major groups. The frequency of diabetes mellitus was least in the sudden out of hospital death group and similar in the other three major groups. The mean heart weight and the percent of patients with a heart of increased weight were highest in the chronic congestive heart failure group; values were lower and similar in the other three major groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mode of death, frequency of healed and acute myocardial infarction, number of major epicardial coronary arteries severely narrowed by atherosclerotic plaque, and heart weight in fatal atherosclerotic coronary artery disease: analysis of 889 patients studied at necropsy. 213 74

The three forms of origin of the atherosclerotic plaque of adults, that is, the fatty streaks, gelatinous elevations, and microthrombi, all occur in arteries of normal infants and children. Some of these may become arrested or regress, but many progress to the prominent lesions that precipitate various clinical catastrophies. The aim of modern medicine is to modify or eliminate many of the factors known to advance the atherosclerotic process and thus decrease the incidence of this disease, which ranks highest on the list of causes of morbidity and mortality in the Western world. Of these factors, some may be controlled by dietary means (low salt; low total fat and cholesterol; appropriate ratios of saturated to mono- and polyunsaturated fatty acids; high content of complex carbohydrates and fiber); controlling hypertension, diabetes, and obesity; abstaining from cigarette smoking; and vigorous physical activities. Because patterns of life-style are determined in childhood and adolescence, and because it is only during that period of life that measures to prevent progression of atherosclerosis may be predictably effective, it becomes increasingly apparent that atherosclerosis is, indeed, a pediatric problem.
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PMID:The genesis of atherosclerosis in pediatric age-group. 217 19


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