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)

A cross-sectional study was designed to evaluate the periodontal status of 85 12-18 year-old French adolescents with insulin-dependent diabetes (IDDM) and 38 healthy controls in the same age group. The clinical examination consisted of plaque control and gingival inflammation evaluation and probing attachment level. The interproximal marginal bone level was assessed with bitewing radiographs taken on the first molars and on areas presenting an attachment loss over 2 mm. Diabetic children had significantly more gingival inflammation than children without diabetes, in spite of similar plaque scores. No significant relation between gingival condition and age, Tanner's index, HbAlc level or disease duration could be demonstrated. None of the subjects had sites with attachment loss > or = 3 mm or radiographic signs of periodontitis.
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PMID:Periodontal status in insulin-dependent diabetic adolescents. 143 Feb 90

Recent studies concerning secular trends in stroke incidence and mortality and identification of independent risk factors for stroke are reviewed. Stroke mortality has declined in many industrialized countries in recent decades. In France, it has been declining by more than 30% between 1968 and 1982 in all age groups and in both sexes except for women under 40 years. The decline in stroke mortality seems to be partly real and partly apparent. In the community-based study of Rochester, Minnesota, stroke incidence decreased by 54% between 1945-49 and 1975-79. Recent data from Rochester, however, suggest that the incidence of stroke may no longer be declining. Survival after stroke has also apparently been improving but several sources of potential bias may also have influenced the decrease in reported survival rates. Hypertension is a major risk factor for stroke. Prolonged differences in "usual" diastolic blood pressure of 5 to 10 mmHg are associated with about 40% difference in stroke incidence. Recent analysis suggests that stroke incidence reduction could arise rapidly after hypertension control and that a lower blood pressure should confer a lower risk of vascular disease, even in individuals conventionally considered as "normotensive". There is evidence that cigarette smoking is an important risk factor for stroke with an overall relative risk of 1.5 and that the risk of stroke declines rapidly after the cessation of smoking. A cardiac condition may be a marker for another risk factor or the primary substrate for cerebral embolism. In patients with atrial fibrillation, the risk of stroke is increased through both of these mechanisms. Diabetes mellitus, chronic alcohol consumption (> 3 drinks/day), and high fibrinogen levels are other independent risk factors for stroke. While high levels of cholesterol may be associated with ischemic stroke, an inverse association of the serum cholesterol with the occurrence of intracerebral hemorrhage in men has been reported. In patients with asymptomatic internal carotid stenosis, higher degrees of stenosis convey a higher risk of stroke. However, far from all these strokes are due to thromboembolism from an atheromatous plaque in the ipsilateral internal carotid artery. The relative risk of stroke during the first 5 years following a transient ischemic attack is 7 times that in persons without transient ischemic attack. More than a third of the subsequent strokes occur in a vascular territory different from that of the incident TIA. While the use of oral contraceptives may increase the relative risk of stroke, postmenopausal estrogen treatment may have a protective effect on the risk of vascular diseases.
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PMID:[Epidemiology of cerebrovascular accidents]. 143 51

1. A polyclonal, monospecific antibody to a constitutive, diabetes-inducible and insulin-reversible cytochrome P-450 isozyme (RLM6) was used to screen a male rat liver cDNA library in lambda gt 11. Six clones harbouring the RLM6 cDNA insert were isolated initially from the expression library and three of these were further plaque-purified and sub-cloned. A 1.1 Kb cDNA insert, representing approximately 65% of the expected full length cDNA was characterized by restriction endonuclease mapping and sequenced by the dideoxy chain-termination method. Comparison of the nucleotide sequence of RLM6 cDNA to that of ethanol-inducible P4502E1 rat cDNA showed the two cDNAs to be identical, the RLM6 cDNA corresponding to nucleotides 310-1402 of the P4502E1 sequence. 2. RLM6 cDNA probe was used in Northern blot and RNA dot blot hybridization analysis to demonstrate that both streptozotocin-induced diabetes and fasting significantly elevated the steady-state level of RLM6 mRNA in male rat liver. Increased RLM6 mRNA level in the diabetic rat resulted in increased RLM6 apoprotein synthesis when polysomal RNA was used in a cell-free, protein-synthesizing system, indicating that the elevated RLM6 level observed in diabetic rats was correlated directly with the increased RLM6 mRNA concentration. 3. Daily insulin treatment of diabetic rats reversed the diabetes-dependent increase in RLM6 mRNA in a time-dependent manner, returning to control values after approximately 2 weeks of continuous insulin treatment. This insulin-dependent decrease of the RLM6 mRNA level was paralleled by a similar time-dependent decrease in serum acetone concentration. 4. Treatment of the male diabetic rat with testosterone also resulted in a decrease in both RLM6 mRNA and in vitro translated apoprotein. 5. Modulation of RLM6 mRNA level in the diabetic rat by insulin and testosterone, and the nucleotide sequence similarity with that of P4502E1 confirms that diabetes-inducible P450RLM6 and ethanol-inducible P4502E1 are coded for by the same gene.
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PMID:Molecular cloning of a cDNA for rat diabetes-inducible cytochrome P450RLM6: hormonal regulation and similarity to the cytochrome P4502E1 gene. 144 86

Diabetes is accompanied by impaired platelet function and accelerated vascular disease. To find out whether a correlation exists between these two complications, and if modifications occurring in diabetic platelets influence their relationship with endothelium, we have studied the interaction between platelets isolated from plasma of diabetic patients and bovine valvular endothelial cells (VEC), in culture. For quantitative analysis, normal and diabetic [3H]-adenine-labeled platelets were incubated with confluent VEC grown in Dulbecco's modified Eagle medium, containing 4.5 g/l glucose, for 30 min at 37 degrees C. After extensive washing and solubilization of the monolayer, the calculated adhesion index showed a two-fold increased adherence of diabetic platelets to VEC as compared to normal platelets. Statistical analysis (by Pitman randomization test) indicated that the adhesion was significantly higher (p = 0.0003) than that of normal platelets to VEC. To partially identify the membrane components implicated in the adhesion process, either platelets or VEC were treated with neuraminidase, trypsin or heparinase prior to the adhesion assay. Trypsin or neuraminidase treatment of platelets significantly diminished their adherence to VEC, suggesting a role of platelets sialylated glycoproteins in the adhesion process. Neuraminidase or heparinase treatment of VEC increased the adhesion of both normal and diabetic platelets, indicating that the cell membrane sialyl residues and heparan sulfate participate in the normal thromboresistant properties of VEC. Transmission and scanning electron microscopy revealed a close apposition between platelets and VEC with the formation of an adhesion plaque, characterized by fine fibrillar bridges between the plasma membranes of the two cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased adhesion of human diabetic platelets to cultured valvular endothelial cells. 145 40

Cigarette smoking is the most preventable cause of cardiovascular morbidity and mortality. Smoking has been associated with a two-to fourfold increased risk of coronary heart disease, a greater than 70% excess rate of death from coronary heart disease, and an elevated risk of sudden death. These risks are compounded in the presence of hypertension, hypercholesterolemia, glucose intolerance, and diabetes, all of which exhibit a synergistic effect with smoking. The relationship between smoking and the risk of peripheral vascular disease has also been well documented. Smokers account for approximately 70% of patients with atherosclerosis obliterans and virtually all those with thromboangiitis obliterans. An association between smoking and cerebrovascular disease remains a matter of debate, although a higher risk of stoke and stroke-related mortality has been observed in smokers than in nonsmokers. Smoking has also been implicated in the development of cor pulmonale, but a direct association with congestive heart failure has not been established. Nicotine and carbon monoxide appear to play major roles in the cardiovascular effects of smoking. Both components adversely alter the myocardial oxygen supply/demand ratio and have been shown to produce endothelial injury, leading to the development of atherosclerotic plaque. Adverse effects on the lipid profile have been noted as well, but the relationship between these changes and the risk of cardiovascular disease remains to be confirmed. Notably, smoking cessation results in a dramatic reduction in the risk of mortality from both coronary heart disease and stroke. In light of the fact that the incidence of smoking has declined primarily among educated sectors of the U.S. population, future efforts must focus on providing effective education, including smoking cessation techniques, to the less-educated groups.
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PMID:Smoking and cardiovascular disease. 149 5

Conflicting reports exist in dental literature on the relationship of diabetes mellitus to periodontal disease. Among the controversies about this relation, the role played by the age of patient has been widely investigated. Some authors, in fact, reported an increased prevalence and severity of gingivitis and periodontitis in children and young individuals with insulin dependent diabetes mellitus (IDDM) in comparison to healthy subjects, while other researchers were not able to confirm this finding. In particular some authors postulated the hypothesis that the diabetic state could influence periodontal conditions just after the age of 30-35. The aim of the present study has been to verify this hypothesis. One hundred thirty-two subjects participated in this study; among them 66 were IDDM patients and 66 were healthy controls comparable to the diabetics for the main epidemiological features. In particular, control subjects were similar to the diabetics for oral hygiene level in order not to attribute eventually occurring differences by mistake to the diabetic state instead of to a not comparable amount of bacterial plaque present on the teeth. Among 66 IDDM patients 33 were younger than 30 (medium age = 14; extremes: 6-22) and were indicated as DG (young diabetics) group; others 33 were older than 30 (medium age = 45.1; extremes: 31-66) and were indicated as DA (adult diabetics) group. A similar differentiation was made in the control group obtaining, in this way, two subgroups (CG = young controls and CA = adult controls). In the diabetic groups males were 53% while among controls they represented 58%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The influence of the "age factor" on periodontal conditions in the diabetic patient]. 150 26

Although there have been significant advances in the care of many of the extrapancreatic manifestations of diabetes, acute myocardial infarction continues to be a major cause of morbidity and mortality in diabetic patients. Factors unique to diabetes increase atherosclerotic plaque formation and thrombosis, thereby contributing to myocardial infarction. Autonomic neuropathy may predispose to infarction and result in atypical presenting symptoms in the diabetic patient, making diagnosis difficult and delaying treatment. The clinical course of myocardial infarction is frequently complicated and carries a higher mortality rate in the diabetic than in the nondiabetic patient. Although the course and pathophysiology of myocardial infarction differ to some degree in diabetic patients from those in patients without diabetes, much more remains to be known to formulate more effective treatment strategies in this high risk subgroup.
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PMID:Acute myocardial infarction in the diabetic patient: pathophysiology, clinical course and prognosis. 151 57

Acute myocardial infarction is the result of sudden coronary occlusion in the absence of a collateral circulation. There main factors are required for this to occur: an acute parietal lesion on a stenosis of variable, sometimes minor, importance; local coronary vasoconstriction and a platelet and fibrin thrombus. Parietal fissuration is the commonest "trigger" of coronary spasm and the thrombotic cascade. All factors of coronary occlusion are potentially reversible--vasodilation--platelet anti-aggregation--physiological fibrinolysis--remodeling and cicatrisation of the plaque, thereby explaining cases of spontaneous regression of occlusion (10% at 1 hour; 20% at 6 hours; 30% at 24 hours; 50 to 70% at 1 year). The pathogenesis of myocardial infarction with angiographically normal coronary arteries may be reviewed and attributed to acute parietal fissuration at a non-significant or angiographically undetectable plaque resulting in occlusive thrombosis. In this case, the role of other pathogenic factors is also discussed (diabetes, oral contraception, haemostatic abnormalities, platelet disorders...).
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PMID:[Acute myocardial infarction: recent physiopathological data. 1: acute coronary occlusion]. 153 Apr 7

Under certain circumstances the effect of insulin to promote glucose uptake in peripheral tissues is reduced because of a resistance to insulin action. This insulin resistance and the resulting hyperinsulinaemia are now recognised as common background factors that may be responsible for hypertension, hyperlipidaemia, decreased thrombolysis and also impaired glucose tolerance and diabetes. Hyperinsulinaemia has also been identified as an independent risk factor for coronary heart disease and promotes smooth muscle cell growth and plaque formation. A series of studies have now demonstrated that treatment with selective beta-blockers as well as thiazide diuretics impair insulin sensitivity by 15-30% and causes a compensatory increase in insulin concentrations. Furthermore, lipoprotein concentrations are affected in an unfavourable way. This is in contrast to the drugs belonging to ACE-inhibitors, calcium-channel blockers and alpha 1-blocker classes that are either neutral or may have the opposite effects in these respects.
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PMID:Insulin resistance and cardiovascular drugs. 154 Oct 35

A single administration of complete Freund's adjuvant (CFA), type 1 carrageenan (Car), or silica 7, 2, and 2 days, respectively, before infection with a low dose (1 x 10(2) plaque-forming units/mouse) of encephalomyocarditis D (EMC-D) virus resulted in a significant increase in the incidence of diabetes in SJL/J mice (100%) compared with untreated EMC-D virus-infected mice (40%). Peritoneal macrophages were isolated from uninfected SJL/J mice, which had been treated once with silica, and transferred into SJL/J mice 2 days before low-dose EMC-D infection. Approximately 90% of the mice became diabetic, whereas 30% of mice that received virus alone became diabetic. The depletion of macrophages by treatment with the combined anti-Mac-1 and anti-Mac-2 monoclonal antibodies after a single administration of CFA, Car, or silica resulted in almost complete prevention of beta-cell destruction in EMC-D virus-infected mice. Furthermore, none of the mice in which macrophages were depleted by long-term treatment with silica and 10% of the mice treated with Car before virus infection became diabetic. On the basis of these observations, we conclude that macrophages are directly involved in the destruction of beta-cells, leading to the development of clinical diabetes in EMC-D virus-infected mice.
Diabetes 1991 Dec
PMID:Direct involvement of macrophages in destruction of beta-cells leading to development of diabetes in virus-infected mice. 166 90


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