Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case-control study of diet and bladder cancer was conducted during 1979-1982 in Edmonton, Calgary, Toronto, and Kingston, Canada. A total of 826 histologically verified cancer cases were individually matched by age, sex, and area of residence to 792 randomly selected population controls. Subjects were interviewed concerning their histories of exposure to a number of dietary factors, including table-top artificial sweeteners, low calorie foods and drinks, beverages containing caffeine or ethanol, and certain other food items. Also, subjects provided information on their past medical, occupational, and residential histories, in addition to their exposures to tobacco and other life-style factors. For the analysis, conditional logistic regression methods were used. Under adjustment for cumulative lifetime amount of cigarette smoking, the dietary factors, with little exception, were not associated with significant alteration of risk for bladder cancer. In particular, ever regular use of artificial sweeteners did not appear to be associated with increased risk, either among men (odds ratio = 0.95, p = 0.70) or among women (odds ratio = 1.15, p = 0.53). However, daily intake of cholesterol, calculated from reported frequencies of consumption of nine relevant food items, suggested a mild increase in risk; the odds ratio estimate of trend was 1.07/100 mg average daily intake (i.e., 1.07(5.5) = 1.45 for 550 mg cholesterol per day, as might be consumed in one egg; p = 0.009). A history of diabetes mellitus of onset after age 20 years also seemed to be associated with increased risk of bladder cancer (odds ratio = 1.65, p = 0.019), but this increase did not appear to be the result of use of insulin or other medications, or use of artificial sweeteners or low calorie foods. Thus, this study tends to confirm reports of a lack of association between use of artificial sweeteners and subsequent risk of bladder cancer.
 ...
PMID:Dietary factors and the incidence of cancer of the urinary bladder. 336 17

Many Authors agree about a relationship between higher estroprogestinic levels and periodontal inflammation. This study tries to define the relationship between oral contraceptives (OC) and specific gingival signs, like bleeding and plaque. 51 women (15 to 19 years) were studied while using OC, and 36 of the same age group were studied as controls. Only women who had no past medical history of hormone imbalance, diabetes mellitus or dentures were selected. The patients were examined at the beginning of the study and were assigned scores related to the amount of plaque, inflammation and pockets (Loe and Silness gingival index). Use of alcoholic beverages, medications, tobacco, and caffeine were also noted. The only significant difference between the control group and the women taking OC was cigarette smoking: 52.9% versus 41.6% respectively. The average time of treatment was 11.5+5 months. No changes were observed in the buccal and lingual mucosa in both populations. The plaque indexes were very close. The bleeding was significantly higher in the group using OC; same for the gingival index. Pockets deeper than 2 mm were present in 33.3% of the treated women, versus 13.8% of the controls. The results point out a significant direct relationship between OC and gingival inflammation after several months of use. It possible that by prolonging the length of the study the gingival lesions would become even more significant.
 ...
PMID:[Drugs with contraceptive actions and periodontal status. Epidemiological survey]. 347 42

The metabolic actions of caffeine were investigated in the rat (90 mg/kg bw caffeine intravenously during 3 hours) and in human volunteers (35 mg/kg bw caffeine orally) in the fasting state. Additionally, the effects of caffeine were measured during simultaneous intravenous glucose infusion (0.25 mg/kg bw/h during 6 hours in humans and 1.8 mg/kg bw/h during 3 hours in the rat). In the fasting rat, intravenous caffeine caused an increase in the serum concentrations of glucose, urea, insulin, and free fatty acids, whereas a decrease in glucoplastic amino acids was found. As the liver glycogen concentration was not altered, the increase in blood glucose should be due to an increase in glyconeogenesis. During simultaneous application of carbohydrates and caffeine, the increases in the concentration of blood glucose and serum insulin were intensified, whereas the serum concentrations of lactate and urea as well as hepatic glycogen were not altered. In fasting male volunteers caffeine caused an increase in the concentrations of blood glucose, cortisol, insulin, free fatty acids, free glycerol and ketone bodies. During intravenous glucose infusion, caffeine intensified the decrease in serum phosphate induced by carbohydrates. Neither in volunteers nor in the experimental animal, an alteration in the concentrations of cholesterol or serum triglycerides or serum uric acid was effected by caffeine. It is concluded that high dosed caffeine causes peripheral insulin resistance in the human being as well as in the experimental animal. This peripheral insulin resistance is shown by the simultaneous large increases in concentrations of serum insulin, blood glucose and concentration of free fatty acids. In this situation insulin obviously is not able to inhibit lipolysis or gluconeogenesis nor to increase peripheral glucose utilisation. These metabolic effects of caffeine show some similarities to the metabolic situation in diabetes mellitus type 2 (Non Insulin Dependent Diabetes mellitus).
 ...
PMID:[Effect of caffeine on various metabolic parameters in vivo]. 639 Sep 95

Analgesic nephropathy has long been considered a potentially preventable cause of renal disease. Early reports were described in patients who consumed analgesics containing phenacetin. In recent data, the removal of phenacetin from analgesic preparations resulted in a reduction in analgesic-induced end stage renal disease in Europe and Australia. However, a reduction in the incidence of analgesic nephropathy has not occurred uniformly, suggesting that phenacetin is not the sole cause. Current data raise concerns regarding adverse renal effects of acetaminophen and nonsteroidal antiinflammatory drugs. Aspirin taken alone may be of least concern. The diagnosis of analgesic nephropathy is suggested in subjects with chronic renal failure, a history of daily consumption of analgesic preparations, small bumpy kidneys, and renal papillary necrosis or chronic interstitial nephritis. However, the spectrum of disease may be changing, because these agents also may increase the risk of cardiovascular disease and chronic renal disease due to nephrosclerosis, glomerulonephritis, and diabetes mellitus. Potential pathogenetic mechanisms in analgesic nephropathy include direct cellular injury induced by analgesics, prostaglandin inhibition with reduction or redistribution of renal blood flow, and interesting new concepts regarding the role of caffeine in increasing oxygen demand and reducing oxygen supply in the medulla. The primary goal of therapy is discontinuation of analgesic consumption. Because of the association between analgesic intake and uroepithelial tumors, surveillance of patients for neoplasm is suggested.
 ...
PMID:Case report: analgesic nephropathy: a soda and a powder. 757 21

Oral glucose tolerance was tested in a heterogeneous group of 108 patients with liver cirrhosis. Data were compared with those from 181 subjects without liver disease (44% normal, 35% impaired glucose tolerance and 21% type 2 diabetes mellitus). In cirrhosis, 27% of the patients had normal, 36% had impaired glucose tolerance, and 37% were diabetic. There was no association between glucose intolerance or diabetes and the aetiology of cirrhosis, the duration of the disease, the biochemical indicators of hepatocyte damage, cholestasis and/or liver function. Only weak associations were found between the results of quantitative liver functions tests (caffeine, xylocaine, indocyanine green) and basal and post load glucose and insulin concentrations. Cirrhotics with 1st degree relatives with type 2 diabetes mellitus (n = 16) did not show an increased prevalence of diabetes. Older and/or malnourished patients were more frequently glucose intolerant. Using the plasma glucose concentration 120 minutes after glucose load as the dependent variable, multivariate regression analysis showed that 54% of its variance is associated with the following variables: basal plasma glucose (36%) and free fatty acid concentration (5%), age (3%), basal glucose oxidation rate (3%), muscle mass (3%) and plasma free glycerol at 120 minutes after glucose load (3%). By contrast, the clinical state of the patients (i.e. the CHILD-Pugh score) accounted for only 2% of the variance. We conclude that glucose tolerance is variable in cirrhosis. After manifestation of liver disease, glucose intolerance or diabetes cannot be explained by the clinical, histological or biochemical signs of liver disease.
 ...
PMID:Glucose intolerance in liver cirrhosis: role of hepatic and non-hepatic influences. 786 13

The relationship between consumption of decaffeinated coffee and acute myocardial infarction was analyzed in a case-control study conducted in Italy between 1983 and 1992. Case patients were 433 women with acute myocardial infarction, aged 24 to 69 years (median age, 52 years), and control subjects included 869 women in hospital for a wide spectrum of acute conditions, other than cardiovascular, neoplastic, digestive, and hormone-related diseases or conditions associated with long-term modification of diet. Regular use of decaffeinated coffee was reported by 11% of the case patients and 7% of the control subjects. Compared with women who did not drink decaffeinated coffee, the relative risk (RR) was 1.3 (95% confidence interval (CI), 0.8 to 2.2) for one cup/d and 2.1 (95% CI, 1.1 to 3.9) for 2 or more cups (chi 2(1) for trend = 5.62, P = 0.02). The estimates were somewhat higher after allowance for education, marital status, body mass index, and smoking status (RR for > or = 2 cups of decaffeinated coffee per day, 2.5; 95% CI, 1.2 to 4.9), and somewhat lower after further allowance for diabetes, hypertension, and hyperlipidemia (RR, 1.7; 95% CI, 0.8 to 3.6). There was no association between duration of use of decaffeinated coffee and infarction risk. The relationship between decaffeinated coffee and infarction was consistent across strata of age, education, smoking, and history of hyperlipidemia. Thus, a relationship of marginal significance was observed in this study between decaffeinated coffee and myocardial infarction, of similar magnitude to that described for caffeinated coffee. This indicates that (i) caffeine is unlikely to be a relevant factor in any potential coffee-myocardial infarction relationship, and (ii) shifting from caffeinated to decaffeinated coffee is unjustified in order to reduce any possible coffee-related infarction risk.
 ...
PMID:Decaffeinated coffee and acute myocardial infarction. A case-control study in Italian women. 792 7

A preliminary case-control study was conducted on Saudi women to detect possible risk factors for spontaneous abortion (SA). Two hundred and twenty six consecutive women hospitalised for SA and 226 women admitted for normal delivery and used as controls, were studied. Women with SA were significantly older at menarche (Relative Risk (RR) = 3.2), more frequently married to blood-related husbands (RR = 2.1) and husbands older than 50 years (RR = 2.4). Number of previous abortions related linearly to the risk of aborting spontaneously in the next pregnancy. Compared to primigravidas, the RR was 3.2 if the outcome of the most recent pregnancy was SA, and 0.8 if it was a livebirth. A family history of SA was more common among cases (RR = 4.6). Spontaneous abortion was also associated with daily consumption of more than 150 mg of caffeine, abdominal trauma, infection and fever during pregnancy. No significant association, however, emerged with maternal age, social class, education, exposure to video display terminals, parity, use of contraception, diabetes or obesity. The application of these data in clinical practice and future research needs are discussed.
 ...
PMID:Risk factors for spontaneous abortion: a preliminary study on Saudi women. 793 96

The phasic contractions induced by noradrenaline and caffeine were compared in aortic rings from rats with 8-12 week streptozotocin-induced diabetes and age-matched control rats. In Ca(2+)-free medium, no difference was found in the magnitude of the contractile responses to 10 microM noradrenaline between control and diabetic aortas. The transient contraction induced by 20 mM caffeine was significantly diminished in diabetic aorta compared aorta. The results suggest that the ability of caffeine, but not of inositol 1,4,5-trisphosphate, to mobilize Ca2+ from intracellular stores is impaired in diabetic rat aorta.
 ...
PMID:Attenuated contractile response of diabetic rat aorta to caffeine but not to noradrenaline in Ca(2+)-free medium. 805 Apr 73

To study the mechanisms of cardiac dysfunction in experimental diabetes, adult rat cardiomyocyte shortening (measured with a video edge-detector system), the sarcoplasmic reticulum (SR) Ca2+ content [assessed by rapid-cooling contracture (RCC) and caffeine contracture (CC)] was examined. Ryanodine binding to the SR Ca(2+)-release channel of myocardium homogenate was also studied. Myocytes from diabetic rats showed depressed shortening (44% decrease compared with controls), reduced maximum rates of shortening and relengthening (58 and 56% decrease, respectively), and prolonged time to peak shortening (47% increase). RCCs and CCs from diabetic cells were 68 and 75% of the control values, respectively. Most of these cardiomyocyte abnormalities were corrected by daily insulin treatment in the diabetic rats. Ryanodine binding parameters indicated that the number of high-affinity binding sites was decreased in diabetic hearts. These data suggest that changes in contractile parameters as measured in diabetic myocytes are in good agreement with data obtained from intact heart or cardiac tissue preparations. Decreased SR Ca2+ content and reduced ryanodine binding sites indicate that the SR functions of storage and release of Ca2+ were depressed. This consequently may cause depressed contraction in diabetic hearts.
 ...
PMID:Cellular functions of diabetic cardiomyocytes: contractility, rapid-cooling contracture, and ryanodine binding. 820 6

The effect of insulin to attenuate the Ca2+ and contractile response of vascular smooth muscle to a number of agonists has been described previously, but the Ca2+ regulatory mechanisms of insulin action remain unclear. We determined the effect of a physiological insulin concentration (300 pmol/l) on the Ca2+ response of vascular smooth muscle cells of the porcine right coronary artery to endothelin 1 (ET-1); furthermore, we examined the cellular Ca2+ stores affected by insulin (i.e., Ca2+ stores releasable by inositol 1,4,5-trisphosphate, caffeine, and ionomycin). We measured the Ca2+ responses of acutely isolated single smooth muscle cells with the fluorescent Ca2+ indicator Fura-2. Acute insulin exposure (20 min) significantly attenuated the Ca2+ response of single smooth muscle cells to 10 nmol/l ET-1. This inhibitory effect of insulin was observed both in the presence and absence of extracellular Ca2+. In contrast with the effects on ET-1-induced Ca2+ responses, insulin did not inhibit the Ca2+ response to 5 mmol/l caffeine, an agent that directly releases sarcoplasmic reticulum Ca2+ stores. Insulin was also without effect on the total cellular Ca2+ store released by 1 micromol/l ionomycin, a Ca2+-transporting ionophore. When ET-1 and caffeine were given in succession, a sizable caffeine-sensitive Ca2+ store could be released from insulin-treated cells but not control cells, indicating that the sarcoplasmic reticulum Ca2+ store of insulin-treated cells was not depleted by ET-1. Generalized depletion of the sarcoplasmic reticulum Ca2+ store is not one of the cellular mechanisms involved in the effect of insulin on coronary smooth muscle; instead, the effect may be due to an inhibitory influence on transmembrane signal transduction, such as diminished ET-1-induced inositol 1,4,5-trisphosphate production or reduced ability of this phosphoinositol to release stored Ca2+.
Diabetes 1996 Jul
PMID:Effects of a physiological insulin concentration on the endothelin-sensitive Ca2+ store in porcine coronary artery smooth muscle. 866 36


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