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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that histamine receptors mediate increased blood-retinal barrier permeability in experimental diabetes, 51 rats were made diabetic by streptozocin injection (65 mg/kg; jugular vein) and were held for four weeks. The seven animal groups were as follows: untreated controls; untreated diabetic rats; diabetic rats receiving diphenhydramine hydrochloride (Benadryl); diabetic rats receiving cimetidine hydrochloride (Tagamet); diabetic rats receiving diphenhydramine and cimetidine; diabetic rats receiving purified pork insulin (Iletin II); and diabetic rats receiving insulin and diphenhydramine. All treatments were given during the last week. Blood-retinal barrier permeability was assessed through measurement of the vitreous content of fluorescein isothiocyanate conjugated to bovine serum albumin (FITCBSA) after 20 minutes of FITCBSA circulation. Vitreous FITCBSA content of the diabetic group was 64% greater than control content. Diabetic rats treated with either diphenhydramine or diphenhydramine and insulin had respective decreases of 43% and 40% in vitreous FITCBSA content. The vitreous content of the diabetic group receiving insulin was lowered 37% below untreated diabetic values, while the vitreous FITCBSA content of the diabetic group receiving both insulin and diphenhydramine was reduced 63%. These data indicate that retinal histamine H1-receptor activation may be partially responsible for initial blood-retinal barrier leakage of macromolecules into the vitreous and that this abnormal leakage can be prevented both by diphenhydramine and by insulin. Histamine H1 receptors may play an important role in mediating increased blood-retinal barrier permeability in experimental diabetes.
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PMID:Histamine H1 receptors mediate increased blood-retinal barrier permeability in experimental diabetes. 252 87

In a prospective randomized trial, 36 women received cimetidine and 32 magnesium trisilicate mixture BP as antacid therapy every 2 h in labour. The women belonged to a high-risk category and the infants born were less than 36 weeks gestation, or less than 2000 g birthweight or otherwise in jeopardy because of severe maternal pre-eclampsia or diabetes. Measurements of a wide range of haematological and biochemical variables revealed no differences between the two groups of babies. The frequency of complications found in the infants was similar, although infants born to the women who received magnesium trisilicate required oxygen therapy for a longer period. Cimetidine did not appear to affect the development of gastric acidity, or to increase bacterial colonization of the gastrointestinal tract in the infant.
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PMID:Cimetidine in labour: absence of adverse effect on the high-risk fetus. 388 4

There are only 6 published reports of pancreatitis associated with oral contraception (OC). This article presents 1 additional case. A 28 year old white woman was hospitalized for severe abdominal pains; gastroenteritis was diagnosed and the patient treated with Compazine and Maalox. Because of the increasing severity of pains the patient was rehospitalized and pancreatitis secondary to hyperlipoproteinemia was diagnosed. OC treatment was suspended, and the patient was successfully treated with Cimetidine, antacids, and insulin for elevated glucose. Pancreatitis caused by OC is probably due to alterations in lipid metabolism, and related to the estrogen content of the preparation used. A major study done recently with 2 types of synthetic estrogens combined with 3 types of progestogens confirmed that hypertriglyceridemia induced by OC was estrogen dosage-related. It seems apparent that OC use in patients with intrinsic lipid abnormalities may be contraindicated; other risk patients are those who are obese, diabetic, or with family antecedents of diabetes or hyperlipidemia.
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PMID:Birth control pills and pancreatitis. 707 Jan 28

Neutrophil-endothelial adhesion is a crucial step in vascular inflammation and is recognized as a direct cause of serious atherosclerosis-mediated diseases. We previously demonstrated that high concentrations of glucose increased adhesion in a protein kinase C (PKC)-dependent manner within 48 h of administration by increasing the surface expression of endothelial adhesion molecules. In this study, we focused on the effects of histamine 2 receptor antagonists on endothelial-neutrophil adhesion and on the surface expression of endothelial adhesion molecules mediated by high glucose levels. Histamine 2 receptor antagonists have pleiotropic effects; they not only block the secretion of gastric acid, but also inhibit cell-cell adhesion, resulting in inhibition of metastasis. However, relevant mechanisms of action are not yet fully understood. Of three histamine 2 receptor antagonists (cimetidine, ranitidine, and famotidine), only cimetidine significantly attenuated adhesion mediated by 48-h incubation with 27.8 mM glucose. Cimetidine was found to decrease the surface expression of endothelial adhesion molecules intercellular adhesion molecule-1 and P-selectin, but not E-selectin. To determine the effects of cimetidine on intracellular level, we examined the effects of cimetidine on PKC-induced changes in adhesion, as well as the effects of nitric oxide (NO) synthase inhibitors on cimetidine. We found that NO synthase inhibitors reduced the inhibitory effects of cimetidine, whereas cimetidine did not affect adhesion mediated by a PKC activator. These data suggest that cimetidine acts directly on endothelial cells to inhibit high-glucose-induced expression of adhesion molecules and neutrophil adhesion mediated by increasing endothelial NO production, but not by inhibiting PKC.
J Diabetes Complications
PMID:Effects of histamine 2 receptor antagonists on endothelial-neutrophil adhesion and surface expression of endothelial adhesion molecules induced by high glucose levels. 1718 74