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)

Cataract is the major cause of blindness worldwide and at present the only approved treatment in many countries including the UK and USA is surgical removal of the lens. In other countries various anti-cataract drugs are available without proof of their efficacy. Research is continuing into the possible benefits of several groups of drugs and some vitamins. The first to be studied were sorbitol-lowering agents (aldose reductase inhibitors) based on the sorbitol hypothesis for diabetic cataract. Sorbitol-lowering agents have distinct effects in vitro and many of them delay the development of cataract in galactose-fed rats. A few delay cataract in diabetic rats but none have been proved effective in clinical trials, although these continue. Aspirin, paracetamol (acetaminophen) and ibuprofen delay diabetic cataract in rats, and have been shown to delay other experimental cataracts. Case-control studies from 3 continents indicate that these drugs, or at least aspirin, protect against cataract. Results of studies on all 3 drugs indicate a benefit even at low doses. Population-based studies did not identify any protection against early lens opacities but tiny opacities that do not impair vision are not a problem. Bendazac protects lens proteins in vitro and delays cataractogenesis in x-irradiated rats. In humans, it reached the clinical trial stage but most trials have been small and with subjective criteria of opacification. One objectively monitored trial suffered from a high drop-out rate. Other preparations studied less extensively include vitamins, aminoguanidine to prevent protein cross-linking in diabetes and agents designed to boost glutathione levels. It is probable that some agents which may delay or prevent cataract will be proved effective soon, and in the end there may be different drugs to delay cataract in different high risk groups. This is what might be expected of a multifactorial disease, although compounds that intervene in the final common pathways to cataract could have a broad efficacy.
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PMID:Pharmacological treatment strategies in age-related cataracts. 150 43

Enhanced non-enzymic glycation of proteins has been suggested to play a role in the pathogenesis of diabetic microangiopathy. Thus pharmacological inhibition of this reaction could be envisaged to delay the development of late diabetic complications. In the present study we have investigated the effect of a new compound, 1-Benzylindazole-3-oxyacetic acid, Bendazac (BDZ) on the in vitro glycation of soluble proteins (albumin and fibrinogen) and isolated glomerular basement membrane (GBM). The data obtained indicate that BDZ is capable of reducing significantly the glycation of albumin and fibrinogen (p less than 0.001). When present in concentrations usually found in patients undergoing therapy (40-80 micrograms/ml), an inhibitory effect on soluble proteins was also observed. Inhibition of glycation of GBM was found only in the presence of the active metabolite (5 hydroxy BDZ) and at high glucose concentrations. These results suggest that BDZ could interfere with protein non-enzymic glycation and its use in patients with diabetes may be then taken into consideration to evaluate the effect on late diabetic complications.
Diabetes Res 1988 Sep
PMID:Inhibition of protein non-enzymic glycation induced by Bendazac. 324 Jun 33

The possible beneficial effects on the lens and retina which Bendazac Lysine may have in the treatment of adult diabetic patients were investigated. Twenty patients, ranging in age from 54.80 +/- 5.86 years old, were studied. The average duration of the diabetes was 11.32 +/- 4.10 years. Thirteen patients had background retinopathy. The metabolic controls carried out during the study were satisfactory (HbA1 < 11%). Bendazac Lysine (500 mg three times a day) was administered for 6 months. Blood-retinal barrier permeability (VPR and VPRt) and lens transmittance (t) were evaluated prior to and 6 months after treatment by fluorophotometry. No statistically significant differences between the pre- and post-treatment values of the retina permeability were observed, however, there was a statistically significant improvement (p < 0.05) (initial value: t = 0.813 +/- 0.040 and final value: t = 0.823 +/- 0.037) in the lens transmittance. The authors conclude that Bendazac Lysine has a beneficial effect on the lens in the diabetic adult although no improvement in the permeability of the blood-retinal barrier has been observed.
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PMID:Effect of bendazac lysine on lens and retina in diabetics. 783 76

1. Diabetic neuropathy is a many faceted complication of both type I and II diabetes. The aim of the present study was to investigate the effects of bendazac lysine (BDL), an anticataract drug, on experimental diabetic peripheral neuropathy (DPN) in rats. 2. Diabetes was induced in rats by intraperitoneal injection of 75 mg/kg streptozotocin (STZ) dissolved in 0.1 mol/L citrate buffer (pH 4.4). Bendazac lysine was administered to rats at doses of 50, 100 and 200 mg/kg twice a day for 12 weeks. 3. Diabetic rats without treatment showed hypopraxia, polydipsia, polyuria, slow weight gain, cataract, increased tail-flick threshold temperature, decreased motor nerve conduction velocity (nd induced pathological morphological changes of myelinated nerve fibres. All these symptoms were ameliorated in diabetic rats treated with BDL. Bendazac lysine ameliorated the blood glucose concentration, glycosylated haemoglobin levels and insulin levels in the plasma of diabetic rats, reduced aldose reductase activity in erythrocytes and advanced glycation end-products in both nerves and serum and increase the activity of glutathione peroxidase in the nerves and Na(+)/K(+)-ATPase in the nerves and erythrocytes. 4. Bendazac lysine exerts its protective effects against the progression of diabetic peripheral neuropathy in STZ-diabetic rats through multiple mechanisms and is a potential drug for the prevention of deterioration in DPN.
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PMID:Protective effects of bendazac lysine on diabetic peripheral neuropathy in streptozotocin-induced diabetic rats. 1718 6