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)

Development of dementia depends on genetic susceptibility and on risk factors accessible to primary prevention. Among the latter, vascular risk factors are well defined: prevention of hyperhomocysteinemia, diabetes mellitus, hypercholesterolemia, and, to some extent, of arterial hypertension could avoid the cognitive decline of dementia. Estrogen replacement therapy, antiinflammatory drugs, alcohol, vitamin E and intellectual activities seem efficacious in term of primary prevention. When dementia is present, only vitamin E, selegiline and some antiinflammatory drugs have proved efficacy compared to placebo to slow the cognitive decline. Long-term effects of cholinesterase inhibitors need to be investigated in future trials.
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PMID:[Prevention of dementia: is it possible?]. 1286 24

To define the clinical significance of plasma thrombomodulin (TM) values in elderly, we examined plasma TM in healthy young subjects, healthy elderly subjects and patients with cerebral infarction sequelae. We also studied the relationship with effective renal plasma flow (ERPF) and with the liver's protein-production ability. The TM values of healthy elderly subjects were higher than those of healthy young subjects. There existed an inverse correlation between TM values and ERPF. Accordingly, high TM values might significantly influence renal arteriosclerosis. From the inverse correlation identified between TM and serum cholinesterase, it was estimated that high TM might appear in conjunction with the liver's protein production ability. Patients with cerebral infarction showed higher plasma TM values. It is thought that angiopathy has been maintained in patients as the anamnesis of cerebral infarction even though it occurred in the past. The TM values of patients with diabetes mellitus (DM) were higher than those without it. Moreover, the TM values of patients with DM complicated by retinopathy were higher than those uncomplicated by retinopathy. It is therefore estimated that increased TM might occur with angiopathy resulting from DM. A possibility thus exists that plasma TM could be utilized as one of the markers for endothelial injury.
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PMID:Plasma thrombomodulin values and hepatorenal function in the elderly. 1537 35

Significant progress in the field of VaD resulted from publication of the NINIDS-AIREN Diagnostic Criteria for VaD (G.C. Roman, T.K. Tatemichi, T. Erkinjuntti, et al., Vascular dementia (VaD): diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology 43 (1993) 250-260). Epidemiological studies confirmed the importance of VaD as the second most common cause of dementia in the elderly, representing 15-20% of all cases of dementia. In Europe and North America, Alzheimer's disease (AD) predominates over VaD in a 2:1 ratio; in contrast, in Japan and China VaD accounts for almost 50% of all dementias. Case-control studies have identified risk factors for VaD including ageing, hypertension, diabetes mellitus, hyperlipidemia, recurrent stroke, cardiac disease, smoking, sleep apnea, and more recently, hyperhomocysteinemia, among others. Hypertension treatment may prevent VaD and AD. This finding has enormous importance from the Public Health viewpoint to decrease the future number of patients with dementia in the elderly. Along with advances in the field of VaD came a number of controversies and damaging misconceptions and myths. Myth no. 1--Vascular dementia is a non-entity: The false idea that VaD does not exist is particularly destructive because it creates the perspective that VaD is unworthy of study or research. A condition that either does not exist or represents only a minute proportion of all cases of dementia in the elderly, lacks public health relevance and becomes a low priority for research by funding agencies and industry. In fact, vascular brain lesions are the commonest and most important component of dementia in the elderly. Myth no. 2--Vascular dementia is so difficult to diagnose that only experts can recognize and identify it accurately: VaD does exist and the diagnosis of post-stroke VaD, in particular is straightforward. Most cases fulfill NINDS-AIREN criteria for probable VaD; i.e., (1) there is acute onset of dementia demonstrated by impairment of memory and two other cognitive domains, such as orientation, praxis or executive dysfunction; (2) relevant cerebrovascular lesions are demonstrated by neuroimaging; and (3) a temporal relation between stroke and cognitive loss is evident. In the donepezil trials on VaD, post-stroke dementia represented about 75% of the >1,200 patients enrolled. Myth no. 3--Improvement in clinical trials of cholinergics in VaD is due to underlying AD, not to the vascular lesions. Experimental, clinical and pathological evidence has demonstrated cholinesterase deficits in VaD (independently of any concomitant AD pathology), including low acetylcholine in cerebrospinal fluid, and reduced choline acetyltransferase (ChAT) in the brain.
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PMID:Facts, myths, and controversies in vascular dementia. 1553 19

We reported that a leaf extract (GLEt) obtained from an anti-diabetic plant, Gymnema montanum, an endangered species endemic to India, has anti-peroxidative and antioxidant effects on diabetic brain tissue in rats. Here we examined the effect of the extract on the activity of reduced brain and retinal acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in streptozotocin (STZ)-induced diabetic male Wistar rats. Diabetic rats received GLEt orally (200 mg/kg bwt/d) for 12 wk, and changes in blood glucose, plasma insulin, the lipid peroxidation marker thiobarbituric acid-reactive substance (TBARS), and AChE and BChE activity were measured. The results confirmed prior reports that hyperglycemia significantly enhances TBARS levels in brain and retinal tissue and decreases AChE and BChE activity. Treatment with GLEt significantly reversed the impairment in enzymatic activity in addition to reducing the level of TBARS, suggesting that GLEt protects against the adverse effect of lipid peroxidation on brain and retinal cholinesterases. We suggest that GLEt could be useful for preventing the cholinergic neural and retinal complications of hyperglycemia in diabetes.
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PMID:Modulation of impaired cholinesterase activity in experimental diabetes: effect of Gymnema montanum leaf extract. 1618 84

Serum cholinesterase activity was measured in diabetes, hypertensive and diabetic/hypertensive patients. The sample consisted of volunteer patients and was divided in a control group (n=26), type 2 diabetic group (n=16), hypertensive group (n=12) and type 2 diabetic/hypertensive group (n=26). In addition, blood glucose, cholesterol and triglyceride levels were determined. Serum cholinesterase activity in the control group was significantly lower in relation to the other groups (p<0.001). Blood glucose levels were elevated in type 2 diabetic and type 2 diabetic/hypertensive groups. In vitro studies showed increased cholinesterase activity in the presence of glucose 5-100mM or insulin 0.5-25 UI (p<0.001). Cholesterol and triglycerides were at normal levels only in the control group. Possibly, a relationship exists between the increase in serum cholinesterase and the vascular complications in the diabetic patients, potentially stimulated by the levels of glycemia and dyslipidemia. Although patients were receiving different medicines, the increase in enzyme activity was similar in all groups. This enzymatic profile suggests a possible interference of the diseases in the catalytic mechanism of the serum cholinesterase enzyme.
Diabetes Res Clin Pract 2006 Apr
PMID:Serum cholinesterase activity in diabetes and associated pathologies. 1623 31

Controversial data exists concerning the impact of immunosuppressive therapy on the development of post-transplantation diabetes mellitus (PTDM). Therefore, we investigated glucose metabolism in healthy donors and in recipients of living-donor liver transplants (LD-LTX, n=18) without pre-existing diabetes mellitus before, on day 10, month 6, and month 12 after intervention. The computer-assisted analysis of glucose, insulin, and C-peptide profiles obtained from frequently sampled intravenous glucose tolerance tests allows to achieve an integrated view of factors controlling glucose tolerance, i.e., insulin sensitivity (SI), first and second phase insulin secretion (phi1 and phi2). SI of donors declined by day 10 after operation (SI 2.65 +/- 0.41 vs. 4.90 +/- 0.50 10(-4) minute(-1) microU ml(-1), P < 0.01) but returned to values as before after 6 months. Phi1 did not change. Phi(2), however, significantly increased by day 10 (8.57 +/- 0.82 10(9) minute(-1) to 13.77 +/- 1.53 10(9) minute(-1), P < 0.01) but was in the same range as before after 6 months. In parallel to donors SI of recipients progressively increased after LD-LTX. Phi1 did not alter in recipients. Phi2 continuously decreased and was not different from donors by month 12. The extent of liver injury assessed by liver enzyme concentrations and liver function represented by cholinesterase activity, albumin, and INR were closely related with changes of SI in donors and recipients during the first year after intervention. In conclusion, the extent of liver damage plays a predominant role in regulating glucose tolerance. No impact of immunosuppressive therapy on SI, phi1 and phi2 was detected.
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PMID:Major influence of liver function itself but not of immunosuppression determines glucose tolerance after living-donor liver transplantation. 1649 77

As people grow old, their need for medications increases dramatically because of the higher incidence of chronic pain, diabetes mellitus, cardiovascular and neurological diseases in the elderly population. Furthermore, the elderly require special consideration with respect to drug delivery, drug interactions and adherence. In particular, patients with chronic neurological diseases often require multiple administration of drugs during the day to maintain constant plasma medication levels, which in turn increases the likelihood of poor adherence. Consequently, several attempts have been made to develop pharmacological preparations that can achieve a constant rate of drug delivery. For example, transdermal lisuride and apomorphine have been shown to reduce motor fluctuations and duration of 'off' periods in advanced Parkinson's disease, while rotigotine allows significant down-titration of levodopa without severe adverse effects. Thus, parkinsonian patients with long-term levodopa syndrome or motor disorders during sleep could benefit from use of transdermal lisuride and apomorphine. Moreover, transdermal dopaminergic drugs, particularly rotigotine, seem the ideal treatment for patients experiencing restless legs syndrome or periodic limb movement disorder during sleep, disorders that are quite common in elderly people or in association with neurodegenerative diseases. Unlike dopaminergic drugs, transdermal treatments for the management of cognitive and behavioural dysfunction in patients with Parkinson's disease and Alzheimer's disease have inconsistent effects and no clearly established role. Nevertheless, because of their favourable pharmacological profile and bioavailability, the cholinesterase inhibitors tacrine and rivastigmine are expected to show at least the same benefits as oral formulations of these drugs, but with fewer severe adverse effects. Transdermal delivery systems play an important role in the management of neuropathic pain. The transdermal lidocaine (lignocaine) patch is recommended as first-line therapy for the treatment of postherpetic neuralgia. Furthermore, in patients with severe persistent pain, transdermal delivery systems using the opioids fentanyl and buprenorphine are able to achieve satisfactory analgesia with good tolerability, comparable to the benefits seen with oral formulations. Transdermal administration is the ideal therapeutic approach for chronic neurological disorders in elderly people because it provides sustained therapeutic plasma levels of drugs, is simple to use, and may reduce systemic adverse effects. Several transdermal delivery systems are currently under investigation for the treatment of Parkinson's disease, Alzheimer's disease and neuropathic pain. Although most transdermal delivery systems treatments cannot be considered as first-line therapy at present, some of them provide clear advantages compared with other routes of administration and may become the preferred treatment in selected patients. In general, however, most transdermal treatments still require long-term evaluation in large patient groups in order to optimise dosages and evaluate the actual incidence of local and systemic adverse effects.
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PMID:Transdermal treatment options for neurological disorders: impact on the elderly. 1682 90

Cerebrovascular disease (CVD) is an important cause of psychiatric disability in the elderly. Much of this disability can be attributed to dementia and lesser degrees of cognitive impairment, which result from strokes and other forms of cerebrovascular pathology. While vascular dementia is common, estimates of its frequency vary due to its clinical and pathologic heterogeneity, the challenges involved in its measurement and its frequent co-occurrence with Alzheimer's disease. Nevertheless the clinical features and natural histories of vascular dementia can be described, and risk factors have been identified and include hypertension, diabetes mellitus, hyperlipidaemia, other conditions that promote atherosclerosis, and rare genetic mutations. While vascular dementia is not curable, treatments are available. For example, a few recent clinical trials suggest that cholinesterase inhibitors have some efficacy. Our knowledge of the risk factors has also provided opportunities for the primary and secondary prevention of vascular dementia, and indicates promising avenues for research.
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PMID:Cerebrovascular disease and dementia. 1708 61

Alzheimer's disease and type 2 diabetes mellitus tend to occur together. We sought to identify protein(s) common to both conditions that could suggest a possible unifying pathogenic role. Using human neuronal butyrylcholinesterase (AAH08396.1) as the reference protein we used BLAST Tool for protein to protein comparison in humans. We found three groups of sequences among a series of 12, with an E-value between 0-12, common to both Alzheimer's disease and diabetes: butyrylcholinesterase precursor K allele (NP_000046.1), acetylcholinesterase isoform E4-E6 precursor (NP_000656.1), and apoptosis-related acetylcholinesterase (1B41|A). Butyrylcholinesterase and acetylcholinesterase related proteins were found common to both Alzheimer's disease and diabetes; they may play an etiological role via influencing insulin resistance and lipid metabolism.
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PMID:Alzheimer's disease and type 2 diabetes mellitus: the cholinesterase connection? 1709 57

As a strategy to prevent the progression of diabetes mellitus, it is important to screen out the subjects who will develop a pre-diabetic state (PDS) in the future. To find out the potential risk factors for PDS, we employed the values of fasting plasma glucose and hemoglobin A1c (HbA1c), which are routinely measured in our health checkup. We selected 3,879 individuals who had normal glucose regulation at both fasting plasma glucose < 6.1 mmol/l and HbA1c < 5.5% in 1997 and investigated whether they would develop PDS in the next 5 years. PDS is defined at fasting plasma glucose >or= 6.1 mmol/l and HbA1c >or= 5.5%. Among 3,879 individuals, 21 developed PDS and 2,128 maintained normal glucose regulation in 2001. The remaining 1,730 subjects fit one of the two criteria for PDS. The parameters measured in 1997, including fasting plasma glucose, HbA1c, triglyceride, alanine aminotransferase, gamma-glutamyltranspeptidas, cholinesterase, uric acid, red blood cells, hemoglobin, percent body fat and diastolic blood pressure, were significantly higher in the individuals who developed PDS than in those who maintained normal glucose regulation. On the other hand, hematocrit was significantly lower in PDS than in normal glucose regulation. Logistic regression analysis identified alanine aminotransferase >or= 40 U/l, triglyceride >or= 1.69 mmol/l, low-density lipoprotein cholesterol >or= 3.62 mmol/l and hematocrit < 38% as valuable factors for predicting the development of PDS. The present study demonstrates that the subjects with high risks for PDS could be identified from several clinical parameters and that they should be encouraged to improve their living habits not to develop diabetes mellitus.
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PMID:Risk factors for development of pre-diabetic state from normal glucose regulation. 1714 92


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