Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the basis of vascular involvement, an open clinical trial was performed to determine whether or not the antithrombotic drug cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl) butoxy]-3,4-dihydro-2(1H)-quinolinone, OPC-13013, Pletaal, CAS 73963-72-1) applied as a single 100 mg tablet increases peripheral blood flow and prevents diabetic neuropathy in 30 patients with non-insulin dependent diabetes mellitus. The hemodynamic effects of this drug on the a. dorsalis pedis were examined using a new real-time two-dimensional Doppler echography. 1 h after oral administration of cilostazol, the cross-sectional area of the a. dorsalis pedis significantly increased from 2.2 +/- 0.2 to 2.9 +/- 0.3 mm2 (p less than 0.05). Also, the a. dorsalis pedis blood flow index significantly increased from 16 +/- 1 to 31 +/- 4 (p less than 0.05). Cilostazol did not affect plasma glucose level (from 213 +/- 14 to 198 +/- 15 mg/dl), but slightly plasma ratio of 6-keto PGF1a to TXB2 (from 0.71 +/- 0.09 to 0.83 +/- 0.12). These effects of cilostazol might ameliorate diabetic neuropathy by improving blood flow and preventing nerve tissue ischemia.
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PMID:Hemodynamic effects of cilostazol on peripheral artery in patients with diabetic neuropathy. 164 79

We report the results of a study of serum antibodies to proteins of the nerve cytoskeleton in patients with Type I and Type II diabetes mellitus, both with and without clinical signs of diabetic neuropathy. In contrast to previous reports, elevated levels of antibody to tubulin or glycated tubulin were not associated with either diabetes or diabetes with related neuropathy. Similarly, clinical evidence of neuropathy in patients with diabetes did not relate to increased levels of antibody to native or glycated microtubule-associated proteins (MAPs). The levels of antibody to MAPs and glycated MAPs were higher in control subjects over the age of 45 years compared with younger control subjects. Increased levels of antibody to tubulin and glycated tubulin were found in the sera of patients with systemic lupus erythematosus, but not rheumatoid arthritis.
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PMID:Antibodies to tubulin and microtubule-associated proteins. A study in diabetes mellitus, systemic lupus erythematosus, and rheumatoid arthritis. 177 91

We studied whether lifetime cigarette smoking is associated with the presence of diabetic neuropathy. The research design consisted of a case-control study conducted from a referral-based diabetes clinic at a major medical center. The patients were a 65% sample (163 insulin-dependent diabetes mellitus [IDDM] and 166 non-insulin-dependent diabetes mellitus [NIDDM] patients) of all patients admitted during a 26-mo period. Neuropathy was diagnosed on the basis of signs and symptoms. Smoking history was obtained by mailed questionnaire (66% response rate). Diabetes duration, HbA1, age, sex, peripheral vascular disease, hypertension history, and lifetime alcohol consumption were measured as covariates. The prevalence of neuropathy was 49 and 38% in IDDM (n = 113) and NIDDM (n = 104) patients, respectively. In IDDM, but not NIDDM, current or ex-smokers were significantly more likely to have neuropathy than individuals who had never smoked (odds ratio 2.46, P = 0.02), and the prevalence of neuropathy increased with increasing number of pack-years smoked (P less than 0.001). After adjustment for covariates, IDDM patients smoking greater than or equal to 30 pack-yr were 3.32 times more likely to have neuropathy than patients smoking less than this amount (95% confidence interval 1.15-9.58, P = 0.026). Cigarette smoking was associated with the presence of neuropathy in this clinic-based population of IDDM patients. The hypothesis that cigarette smoking is associated with diabetic neuropathy should be investigated further, both prospectively and in a more representative population.
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PMID:Cigarette smoking and neuropathy in diabetic patients. 231 3

A unifying metabolic hypothesis completely accounting for the development of one or more of the chronic complications of diabetes on the basis of a single aspect of disturbed glucose metabolism resulting from insulin deficiency and/or hyperglycemia has been sought by clinical and basic scientists for decades. A growing body of loosely related but internally consistent scientific data obtained from cultured cells, incubated tissue preparations, animal models, and man implicate sorbitol- and glucose-induced myo-inositol depletion and altered phosphoinositide metabolism in a series of secondary biochemical, functional, and architectural abnormalities in the PNS in diabetes. These early metabolically based functional and structural changes simulate those that characterize human diabetic neuropathy. Can abnormal phosphoinositide metabolism in diabetic nerve thereby by itself explain the development of chronic diabetic neuropathy with all of its clinical complexity and heterogeneity? Almost certainly not. Even if the entire contribution of hyperglycemia to the development of diabetic neuropathy were mediated by secondary abnormalities in phosphoinositide metabolism, other factors must also play a role. Witness the differences in the histopathological picture of neuropathy in patients with IDDM and NIDDM despite similar durations and severity of diabetes, the apparent influence of age and gender on the appearance of early neuropathy in patients with IDDM, and the association of alcohol consumption with diabetic neuropathy. While early metabolic and functional disturbances in diabetic nerve such as impaired (Na,K)-ATPase function and paranodal swelling are empirically attributable to abnormal myo-inositol and phosphoinositide metabolism, more advanced abnormalities such as axo-glial dysjunction may reflect superimposed independent biochemical and/or hormonal defects (although, as mentioned previously, aldose reductase inhibition decreases axo-glial dysjunction in diabetic humans). The PNS has only a limited repertoire of responses to a variety of insults, so that Wallerian degeneration, axonal atrophy, impaired axonal transport, and dystrophic changes in diabetic neuropathy may represent multiple factors. On the other hand, the increasingly recognized importance of the phosphoinositide cascade in neuromodulation may attribute a progressively wider range of disturbances in the diabetic PNS to myo-inositol depletion and associated defects in phosphoinositide metabolism. Thus, while all effects of aldose reductase inhibitors in the PNS of diabetic rats have been reproduced by myo-inositol supplementation when this alternative intervention has been tested, the exact role of phosphoinositide metabolism in most of these responses is not well understood.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathogenesis of diabetic neuropathy: role of altered phosphoinositide metabolism. 256 4

In 1987-1988 160 type 2 diabetics, dispensarized in diabetological out-patient departments of the medical clinic of the Institute for Postgraduate training were subjected to neurological examinations. The selection of the group was governed by an effort to reduce to a minimum the association of other neurotoxic influences. The group therefore comprised subjects under 60 years of age; diabetics with other diseases with a possible neurotoxic action, drug abuse, alcohol abuse, etc. were eliminated. After a detailed neurological examination signs of affection of the peripheral nervous system were detected in 87.5%, clinically manifest diabetic neuropathy was found in 78 diabetics (48.75%); 12 had moreover mononeuropathy of the median nerve. The clinical picture was uniform: impaired perception of vibrations on the acra of the lower extremities with ascendent propagation, reduction to disappearance tendinous-muscular reflexes on the lower extremities. Subjectively more frequently cramps of the feet than paraesthesias were reported. The authors revealed that long-term compensation of diabetes, the duration of diabetes and the biological age of the diabetics were statistically significant for the manifestation of diabetic neuropathy. This significance was proved for the factor of biological age (p less than 0.05); there was also a significant correlation between the long-term state of compensation of type 2 diabetes and the manifestation of neuropathy (p = 0.06).
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PMID:[Incidence and developmental interdependence of peripheral nerve disorders in type 2 diabetics]. 259 49

Vibratory detection threshold (VDT) was determined on the plantar side of the distal phalanx of the right great toe of 22 diabetic (NIDDM) patients. In addition, a neurological examination and a sural nerve conduction study were performed. Peripheral neuropathy, based on our criteria, was found in 41% of the patients. VDT was abnormally high in 23% of the patients. The combined frequency of the abnormality of the amplitude of the action potential of the sural nerve or the conduction velocity or both was 73%. The nerve conduction study showed the highest sensitivity in detecting the abnormality of the peripheral nerve in this study; this is in agreement with the result shown in the literature. Seven patients showed no response to electrical stimulation of the sural nerve, although VDT was obtained in these patients. Among the 6 patients that underwent the normal sural nerve conduction study, no one showed abnormally high VDT. The determination of VDT seems to be a useful examination for the follow-up study of diabetic neuropathy, although it is less sensitive than the sural nerve conduction study.
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PMID:[Correlation between vibratory detection threshold and conduction study of sural nerve in diabetic patients]. 260 39

To investigate whether pain and paresthesias could identify two different subclasses of small-fibre diabetic neuropathy, and to evaluate their relation to the metabolic control, we tested nerve conduction velocity (NCV) of median nerve (sensitive-SM, and motor-MM) and deep peroneal nerve (DP) in 48 diabetics (24 IDDM, 24 NIDDM) reporting pain (group A) or paresthesias (group B) that might be due to diabetic polyneuropathy. Glycated haemoglobin (HbA1c) was also assessed. No difference between group A and group B was found either in NCV, in all nerves tested, or in HbA1c. No relation was observed between NCV of nerves tested and HbA1c, duration of diabetes, age and type of diabetes in both groups.
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PMID:Neuroelectric procedure does not discriminate between painful and paresthetic diabetic neuropathy. 273 2

Diabetes mellitus type II (currently known as non-insulin-dependent diabetes) is apparently the result of genetically imposed insulin resistance. Type II diabetes is far more common than insulin-dependent (type I) diabetes, which is probably an autoimmune disease resulting in inadequate insulin production. The decade of the '80s has seen several changes in the management of type II diabetes, including: more widespread use of glycosylated hemoglobin and home blood glucose monitoring as surveillance tools; modification of the dietary regimen by advocating increased amounts of complex carbohydrates; use in this country of the second-generation oral sulfonylureas; and therapeutic trials of tricyclic antidepressants for relief of painful diabetic neuropathy. Diabetes mellitus type II is potentially preventable through encouragement of weight loss and regular screening for those genetically at risk.
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PMID:Type II diabetes mellitus update: diagnosis and management. 374 79

The incidence and prevalence of diabetic neuropathies in Insulin Dependent (IDDM) and Non-Insulin Dependent (NIDDM) Diabetes Mellitus is not known because in previous studies the heterogeneity of diabetes and of the neuropathies was not taken into account, criteria for diagnosis and surveillance for neuropathy were variable, and studies were not prospective or population based. We have begun such prospective epidemiologic studies using a uniform algorithm for the classification of the diabetic disorders and uniform and validated approaches for the assessment of symptoms, neurologic deficits and various quantitative end-points of neural dysfunction. As regards cause, a key question which we are trying to answer is whether hyperglycemia and associated metabolic alterations affect neural tissue directly or whether there is an intervening tissue alteration between metabolic derangement and tissue change. Improved control of hyperglycemia does not appear to be associated with rapid neurologic improvement, possibly arguing for an intervening tissue alteration. The recently observed decrease in nerve oxygen tension and blood flow in streptozotocin diabetes suggests that an alteration of the nerve microenvironment may relate importantly to the cause of diabetic neuropathy.
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PMID:Diabetic neuropathy. 403 17

Serum immunoglobulin (G, A, M) levels were performed on 66 patients with non-insulin-dependent (type II) diabetes mellitus (NIDDM). When compared with 30 age-matched normal controls and 32 hospitalized controls there was no significant difference between the mean IgG and IgM levels. The IgA levels were significantly higher (P less than 0.005) in the diabetic group when compared with both control groups. This is true regardless of age, sex, duration of disease, and type of treatment (insulin/diet or oral hypoglycemic agents and/or diet). Thirty-six percent of the diabetic patients' IgA levels exceeded the mean +/- 2 SD of the normal control group. There were no significant differences in immunoglobulin levels between insulin-treated and non-insulin-treated diabetic groups. Since diabetic patients may have a number of secondary diseases, attempts were made to correlate the most common of these (acute and/or chronic bacterial infections, hypertension, arteriosclerotic heart disease, and diabetic neuropathy) with elevated IgA levels. Only IgA levels of diabetic patients with infections versus diabetic patients without infections were significantly different (P less than 0.05). However, IgA levels of uninfected diabetic patients remained significantly higher than those of normal controls (P less than 0.005), hospitalized controls (P less than 0.01), and hospitalized controls with bacterial infections (P less than 0.005). Possible reasons for the isolated elevations of IgA are discussed.
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PMID:Elevation of IgA levels in the non-insulin-dependent (type II) diabetic patient. 675 40


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