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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in the control of arginine-vasopressin (AVP) secretion have been described in type I diabetes mellitus. In order to gain a better insight into this problem, we examined whether insulin-dependent diabetics in good metabolic conditions and without diabetic complications had an abnormal AVP responsiveness to metoclopramide (MCP), an AVP-stimulating agent with a central site of action. In addition, we tested the AVP response to insulin-induced hypoglycemia in the same subjects. Twenty insulin-dependent diabetic men without neuropathy or other diabetic complications were divided into two groups according to the duration of their illness (10 patients who had been diabetic for less than 10 years, group 1, and 10 patients who had been diabetic for more than 10 years, group 2). Eleven age- and weight-matched normal men participated as controls. All groups were tested with MCP (20 mg in an intravenous bolus) and, on a different occasion, with insulin-induced (0.15 IU/kg) hypoglycemia. Experiments started after optimization of the metabolic status of the diabetic men by 3 days of treatment with continuous subcutaneous insulin infusion. Basal concentrations of AVP were similar in all groups (diabetics of group 1: 2.2 +/- 0.2 pmol/l, mean +/- SE; group 2: 2.3 +/- 0.2 pmol/l; normal controls: 2.2 +/- 0.2 pmol/l). Administration of MCP induced a striking elevation of plasma AVP levels in the normal controls and in the diabetic subjects of groups 1 and 2. All subjects showed a mean peak response at 15 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal arginine-vasopressin responses to metoclopramide and insulin-induced hypoglycemia in type I diabetes mellitus. 228 81

Diabetic cheiroarthropathy (DCA) or pseudosclerodermatous hand of the diabetic is characterized by nonpainful limited extension of the proximal metacarpophalangeal and/or interphalangeal joints with spontaneous flexum of the fingers. The mechanism of lesion formation is poorly known but apparently associates neurogenic, vascular and cutaneous phenomena. Fifteen patients with DCA (9 men, 6 women; range 20-74 years) were studied by capillaroscopy, photoplethysmography and skin biopsy. Eleven had type 1 diabetes and 4 type 2 over periods ranging from 1 to 42 years (mean 19.9 years). Diabetic retinopathy was noted 10/15 times, nephropathy 5/15 times and neuropathy of the lower limbs 13/15 times. All patients had at least one of these abnormalities. In capillaroscopy, "Shoal of fish" features of diabetic microangiopathy were found only 4 times, but minor dystrophy was noted in 12 cases. In digital photoplethysmography, a drop in digital systolic pressure or an increase in pulse time was noted in 5 cases. The Hillestad test was less than or equal to 2 in 8 patients. Histological study showed constant dermal collagenous fibrosis in diseased skin, which was also found in normal skin in 6/13 patients. PAS staining showed a thickening of vascular basal membrane 14/15 times in diseased skin and 11/13 times in normal skin. The relation between DCA and microangiopathy is discussed in terms of collagen metabolism abnormalities observed during diabetes.
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PMID:[Diabetic cheiroarthropathy. Microcirculatory aspects]. 231 10

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

Ulnar and tibial F response parameters were characterized in 17 healthy controls and 26 subjects with type I diabetes mellitus meeting or exceeding criteria for mild diabetic peripheral neuropathy. The presence of mild diabetic peripheral neuropathy was determined by utilizing conventional nerve conduction studies, the neuropathy symptoms score and a neurologic examination. Ulnar and tibial nerve F response latency, amplitude, duration, chronodispersion and persistence were then compared between populations. The relationship between tibial F response persistence and minimal F response latency was assessed in both populations. In addition, the relationship between tibial F response persistence and tibial nerve conduction velocity and tibial nerve compound action potential characteristics (e.g., latency, amplitude and duration) was assessed in the diabetic population. The results indicate that ulnar F response latency and chronodispersion failed to differentiate the subject and control populations; however, significantly decreased ulnar F response amplitude and duration were noted in the diabetic population. In the tibial nerve, the F response persistence was significantly decreased in the diabetic population but persistence did not correlate with compound muscle action potential latency, amplitude, duration or nerve conduction velocity. Finally, the tibial F response latency, amplitude, duration and chronodispersion failed to differentiate the control and diabetic populations.
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PMID:F response characteristics in type I diabetes mellitus. 236

The function of the local nervous veno-arteriolar reflex regulation of blood flow in subcutaneous tissue of the lower leg was studied in diabetic patients. The material comprised 11 long-term insulin-dependent diabetic (IDDM) patients with retinopathy and nephropathy and eight short-term IDDM patients without retinopathy or nephropathy and 11 non-diabetic subjects. The diabetic patients had no or a slight to moderate degree of peripheral autonomic and sensoric neuropathy. Blood flow was measured by the local 133Xe wash-out technique. Blood flow was determined before, during and after an approximately 40 mmHg increase in venous transmural pressure, induced by lowering the lower leg 50 cm below heart level. During lowering of the leg, the subcutaneous blood flow decreased to the same level in long-term IDDM patients (mean: 46%), short-term IDDM patients (53%) and control subjects (53%). There was no association between the relative local blood flow during lowering and the degree of terminal arteriolar hyalinosis studied in skin biopsies from the same tissue area. Our results suggest that terminal arteriolar hyalinosis does not interfere with the local sympathetic-mediated veno-arteriolar reflex regulation of blood flow. Moreover, the vasoconstriction mediated by the veno-arteriolar reflex probably occurs in the larger arterioles (greater than 50-100 micron) or small arteries.
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PMID:Arteriolar hyalinosis does not interfere with the local veno-arteriolar reflex regulation of subcutaneous blood flow in insulin-dependent diabetic patients. 244 59

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

A high plasma prorenin is a marker of microvascular complications of diabetes. We have followed 56 adults and 120 children with uncomplicated insulin-dependent (type 1) diabetes. When plasma prorenin rises above the normal range in an adolescent or adult with type 1 diabetes, signs of nephropathy, retinopathy, or neuropathy follow within one to two years. The earliest sign may be intermittent microalbuminuria, which can often be abolished by improved control of hyperglycemia. The association between increased plasma prorenin and complications of noninsulin-dependent (type 2) diabetes is less reliable in patients with hypertension and in those receiving medication that affects plasma prorenin. The oral hypoglycemic agent, glipizide, lowers plasma prorenin, but its effect on prognosis is unknown. Plasma prorenin and renin decline as blood pressure rises, whereas the prevalence of micro- and macroalbuminuria increases. Many drugs used to control hypertension affect the level of prorenin. In the majority of our patients with type 2 diabetes who are hypertensive or are taking a medication that affects plasma prorenin, microalbuminuria may prove to be a more reliable warning of vascular complications.
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PMID:Prorenin and vascular complications of diabetes. 265 63

At the University of Iowa, Iowa City, 75 pancreas transplant procedures were performed for type I diabetes mellitus from March 1984 to September 1988. Forty-seven of these transplants were performed simultaneously with kidney transplants from the same donor; 23 followed previous kidney transplants, and 5 were preuremic pancreas-only transplants. The 1-year patient survival rate is 85% and pancreas graft survival rate is 54%. The simultaneous kidney and pancrease group had a 1-year patient survival rate of 82%, a pancreas graft survival rate of 59%, and a renal graft survival rate of 73%. Thirty-one of 70 kidney and pancreas recipients had a functioning pancreas 1 year post transplantation and 26 of 31 currently have a functioning pancreas and are insulin free. Patient symptoms of neuropathy and gastroenteropathy are improved with long-term graft function. Some patients may develop type II diabetes post transplantation with impaired glucose tolerance despite high insulin production by the graft. Pancreas transplantation is the only therapy that achieves a euglycemic state as indicated by glycosylated hemoglobin and glucose tolerance testing. Centers must continue to follow up patients on a long-term basis to determine the final effects on the secondary complications of diabetes.
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PMID:Function of pancreas allografts more than 1 year following transplantation. 266 39

The plasma catecholamine response to a standardized bicycle exercise test was evaluated in 24 insulin-dependent diabetic (IDDM) patients in whom the heart rate reactions to deep breathing (E/I ratio) and to tilt, the immediate acceleration and the transient deceleration (acceleration and brake indices), had been assessed as tests of autonomic neuropathy. Patients with an abnormal acceleration index (n = 8) showed, compared with non-diabetic (n = 18) controls who had participated in previous studies, an impaired increment in noradrenaline during exercise (80% of maximal working capacity) (MWC) (12.38 +/- 1.46 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (50% of MWC: 0.25 +/- 0.04 nmol l-1 vs. 0.54 +/- 0.08 nmol l-1; P less than 0.05). Similarly, patients with an isolated abnormal brake index (n = 6), i.e. with a normal acceleration index and a normal E/I ratio, showed compared with controls an impaired increment in noradrenaline (9.53 +/- 1.66 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (1.41 +/- 0.22 nmol l-1 vs. 2.92 +/- 0.51 nmol l-1; P less than 0.05) during 80% of MWC. IDDM patients with abnormal heart rate reactions to tilt, an abnormal acceleration index or an abnormal brake index show impaired catecholamine responses to exercise, which can be demonstrated also in patients without signs of parasympathetic neuropathy.
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PMID:Impaired responses of plasma catecholamines to exercise in diabetic patients with abnormal heart rate reactions to tilt. 274 44

Two-hundred-and-two impotent diabetic patients gave their consent to be investigated. Impotence is linked to diabetes mellitus in 58.9% of patients so all the other etiologies have to be systematically eliminated. Neuropathy or arteriopathy, when isolated, are found with the same frequency, but these 2 etiologies are often associated (47 patients). No statistical difference between IDDM and NIDDM was found. Mercury strain gauge plethysmography and venous occlusion coupled to ECG allows detection of arterial lesions in diabetic impotence. Patients agreed to submit to all of the various therapeutic possibilities. Combination of alpha-blockade and good glycemic control induced the best results.
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PMID:[Impotence in the diabetic]. 275 49


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