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

The antihypertensive efficacy of enalapril and its effects on renal function and glucose homeostasis were investigated in 9 hypertensive patients with non-insulin-dependent diabetes mellitus. Enalapril therapy produced a significant fall in blood pressure (BP) (p less than 0.05) and a significant increase in renal blood flow (p less than 0.05) without a change in glomerular filtration rate. Furthermore, fasting plasma glucose was significantly reduced (p less than 0.01). Similarly, M value, as an index of plasma glucose control in diabetes, was significantly reduced from 19.6 to 10.1 (p less than 0.01). These findings suggested that the angiotensin-converting enzyme inhibitor enalapril was effective in reducing BP and improving renal function, and might improve glucose homeostasis in hypertensive diabetics.
Nephron 1990
PMID:Beneficial effects of angiotensin-converting enzyme inhibitor on renal function and glucose homeostasis in diabetics with hypertension. 218 76

Unilateral renal agenesis with impaired renal function was found in all 3 siblings of a single family, in association with various metabolic disorders such as diabetes mellitus, hyperuricemia and hyperbilirubinemia with gallstones. The present report suggests that unilateral renal agenesis could occur as a manifestation of a genetic disorder.
Nephron 1990
PMID:Unilateral renal agenesis associated with various metabolic disorders in three siblings. 229 49

This study was aimed at evaluating cardiac function, both systolic and diastolic, in young type 1 diabetics with a mean duration of the disease of 10.9 +/- 6 years and without evidence of cardiac autonomic neuropathy and micro- or macroangiopathy. Thirteen diabetics, with good metabolic control, and 10 normal matched subjects were studied by echocardiography at rest and by radionuclide ventriculography both at rest and during effort. The level of plasma catecholamines was also determined. The echocardiographic data were comparable in the two groups. Scintigraphic data showed an increased peak ejection and peak filling rate (P less than 0.001) in diabetics while the other indices of cardiac function were comparable. Norepinephrine (P less than 0.01) and epinephrine (P less than 0.001) were higher in diabetics. A hypothesis is formulated that the higher indices of flow velocities in type 1 diabetics are supported by a sympathetic overactivity.
Diabetes Res Clin Pract 1990 Jan
PMID:Cardiac function and sympathetic activity in young diabetics. 230 95

Changes in parathyroid hormone (PTH) and osteocalcin over 3 years were studied in hemodialyzed patients with diabetic nephropathy (HD/DM) and hemodialyzed patients without diabetes (HD/non-DM). In HD/DM patients, concentrations of the carboxyl terminal regions of PTH and osteocalcin in the serum did not change significantly, but in HD/non-DM patients, both concentrations increased significantly. In patients in both groups, the mean concentration of the mid-region of PTH increased significantly. Secondary hyperparathyroidism in HD/DM develops slower than in HD/non-DM.
Nephron 1990
PMID:Changes in parathyroid hormone in diabetic patients on long-term hemodialysis. 232 97

Longitudinal data were obtained on 131 diabetic subjects enrolled in a study designed to evaluate the impact of persistent elevation of the blood pressure (BP) upon progression of renal damage in diabetes mellitus. For both insulin-dependent and non-insulin-dependent diabetes, serum creatinine exhibited a more rapid rise in those individuals whose BP remained elevated above 140 mm Hg despite therapy. Since no significant difference in age, duration of diabetes, diabetic control, or renal function at entry in the study could be identified as possible explanations for these differences, the findings support the conclusion that persistent elevation of the BP adds significantly to the risk of renal damage in both insulin-dependent and non-insulin-dependent diabetes, with more rapid decline occurring in non-insulin-dependent diabetes. Hypertensive subjects exhibited higher levels of plasma angiotensin II during the follow-up period.
Nephron 1990
PMID:Prospective study of the impact of hypertension upon kidney function in diabetes mellitus. 234 89

We studied the effect of radiographic contrast media on renal function in both streptozotocin-induced diabetic rats and normoglycemic rats with reduced renal functional mass. Male Sprague-Dawley induced-diabetic rats and weight-matched controls were divided into unilaterally nephrectomized and intact groups prior to an intravenous challenge with sodium diatrizoate (Urografin) at two dose levels, 1,300 and 2,600 mg iodine/kg. Serum creatinine concentration did not change on the 1st and 3rd day after a dose of 1,300 mg/kg of iodine in normal or induced-diabetic rats. Consequent to a dose of 2,600 mg/kg of iodine, induced-diabetic rats had a significant increase in serum creatinine levels to 0.9 +/- 0.45 mg/dl (control 0.68 +/- 0.11 mg/dl). The observed increase in serum creatinine concentration after treatment with sodium diatrizoate was significantly correlated with the degree of hyperglycemia, but not with prior unilateral nephrectomy. Unilateral nephrectomy, prior to administration of sodium diatrizoate did not potentiate the risk of radiocontrast agent injury in induced-diabetic rats. From these findings, we infer that: (1) streptozotocin-induced diabetes in the rat confers a risk for the development of radiocontrast-induced acute renal failure and (2) as judged by the rise in serum creatinine concentration after exposure, there is an increased risk of acute renal failure associated with a higher dose of radiocontrast material.
Nephron 1990
PMID:Uninephrectomy does not potentiate contrast media nephrotoxicity in the streptozotocin-induced diabetic rat. 236 31

The influence of alloxan-induced diabetes mellitus on the sympathetic neuroeffector junction of the rabbit carotid artery denuded of endothelium was studied. Six weeks of diabetes resulted in a neuropathy characterized by a 38% reduction in the arterial content of norepinephrine. Norepinephrine release from the nerves measured from electrically stimulated superfused arterial segments was decreased. The cocaine-sensitive accumulation of [3H]-norepinephrine (NE) was also reduced, reflecting decreased neuronal uptake. The consequences of these prejunctional changes were studied by measuring isometric contractions of arterial rings caused by electrical nerve stimulation or by exogenous norepinephrine. Despite the reduced release of norepinephrine, neurogenic contractions were normal, suggesting an increased sensitivity of the smooth muscle. After neuronal uptake was blocked, the neurogenic contractions of diabetic arteries were less than normal, reflecting the reduction in transmitter release. The sensitivity of diabetic arteries to exogenous norepinephrine was increased under control conditions; maximal contractions were unchanged. Blockade of norepinephrine uptake increased norepinephrine sensitivity more in normal than in diabetic arteries, and there was no longer a significant difference in sensitivity. Thus, under control conditions, neurogenic contractions of the partially denervated diabetic rabbit carotid artery are paradoxically normalized by increased alpha-adrenergic sensitivity of the smooth muscle. The increased sensitivity caused by reduced neuronal uptake can thus preserve neurogenic vasoconstriction and cause supersensitivity to exogenous catecholamines in the sympathetic neuropathy caused by diabetes mellitus.
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PMID:Adrenergic denervation in rabbits with diabetes mellitus. 237 13

Streptozotocin-induced diabetes produced marked alterations of monoamine concentrations in several hypothalamic nuclei of male and female rats. Norepinephrine (NE) concentrations were significantly elevated in the median eminence (ME), supraoptic nucleus (SON) and periventricular nucleus (PEVN) in both sexes of diabetic rats. NE concentrations in the suprachiasmatic nucleus (SCN) and ventromedial nucleus (VMN) of male and female diabetic animals remained unaltered. Serotonin (5-HT) concentrations were increased in PEVN of male and female diabetic rats. No significant changes in hypothalamic dopamine (DA) concentrations were observed. Insulin treatment reversed the diabetes-related changes in monoamine concentrations in most of the nuclei. The significance of these biochemical changes relative to the endocrine and behavioral abnormalities in diabetes is discussed.
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PMID:Diabetes-induced changes in monoamine concentrations of rat hypothalamic nuclei. 243 7

To investigate the influence of diabetes on the responsiveness of the cardiovascular system, we have examined the effects of various agents on the reactivity of the vascular smooth muscle of aortic strips obtained from age-matched control and diabetic rats. Norepinephrine (NE) contracted the aortic strips obtained from age-matched control and diabetic rats in a concentration-dependent manner, but maximal contraction of aortic strips in response to NE was enhanced in diabetic rats. The EC50 value for NE in the diabetic aortic strips was similar to that in the aorta from age-matched controls. Ca-induced contracture of the aortic strips which were depolarized with isotonic K+ (60 mM) was potentiated in aortic strips from diabetic rats, when compared with those from age-matched controls. Ca-induced contracture of aortic strips, preincubated with 10(-6) M NE and 10(-6) M nicardipine in Ca2+-free Krebs-Henseleit solution (KHS), was not significantly different in age-matched control and diabetic rats. Bay K 8644, an activator of calcium channels, produced an increase in the force of contraction of the slightly depolarized aorta from diabetic rats. Phasic contraction induced by phenylephrine (PE) in the presence of 10(-6) M nicardipine in Ca2+-free KHS was significantly enhanced in aortic strips obtained from diabetic rats. These results demonstrate that NE-induced contraction of the aortic strips obtained from diabetic rats was significantly enhanced, and that this increased contractile response of the aorta to NE may be due to an increased influx of extracellular calcium through the voltage-dependent Ca2+ channels, but not through the receptor-operated Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of increased responses of the aorta to alpha-adrenoceptor agonists in streptozotocin-induced diabetic rats. 246 83

1. The effects of a six week period of streptozotocin-induced diabetes on tissue catecholamines and on in vivo noradrenaline turnover were assessed in rats. 2. Noradrenaline concentrations measured in heart ventricle, terminal ileum, vas deferens, spleen and adrenal tissue from the diabetic rats were all found to be elevated compared to those found in control rat tissues. The adrenaline contents of the adrenal glands were also raised in these animals. 3. Noradrenaline turnover in heart ventricle, terminal ileum and vas deferens was estimated from the decline in tissue content of the amine following inhibition of its synthesis with alpha-methyl-p-tyrosine. Turnover was found to be increased in all three tissues. 4. The involvement of the polyol pathway in the above changes was investigated by examining the effects of continuous treatment with an aldose reductase inhibitor, Statil (ICI 128436) or dietary myo-inositol supplementation. Either treatment was found to prevent or reduce the increases in tissue noradrenaline and in its turnover. Myo-inositol treatment also partially prevented the rise in adrenal adrenaline. 5. It is concluded that the elevation of tissue catecholamines and of noradrenaline turnover by diabetes was related to myo-inositol depletion secondary to excessive sorbitol synthesis. Possible mechanisms for the observed increase in noradrenaline turnover could involve Na+, K+-ATPase depression.
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PMID:Tissue noradrenaline and the polyol pathway in experimentally diabetic rats. 250 23


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