Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The magnitude of hGH reserve was investigated in young (16-40 years old) diabetic patients. Forty patients were examined with the arginine infusion test, twenty three with a sensitized version of the L-Dopa test. The patients were divided into four groups based on the type of their illness (IDDM or NIDDY) and the clinical stage of IDDM. It was concluded that the hGH reserve of the various diabetic groups differs from the hGH reserve of healthy persons as well as from one another. Taking into consideration the possible causes of these differences, it is suggested that the hGH reserve depends primarily on the metabolic condition of the patients, while the type of diabetes (IDDM or NIDDY) and the insulin therapy used may also be important contributing factors. Achievement of a good metabolic control within the same type of diabetes leads to the normalization of the previously pathologic hGH reserve.
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PMID:Growth hormone reserve in diabetes mellitus. 368 49

Growth hormone (GH) response was studied in 8 insulin-dependent and 7 non-insulin-dependent diabetics after stimulation with L-Dopa (500 mg orally) and TRH (0.2 mg iv.). L-Dopa induced a clear GH response in insulin-dependent diabetes (IDDM) and in the control group while in non-insulin-dependent diabetes (NIDDM) peak GH levels were lower (P less than 0.05) and 4 of 7 subjects failed to respond to L-Dopa stimulation. TRH had no effect on GH levels in NIDDM and in the controls. Insulin-dependent diabetics responded to TRH stimulation and GH levels at 20 and 30 min were significantly higher as compared with NIDDM and the control group. The degree of hyperglycemia seemed not to influence GH response. The highest GH levels were noted in two patients with proliferative retinopathy. It is suggested that TRH-induced GH release may be a characteristic feature in some patients with IDDM.
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PMID:TRH-induced growth hormone release in insulin-dependent diabetes mellitus. 644 6

Authors refer in this study their clinical experience with brain cortex phospholipids (BC-PL) in patients affected by Parkinson's disease and treated with L-DOPA plus IDD. It's plain from results elaborated through statistical examinations a positive influence more on motor timing performances (screw-test, gait-test, peg-board test) than each item of Webster rating scale. Moreover getting in connection high nervous functions with motor activity, authors suppose BC-PL have a primary and direct action on cortical cholinergic structures correlated with attention, learning and memory and consequently a secondary action on motor performances.
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PMID:[Cerebral phospholipids and Parkinson's disease: cross-over double-blind study versus placebo]. 701 86

Dopamine (DA) functions as an essential neuromodulator in the brain and retina such that disruptions in the dopaminergic system are associated with common neurologic disorders such as Parkinson's disease. Although a reduction in DA content has been observed in diabetes, its effects in the development of diabetes-induced neuropathy remains unknown. Because the retina is rich in DA and has a well known diabetes-induced pathology (diabetic retinopathy or DR), this study was designed to examine the role of retinal DA deficiency in early visual defects in DR. Using rodent models of type 1 diabetes mellitus, we investigated whether diabetes caused a reduction in retinal DA content in both rats and mice and determined whether restoring DA levels or activating specific DA receptor pathways could improve visual function (evaluated with optokinetic tracking response) of diabetic mice, potentially via improvement of retinal function (assessed with electroretinography). We found that diabetes significantly reduced DA levels by 4 weeks in rats and by 5 weeks in mice, coincident with the initial detection of visual deficits. Treatment with l-DOPA, a DA precursor, improved overall retinal and visual functions in diabetic mice and acute treatment with DA D1 or D4 receptor agonists improved spatial frequency threshold or contrast sensitivity, respectively. Together, our results indicate that retinal DA deficiency is an underlying mechanism for early, diabetes-induced visual dysfunction and suggest that therapies targeting the retinal dopaminergic system may be beneficial in early-stage DR.
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PMID:Dopamine deficiency contributes to early visual dysfunction in a rodent model of type 1 diabetes. 2443 31