Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

50 diet-treated, non-insulin-dependent diabetics were tested subjectively and objectively for chlorpropamide-alcohol flushing (CPAF) with a single challenge test. Of the 12 (24%) who reported a subjective flush, 9 (18%) also flushed when a placebo was given instead of chlorpropamide, so the true incidence of chlorpropamide-alcohol flushing was 4% (1 patient was not retested with placebo). In a control group of 21 non-diabetics, 2 showed the specific CPAF phenomenon. Temperature measurement did not improve discrimination, but it did show a faster rise in facial temperature in CPAF-positive subjects than in alcohol flushers. This study does not confirm previous higher estimates of the incidence of the CPAF phenomenon in non-insulin-dependent diabetes.
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PMID:Low incidence of chlorpropamide-alcohol flushing in diet-treated, non-insulin-dependent diabetes. 610 2

A woman had episodic attacks of flushing associated with severe skin, bone, and abdominal pain, accompanied by mood alterations and anxiety, and followed by an organic psychosis. These symptoms and signs could be induced by small doses of clonidine, L-5-hydroxytryptophan, pentagastrin, insulin, epinephrine, compound 48/80, methacholine, morphine, histamine, or d-tubocurarine. Skin testing showed abnormally sensitive mast cells and an exaggerated axon flare. Cimetidine initially prevented the attacks but became less effective after 18 months. Thyrotropin-releasing hormone stopped the skin pain whereas neurotensin reproduced the burning sensation in the skin without inducing the attack. Both the flush and the organic psychosis were reversed entirely by naloxone or naltrexone, and the hallucinosis could be reversed by vasodilators.
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PMID:A case of episodic flushing and organic psychosis: reversal by opiate antagonists. 618 3

The role of opiate receptors in the metabolic response to an intravenous glucose load was determined in eight non-diabetic subjects (four of whom showed a positive chlorpropamide alcohol flush response and four who did not). Subjects were studied in a double blind randomised fashion receiving either a saline control or the specific opiate receptor antagonist, naloxone (0.4 mg/min), as an infusion for 5 minutes before and 20 minutes after an intravenous bolus of glucose (0.5 g/kg body weight). Naloxone decreased the early plasma glucose peak in all subjects by increasing the distribution volume but did not alter the fractional glucose clearance. Insulin and glucagon responses to glucose were not altered by naloxone. Naloxone delayed the normal post-glucose rise in the levels of the gluconeogenic precursors alanine, lactate, pyruvate and glycerol suggesting a delay in the usual inhibition in gluconeogenesis following a glucose load. There was no difference in the metabolic response between those subjects who were liable to chlorpropamide alcohol flushing and those who were not either with or without naloxone. We conclude that opiate receptors may influence distribution volume and gluconeogenesis but do not play a major role in either insulin or glucagon secretion or in glucose disposal following an intravenous glucose load.
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PMID:Opiate receptors and the metabolic response to intravenous glucose. 629 13

By and large, essential diabetes mellitus is thought to be 50% inherited and 50% environmental. In insulin-dependent diabetes mellitus (IDDM) there is a strong link with the HLA system with regard to the inheritance of 'susceptible' diabetic genes, especially the DR3 and DR4 alleles. In IDDM environmental factors act in a predisposed individual to initiate an immune response with resultant beta-cell damage and destruction. Non-insulin-dependent diabetes mellitus (NIDDM) has no clear HLA link, but has been shown in studies of twins to have a stronger genetic basis than IDDM. In NIDDM environmental factors (race, ethnicity, diet, obesity) have an important influence on the clinical expression of the disease and the severity of complications in a genetically predisposed individual. The non-insulin-dependent diabetes of the young (NIDDY) variant and the phenomenon of chlorpropamide-primed alcohol-induced flushing both underline the heterogeneity of NIDDM. Because of the heterogeneous nature and multifactorial inheritance pattern of diabetes mellitus, accurate genetic counselling is not possible as yet. However, data to date suggest that it is unwise to advise prospective parents not to procreate, since the overall risk of the development of clinical diabetes mellitus is extremely low.
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PMID:The genetics of diabetes mellitus, including the South African perspective. 638 8

A synthetic replicate of human pancreas growth hormone-releasing factor, hpGRF1-44-NH2, (hpGRF44), a 44-amino acid amidated peptide, was administered to seven normal men. In addition to placebo, 4 subjects received 3 doses of hpGRF44 (0.5 microgram/kg, 5 micrograms/kg, 10 micrograms/kg), while one subject received 2 doses (5 micrograms/kg, 10 micrograms/kg) and 2 subjects received one dose (0.5 microgram/kg or 5 micrograms/kg), each as a rapid intravenous injection. A significant increase in circulating growth hormone (GH) was observed at each dose (0.5 microgram/kg, p = 0.05; 5 micrograms/kg, p less than 0.005; 10 micrograms/kg, p = 0.01) when compared to placebo, with equivalent maximal responses. At all doses studied a rise in plasma GH occurred within 5 min, with a peak response in most patients at 30-45 min. There were no associated changes in any of the other anterior pituitary hormones or insulin. Other than transient flushing and minimal changes in vital signs, no side effects were noted. The results of these studies support the potential usefulness of hpGRF44 for the assessment of GH secretion and reserve, and of this peptide or an analog as a therapeutic agent to stimulate GH release.
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PMID:Synthetic human pancreas growth hormone-releasing factor (hpGRF1-44-NH2) stimulates growth hormone secretion in normal men. 640 19

An epidemiological study was carried out to compare the prevalence of facial flushing in non-diabetics, patients with insulin dependent diabetes, and patients with non-insulin dependent diabetes in response to 40 ml sherry taken 12 hours after 250 mg chlorpropamide or placebo, administered double blind in randomised order. A flush after chlorpropamide but not placebo was reported by 6.2% of non-diabetics (17/273), 9.7% of insulin-dependent diabetics (14/145), and 10.5% of non-insulin dependent diabetics (25/239), excluding those receiving long term chlorpropamide treatment. The differences were not significant. This response was unrelated to age, sex, body mass index, and family history of diabetes in all three groups. Patients taking long term chlorpropamide, however, showed a significantly (p less than 0.01) higher prevalence of flushing after both chlorpropamide and placebo (56.3%; 9/16) compared with the rest of the non-insulin dependent diabetics (16.7%; 40/239), the insulin dependent diabetics (6.9%; 10/145), and the non-diabetics (5.9%; 16/273). Patients receiving long term chlorpropamide would be expected to flush with sherry after a placebo tablet because of therapeutic plasma concentrations of the drug. It is concluded that there is no evidence of an increased prevalence of chlorpropamide alcohol flushing in response to the single challenge test in non-insulin dependent diabetics compared with insulin dependent diabetics and non-diabetics except in selected patients taking chlorpropamide long term. This study does not support the hypothesis that the chlorpropamide alcohol flush is a specific marker for a subtype of non-insulin dependent diabetes.
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PMID:Epidemiological study of prevalence of chlorpropamide alcohol flushing in insulin dependent diabetics, non-insulin dependent diabetics, and non-diabetics. 641 76

Human pancreatic GRF (hpGRF-40; 1 microgram/kg, iv) selectively stimulates GH release in normal men (9). We now report the effects of graded doses of hpGRF-40 on GH release in 12 normal men. Mean peak increments in serum GH after vehicle and the various doses of hpGRF-40 were 1.13, 11.40, 14.60, 17.01, 14.45, and 15.60 ng/ml after vehicle and 0.1, 0.33, 1.0, 3.3, and 10 micrograms/kg hpGRF-40 (iv bolus), respectively. Peak values were observed 30-60 min after hpGRF-40 treatment. There was considerable variability of responsiveness among individual subjects, and no dose-response relationship between the doses and maximal GH values was found. However, the higher doses of 3.3 and 10.0 micrograms/kg resulted in a more prolonged and biphasic pattern of GH release. A side effect of facial flushing of less than 5-min duration occurred in 4 or 6 subjects who received 3.3 micrograms/kg and in all 5 who received 10 micrograms/kg of hpGRF-40. No changes in serum glucose, LH, TSH, PRL, plasma cortisol, or 8 enteropancreatic hormones occurred after hpGRF-40 treatment. There were small increases in serum somatomedin C levels 24 h after the administration of various doses of hpGRF-40 in 11 of 13 studies. Plasma immunoreactive GRF levels measured 5 min after injection were 0.09, 2.0, 4.9, 23.9, and 66.6 ng/ml after 0.1, 0.33, 1.0, 3.3, and 10 micrograms/kg hpGRF-40, respectively. Serum GH responses after insulin-induced hypoglycemia were compared to GH responses after hpGRF-40. Comparable peak GH stimulation occurred with both provocative tests. Mean +/- SEM peak GH was 20.2 +/- 1.0 ng/ml after insulin and 20.9 +/- 3.2 after hpGRF-40 treatment. hpGRF-40 selectively stimulates GH release in normal men over a dose range of 0.1-10 micrograms/kg and is an effective probe to investigate the dynamics of GH release.
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PMID:Human pancreatic tumor growth hormone-releasing factor: dose-response relationships in normal man. 642 60

Levels of immunoreactive 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) and thromboxane B2 (TXB2) were measured in peripheral venous plasma in a group of volunteers and non-insulin dependent diabetic patients (NIDDS). Levels of these eicosanoids were close to the limit of sensitivity of the radioimmunoassays and consequently data are reported as maximal values. Basal plasma levels of 6-oxo-PGF1 alpha did not exceed 5 pg/ml in either group and maximal levels of immunoreactive TXB2 were 125 +/- 14 and 128 +/- 8 pg/ml for volunteers and NIDDS respectively. Attempts to elicit peripheral vascular prostacyclin biosynthesis in volunteers by using forearm ischaemia produced no increase in plasma 6-oxo-PGF1 alpha levels. Measurement of the combined plasma levels of 6-oxo-PGF1 alpha, 13,14-dihydro-6-oxo-PGF1 alpha, 13,14-dihydro-6,15-dioxo-PGF1 alpha and 6-oxo-PGE1 indicated that these were also low (less than 5 pg/ml) and that failure to demonstrate increased 6-oxo-PGF1 alpha levels was unlikely to have arisen from metabolism of prostacyclin to one or more of these metabolites. Measurement of 6-oxo-PGF1 alpha and TXB2 in peripheral venous plasma before and during chloropropamide alcohol flushing (CPAF) did not provide evidence for a role for these eicosanoids in the etiology of this phenomenon. These findings point to the need for a reappraisal of studies that have described altered plasma levels of 6-oxo-PGF1 alpha and TXB2 in CPAF and other pathophysiological conditions in man.
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PMID:Prostacyclin and thromboxane in non-insulin dependent diabetes: the chlorpropamide alcohol flush reaction revisited. 654 28

We examined the role of endogenous opiates and/or prostaglandins on the abnormal insulin secretion characteristic of some non-insulin-dependent diabetic subjects. A group of chlorpropamide-alcohol flush positive (CPAF+) and a group of flush negative (CPAF-) non-insulin-dependent subjects were compared as to their pancreatic beta-cell responses to intravenous glucose tolerance tests before and after sodium salicylate infusion, and before and after naloxone infusion. There was no difference in mean insulin secretion (either first or second phase) between CPAF+ versus CPAF- groups. Both groups increased their insulin secretion with salicylate infusion, and both had a small decrease with naloxone infusion. There was no correlation between chlorpropamide-alcohol flushing and beta-cell response to glucose.
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PMID:Insulin responses to glucose in non-insulin-dependent diabetic subjects with and without the chlorpropamide-alcohol flush: effect of salicylate and naloxone. 675 79

Glibenclamide was administered to five non insulin dependent diabetic (NIDD) patients, whose hyperglycaemia was not controlled by diet alone. The plasma glucose and insulin porfile was determined under strictly standardised conditions before, after the first administration and after 6 months of treatment with glibenclamide. A rapid and satisfactory lowering of plasma glucose was observed in all patients after the first administered dose and a very similar response was seen after 6 months of therapy, when glibenclamide was administered once a day. Despite a consistent plasma glucose lowering effect a very variable plasma insulin response was evident between the patients. This difference may be of relevance in the long term prognosis of these patients with respect to atherogenesis. For the period of the study weight gain was minimal, no episodes of hypoglycaemia or alcohol induced flushing were recorded.
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PMID:The effect of glibenclamide on the glucose and insulin profile in maturity onset diabetics following both acute and long term treatment. 677 11


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