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)

Non-insulin-dependent diabetes is associated with facial flushing after alcohol in patients on chlorpropamide (chlorpropamide alcohol flushing, C.P.A.F.) especially when there is a family history of diabetes. C.P.A.F. in three subjects (two diabetics, one non-diabetic) was blocked by the specific opiate antagonist naloxone. In nine subjects (six diabetics) C.P.A.F. was reproduced by the enkephalin analogue with opiate-like activity [D-Ala2, MePhe4, Met (O)-ol] enkephalin (DAMME). C.P.A.F. thus may be due to increased sensitivity to endogenous opiates. DAMME and other substances with opiate-like activity, such as morphine and beta-endorphin, affect carbohydrate metabolism and insulin secretion. Increased sensitivity to endogenous opiates such as enkephalin may thus give rise to non-insulin-dependent diabetes associated with C.P.A.F.
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PMID:Sensitivity to enkephalin as a cause of non-insulin dependent diabetes. 8 99

"Mason-type" diabetics (mild diabetes which is dominantly inherited) are relatively free of retinopathy. Alcohol almost invariably causes facial flushing in these patients when they are given chlorpropamide (chlorpropamide alcohol flush, C.P.A.F.). 291 non-insulin-dependent diabetics were examined to see whether there was a difference in frequency of retinopathy between C.P.A.F. positive and negative cases who were of comparable age and duration of diabetes. Retinopathy was commoner and often severe in CPAF negative patients. Blindness from retinopathy was almost confined to C.P.A.F.-negative cases. Lens opacities, on the other hand, were equally common in both groups. Since C.P.A.F. is an inherited trait, retinopathy in non-insulin-dependent diabetics is to a considerable extent, although not entirely, determined by genetic factors.
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PMID:Chlorpropamide alcohol flushing and diabetic retinopathy. 8 72

Insulin dependent (IDD) and non-insulin dependent diabetes (NIDD) are separate disorders. Twin studies show that IDD cannot be entirely due to genetic causes as concordance is no more than about 50%, but there is some inherited predisposition to it as shown by HLA patterns. NIDD, on the other hand, is predominantly due to genetic causes since identical twins are nearly always concordant. Many cases of NIDD show chlorpropamide alcohol flushing (CPAF), a dominantly inherited feature which may precede the appearance of diabetes and thus act as a genetic marker for this type of diabetes. Diabetics who show chlorpropamide acohol flushing are less likely to develop retinopathy than those who do not. Genetic factors must therefore affect the incidence and severity of diabetic retinopathy. Chlorpropamide alcohol flushing is due to sensitivity to enkephalin. Enkephalin and other opioids affect carbohydrate metabolism and insulin release. It is possible therefore that they act as neurotransmitters and cause NIDD by a sympathetically mediated effect on the liver and pancreas--in other words, that as far as NIDD is concerned Claude Bernard's views on the cause of diabetes may have been right.
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PMID:Diabetes: the genetic connections. 39

A simple test was devised to identify people susceptible to chlorpropamide-alcohol flushing (CPAF). Subjects were given a placebo tablet, followed by sherry 12 and 36 hours later. They then received a chlorpropamide tablet and sherry again after 12 and 36 hours. This single-dose challenge test was given to non-insulin-dependent diabetics, insulin-dependent diabetics, and normal subjects. CPAF was common in the non-insulin-dependent diabetics but rare in the other groups. When the test was used in identical twins and families of affected subjects CPAF appeared to be a dominantly inherited trait. We conclude that facial flushing after alcohol in people taking chlorpropamide is related to non-insulin-dependent diabetes, especially when there is a strong family history of diabetes, but not to insulin-dependent diabetes. It is a dominantly inherited trait.
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PMID:Chlorpropamide-alcohol flushing: a dominantly inherited trait associated with diabetes. 72 7

The single-challenge test for chlorpropamide-alcohol flushing (CPAF) was used to study two groups of patients with non-insulin-dependent diabetes and a family history of the disease who were distinguished only by their age at diagnosis (under and over 30). Their relatives were also studied. The proportions of patients showing CPAF in both groups were similar, and the family histories suggested dominant inheritance. When offspring of diabetics in whom the disease was diagnosed early were studied CPAF seemed to precede the appearance of diabetes. We conclude that the patients in both groups had the same, distinct syndrome, which is characterised by diabetes diagnosed at any age that is inherited as an autosomal dominant trait and associated with CPAF. This syndrome, which constitutes about one-fifth of all cases of non-insulin-dependent diabetes, may be detected with a single-challenge CPAF test before the onset of glucose intolerance. CPAF therefore acts as a genetic marker for the syndrome.
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PMID:Chlorpropamide-alcohol flushing: a definition of its relation to non-insulin-dependent diabetes. 72 8

The effect of 3-methylpyrazole-5-carboxylic acid (MPC) on carbohydrate and lipid metabolisms was studied in 18 patients with diabetes mellitus. In addition to diet 17 patients had basic treatment with sulfonylureas with or without biguanides, one patient was treated with insulin. In all patients carbohydrate metabolism was not well controlled, 14 patients had elevated triglycerides. Following a control period of 2 weeks the patients received increasing doses of MPC in addition to basic treatment (25825825 mg; 50,25,25 mg; 50, 50, 25 mg). Blood samples were taken in the fasting state before the first dose of MPC. Free fatty acids almost doubled under the influence of MPC. This was due to a rebound effect at night following suppression of lipolysis during the day. Blood glucose levels showed a tendency to fall, urinary glucose excretion, separately examined for day and night ,did not change consistently. Triglycerides fell markedly by 25%, but this reduction was not statistically significant. Cholesterol decreased by 5%. 40% of the patients showed an increase in urinary ketone bodies. Body weight did not change. Side effects due to MPC included flushing, gastrointestinal distress and cardiovascular complaints and were observed in 75% of the patients. Due to the high frequency of side effects it does not seem to be worthwhile to further investigate the therapeutic effect of MPC in a larger number of patients with different dosage regimens.
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PMID:[Effect of methylpyrazole-carboxylic acid on carbohydrate and lipid metabolisms in patients with diabetes mellitus]. 80 21

Reactive hypoglycemia was documented in ten postgastrectomy patients by a control oral glucose tolerance test (OGTT). Nine patients experienced nausea, flushing, and fatigue during the first hour of the test. Neuroglycopenic or adrenergic symptoms of hypoglycemia occurred in eight patients two to five hours after oral glucose. The oral administration of phenylephrine elixir, 15 mg., thirty minutes before a repeat OGTT, significantly raised thelowest plasma glucose from 37.5 +/- 2.8 mg./dl. to 45.2 +/- 3.8 mg./dl. (p less than 0.05) but did not affect the occurrence of either the early or the late symptoms. In contrast, propranolol, 10 mg., raised the lowest plasma glucose from 37.5 +/- 2.8 mg./dl. to 57 +/- 5.2 mg./dl. (p less than 0.02) and prevented the occurrence of early and late symptoms. Neither peak nor total plasma insulin levels were affected by either drug. The rate of glucose utilization, as determined by intravenous glucose tolerance tests, did not significantly change after the oral administration of either drug. It is concluded that propranolol ameliorated the symptoms and chemical hypoglycemia after oral glucose and merits more detailed study as a long-term therapy for this disorder.
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PMID:Effect of adrenergic agents on postgastrectomy hypoglycemia. 118 31

Fifty-two rat pancreas transplants were performed to investigate which components of the UW solution were essential for successful pancreas preservation. LEW rats were used and the pancreata stored at 4 degrees C for 48 hr after flushing with commercial UW solution (ViaSpan, DuPont Pharmaceuticals) or a number of simplified solutions. Following storage the pancreata were transplanted into syngeneic recipient animals with streptozotocin-induced diabetes mellitus. Graft function was assessed by regular postoperative blood sugar measurements and a glucose tolerance test on the 14th postoperative day. With commercial UW solution, 4 of 9 recipients (44%) showed satisfactory graft function, while only one of 5 pancreata preserved using Eurocollins solution demonstrated satisfactory function. With solution A, in which hydroxyethyl starch and insulin were omitted from the standard UW solution, 3 of 7 recipients (43%) showed satisfactory function. Omission of glutathione, allopurinol, and adenosine from this solution (solution B) gave satisfactory function in 4 of 8 cases (50%). Substitution of raffinose in solution B with an equimolar concentration of glucose (solution C) resulted in acceptable function in 5 of 8 cases (62%). Increasing the raffinose concentration in solution B to 100 mM/L resulted in only 2 of 8 grafts (25%) with adequate function. By contrast, reversing the Na/K concentrations in solution A resulted in 100% (7/7) satisfactory graft function. We conclude that the rat pancreas can be successfully transplanted following 48-hr cold preservation using UW solution and some simplified versions, and that a substantially simplified lactobionate-based solution with a reversed sodium/potassium ratio improved survival.
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PMID:A comparison of some simplified lactobionate preservation solutions with standard UW solution and Eurocollins solution for pancreas preservation. 156 38

Not all episodes of hypoglycemia are recognized as such by diabetic patients, suggesting that it is possible for them to adapt to a low blood glucose level, although the mechanism involved is not known. The aim of this study was to examine whether insulin has an effect, independent of blood glucose, on the subjective, cognitive, and hormonal responses to hypoglycemia. Nine patients with insulin-dependent diabetes mellitus (IDDM) participated in three hyperinsulinemic glucose-clamp studies. After 60 min at 4.5 mM, blood glucose was randomized to be 1) maintained at 4.5 mM for 240 min, 2) lowered to 2.8 mM for 180 min followed by 60 min at 2 mM with an insulin infusion rate of 40 mU.m-2.m-1, and 3) fitted to the same protocol as 2 but with an infusion rate of 120 mU.m-2.min-1. Symptoms and awareness of hypoglycemia (100-mm visual analogue scales), cognitive function, and counterregulatory hormone levels were assessed every 30 min. There were no subjective or cognitive changes during the euglycemic study. Awareness and hypoglycemic symptoms (hunger, facial flushing, trembling, and sweating) were attenuated by the higher insulin infusion rate (P less than 0.05 and P less than 0.01, respectively). Cognition was significantly impaired after 60 min at 2.8 mM (P less than 0.001) and deteriorated further when the blood glucose level was lowered to 2 mM (P less than 0.01). Levels of cortisol (P less than 0.01) and growth hormone (P less than 0.05) but not epinephrine were suppressed by the higher insulin infusion rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of insulin in subjective, cognitive, and hormonal responses to hypoglycemia in patients with IDDM. 186 May 57

It has been suggested that raised post-ethanol plasma acetaldehyde levels, from inhibition of aldehyde dehydrogenase, underlie the liability to chlorpropamide, alcohol flushing (CPAF). We tested the hypothesis that acetate formation from acetaldehyde, the reaction catalysed by that enzyme, was also likely to be affected by chlorpropamide (CP) medication. In six healthy non-diabetic 'non-flushers', fasting acetate (Ac +/- s.d. mmol/l) was 0.22 +/- 0.12, and increased by 0.47 +/- 0.14 to peak levels by 30 min after intake of 40 ml dry sherry, which increased plasma ethanol (mmol/l) levels to 10.2 +/- 6.0. After 5 days of CP (250 mg daily), fasting Ac (0.17 +/- 0.05) and increase to peak of Ac and ethanol after 40 ml sherry (0.56 +/- 0.12 and 8.9 +/- 7.2 respectively), were not changed (P n.s.). There was no correlation between Ac and ethanol at any time point. When the studies were repeated in five non-insulin-dependent diabetic 'flushers', both on regular CP medication and after 3 days without CP, there was again no significant difference in fasting and post-ethanol Ac levels between the two studies (fasting 0.18 +/- 0.04 v. 0.17 +/- 0.02, and increase to peak 0.62 +/- 0.13 v. 0.72 +/- 0.18, P n.s.). These results indicate that the conversion of ethanol to acetate is unaffected by CP medication, and furthermore that post-ethanol acetate levels do not predict liability to CPAF.
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PMID:The formation of acetate from ethanol with and without prior chlorpropamide intake in diabetic and non-diabetic subjects. 190 25


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