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

A reversible deterioration of the oral glucose tolerance has been reported in subjects with initially impaired glucose tolerance when starting to take oral diuretics. This does not seem to be the case in subjects with an initially unimpaired glucose tolerance. A deterioration in the diabetic state is commonly seen when diuretics are given to subjects with clinical diabetes. Our knowledge about the effect of beta-blockers on the glucose tolerance is limited. As for diuretics there seems to be an overrepresentation of diabetics among subjects taking beta-blockers. This overrepresentation can probably be explained by an association between diabetes and disturbances in which diuretics and beta-blockers are commonly used such as arterial hypertension and ischaemic heart disease.
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PMID:Impairment of glucose metabolism during treatment with antihypertensive drugs. 3 6

In view of reports that accessory pathways of glucose oxidation are enhanced in the diabetic state, we have determined the levels of key enzymes of the glucuronate-xylulose cycle in the livers of diabetic mice and rats. Genetically diabetic mice (db/db) were found to have increased levels of two NADP-linked enzymes of this cycle [NADP-xylitol dehydrogenase and NADP-L-hexonate dehydrogenase (aldehyde reductase II)], whereas other NAD- and NADP-linked dehydrogenase activities of the pathway were not changed. On the other hand, the livers of streptozotocin-diabetic mice and rats showed normal levels of all these enzymes. In the course of this study, evidence was obtained for the presence in db/db mouse liver of low molecular weight material inhibitory for glucose 6-phosphate dehydrogenase. The use of these animal models in diabetes research is briefly discussed.
Diabetes 1979 Sep
PMID:Studies on dehydrogenases of the glucuronate-xylulose cycle in the livers of diabetic mice and rats. 3 60

In adrenalectomized rats the effect of i.v. injection of glucose and ATP on insulin changes in external jugular vein was determined in normal and alloxan diabetic animals. In another set of experiments the direct effect of ATP on insulin secretion was investigated. Glucose and ATP were injected in the carotid artery and the blood samples were withdrawn from the portal vein. In these experiments there was immediate and excessive production of insulin release in the portal vein after ATP injection in the carotid artery. In alloxan diabetic rats, despite the high blood glucose levels, the plasma insulin was low and did not respond to glucose stimulation. ATP could increase the sensitivity of the diabetic rats to glucose. The possible role of purinergic nerves in insulin secretion is discussed. It is concluded that multiple innervation of the islets by purinergic, cholinergic and adrenergic nerves, regulate insulin secretion. It is suggested that: 1. Purinergic nerve stimulation is more specific for insulin secretion. 2. ATP is considered the principal transmitter released from purinergic nerves causing insulin secretion. 3. The insulin stimulatory effect normally produced by glucose is through purinergic nerves. 4. It could be possible that one of the causes of diabetes is a defect in the purinergic innervation of the islet cells thus the sensitivity of the islets to glucose is decreased.
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PMID:The purinergic nerve hypothesis and insulin secretion. 4 35

The following evidence suggests that diabetes mellitus may not be the simple consequence of relative or absolute insulin deficiency by itself, but may require the presence of glucagon: (1) relative or absolute hyperglucogonaemia has been identified in every form of endogenous hyperglycaemia, including total pancreatectomy in dogs; (2) insulin lack in the absence of glucagon does not cause endogenous hyperglycaemia, but when endogenous or exogenous glucagon is present, it quickly appears, irrespective of insulin levels at the time. These facts are compatible with a bihormonal-abnormality hypothesis, which holds that the major consequence of absolute or relative insulin lack is glucose underutilisation and that absolute or relative glucagon excess is the principal factor in the over-production of glucose in diabetes.
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PMID:The essential role of glucagon in the pathogenesis of diabetes mellitus. 4 37

The definition of prediabetes by genetic criteria alone has limitations since not all such subjects progress to overt diabetes. Sequential oral glucose tolerance testing in a population has enabled the identification of 14 "true prediabetic" subjects with baseline two-hour plasma glucose levels smaller than 160 mg. per 100 ml. who subsequently developed unequivocal diabetes (two-hour plasma glucose level larger than 275 mg. per 100 ml.). All but one were matched for baseline two-hour plasma glucose and relative weight with a subject whose glucose tolerance remained unchanged during a mean follow-up period of 4 years. Fasting insulin levels and responses at 1/2, 1, and 2 hour sampling times were similar in both group and matched pair analysis at baseline. No evidence was found that subjects destined to develop diabetes have either excessive or diminished insulin secretion.
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PMID:Insulin responses to oral carbohydrate in true prediabetics and matched controls. 4 45

A 53 year old woman presented with diabetes mellitus, hyperglucagonemia (600 to 1,500 pg/ml), clinical hyperparathyroidism and an abdominal mass diagnosed on biopsy as an islet cell carcinoma. Glucagon content of the tumor was 0.78 mug/g wet weight. Hourly blood samples during a 24 hour period revealed a direct correlation between plasma glucose and glucagon. The oral administration of glucose paradoxically increased whereas the intravenous administration decreased plasma glucagon. Circulating glucagon levels were markedly increased with arginine and epinephrine infusion. Both short- and long-term administration of alpha adrenergic blockade depressed the glucagon response to epinephrine infusion. In contrast, long-term alpha adrenergic blockade increased glucagon secretion despite improved glucose tolerance during a second 24 hour study. Although the patient demonstrated overt clinical and chemical findings of hyperparathyroidism, parathyroid hormone (PTH) was not detected in her plasma. The pattern of tumor growth was consistent with an origin from pancreatic islets. We conclude that (1) the tumor was responsive to physiologic stimuli known to affect glucagon secretion; (2) elevations of plasma glucagon levels with oral and dietary glucose suggest regulation of secretion by intestinal factors; and (3) improvement of glucose tolerance with alpha adrenergic blockade may be related to increased insulin secretion.
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PMID:Uncontrolled diabetes mellitus and hyperglucagonemia associated with an islet cell carcinoma. 4 4

The development of diabetes in a small percentage of female beagles receiving large doses of synthetic progestogen for one year is described. The abnormalities in blood sugar and plasma insulin responses to oral glucose arising during induction of diabetes are presented. After a two-year period of diabetes, two animals were examined histologically. Lesions in the kidney and retina, similar to early lesions associated with human diabetic nephropathy and retinopathy, were present. Histologic changes related to the diabetes were also seen in the pancreas and pituitary. The means of induction of the diabetes is discussed. The study supports the view that the dog is a useful species in which to study the long-term pathology of diabetes,
Diabetes 1975 Apr
PMID:Progestogen-induced diabetes in the dog. 4 86

Oral glucose-tolerance test (O.G.T.T.) plasma sugar and insulin levels were measured in 118 newly diagnosed maturity-onset diabetic patients before and after treatment with diet alone for periods of 2 and 6 months. The results of glucose-tolerance tests carried out during treatment could be predicted from the initial test and the weight reduction between the tests. This prediction was not improved by the addition of further variables, including age, obesity, and plasma-insulin levels during the first test. The change in O.C.T.T. plasma-insulin between the first and second tests was predicted by the result of the initial tests, the improvement of glucose tolerance between the two tests, and the degree of weight reduction. 95% of the group achieved some improvement of glucose tolerance after 2 months of dietary treatment, and 59% of the group achieved adequate diabetic control by this time. It is concluded that treatment with diet alone should be the first-line management for patients with newly diagnosed maturity-onset diabetes mellitus.
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PMID:Influence of treatment with diet alone on oral glucose-tolerance test and plasma sugar and insulin levels in patients with maturity-onset diabetes mellitus. 4 96

Isolated, small intestinal microvillous membranes from normal and acutely diabetic rats were compared with respect to D-glucose transport. D-Glucose was accumulated to a greater extent by diabetic membrane vesicles when supplied with energy in the form of a NaC1 or a NaSCN gradient across the vesicle membrane. The difference appeared to be caused by an ability of the diabetic membranes to maintain a higher driving force for active D-glucose transport and not by changes in the glucose "carrier." Increasing the glucose-independent Na-+-conductance of the membrane with monactin or gramicidin D reduced the active accumulation of D-glucose by membrane preparations from both control and diabetic groups. Concentrations of monactin and gramicidin D in the incubation medium of membrane vesicles from diabetic animals could be adjusted so that their D-glucose transport became indistinguishable from that of membranes from normal animals not treated with ionophores. These observatins suggest the microvillous membranes as one site where changes occur in acute diabetes. In addition, the change in the transport properties of the isolated membranes offer a rational explanation for the simultaneous elevation of active intestinal sugar, amino acid, and bile salt transport observed for intact intestinal tissue.
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PMID:Diabetes mellitus: changes in the transport properties of isolated intestinal microvillous membranes. 4 51

Serum-lipid concentrations and their relationship to blood-glucose and serum-insulin were examined in non-insulin-requiring diabetics, 62 with and 45 without retinopathy. The age, sex-body-weight, and duration of known diabetes was comparable in the two groups. All were treated by diet only or diet and oral hypoglycaemic agents. Patients with retinopathy had higher fasting serumtriglyceride and serum--cholesterol levels than those without. Compared with a non-diabetic population, significantly more diabetics with retinopathy had raised derum-lipids. The lipid concentrations did not correlate with body-weight, serum-thyroid-stimulating-hormone levels, renal involvement, or fasting blood-sugar. While the blood-sugar concentrations were similiar in the two groups the absolute insulin increment and the relative insulin response to a 50 g. oral glucose load were significantly lower in those with retinopathy than in those without. The impairment of insulin response correlated significantly with the frequency of hyperlipidaemia. It is suggested that insulin deficiency with secondary hyperlipidaemia is characteristic of diabetic patients with retinopathy.
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PMID:Plasma-lipids and glucose/insulin relationship in non-insulin-requiring diabetics with and without retinopathy. 4 69


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