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

Epinephrine raises plasma lactate concentrations when infused intravenously in normal subjects. We studied a patient with non-insulin-dependent diabetes mellitus who developed lactic acidosis and marked insulin resistance when treated with epinephrine after open heart surgery.
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PMID:Lactic acidosis and insulin resistance associated with epinephrine administration in a patient with non-insulin-dependent diabetes mellitus. 363 50

This study evaluated the association between intraocular pressure and various sociodemographic characteristics, ocular findings, and cardiovascular risk factors in a population screened for glaucoma. A total of 2594 subjects older than 40 years residing in three urban areas of southern Israel participated. Of those screened 6.1% had a raised intraocular pressure (IOP greater than or equal to 21). The mean IOP increased with age, was higher among persons born in Africa or Asia than those born in Europe or America, higher among myopes than hypermetropes and among those with an enlarged cup-disc ratio (CDR). Analysis of variance tests indicated that refractive status, CDR, age, country of birth, and diabetes were each independently associated with IOP. In addition, associations between raised intraocular pressure and age, country of birth, myopia, CDR, diabetes, and glaucoma in the family were found.
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PMID:Epidemiology of intraocular pressure in a population screened for glaucoma. 367 47

The effect of physical training on glucose, insulin, and glucagon response to epinephrine was assessed in normal and diabetic rats. Male Wistar rats were injected with streptozocin (STZ, 45 mg/kg) and those presenting 1 wk later a blood glucose value between 250 and 400 mg/dl were retained in the protocol and randomly assigned to a sedentary or trained group. Similar studies were conducted in control animals. Physical training was done on a treadmill according to a 10-wk program. Epinephrine (0.75 microgram/kg/min) was infused intravenously (i.v.) in previously cannulated rats for 1 h and arterial blood samples obtained at 15-min intervals for glucose, insulin, and glucagon measurements. Pancreatic insulin and glucagon content was also determined. Basal glucose levels were significantly lower in trained than in sedentary diabetic rats (P less than 0.01). The hyperglycemic response to epinephrine was diminished by 19% and 23% in trained control and diabetic animals, respectively, with a faster return to baseline after stopping epinephrine infusion in both trained groups. Although in nondiabetic rats this could be related to some diminution in the suppressive effect of epinephrine on insulin secretion, this was not the case in diabetic animals. Moreover, while training did not modify epinephrine-induced glucagon response in control rats, the twofold greater (P less than 0.01) glucagon response observed in sedentary diabetic rats was restored to normal in trained diabetic rats. After stopping epinephrine infusion, glucagon levels dropped below the baseline in both groups of trained rats but not in their sedentary counterparts. These effects of training on glucagon response could not be explained by changes in pancreatic glucagon content.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Dec
PMID:Diminished glucagon response to epinephrine in physically trained diabetic rats. 390 62

The clinical course of eight boys and six girls with Addison's disease has been reviewed. Adrenal antibodies were found in five boys and five girls, and four children showed clinical evidence of other autoimmune disease (hypoparathyroidism (three); diabetes (one)). The presentation was insidious in 12 children but acute in two. On treatment, linear growth was normal and, with the exception of one girl with theca cell antibodies, pubertal development proceeded normally in the older patients.
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PMID:Clinical presentation, growth, and pubertal development in Addison's disease. 406 44

Adrenal cortical response in acute medical illness has been studied by measuring the plasma 11-hydroxycorticosteroid (11-OHCS) concentration in 178 patients. Those with unbalanced diabetes, acute infections, and severe myocardial infarction had high levels. The results obtained suggest that in a patient with a severe infection and hypotension a plasma 11-OHCS level of less than 15 mug./100 ml. indicates an inadequate adrenal cortical response, and one patient with septicaemia and temporary adrenal cortical insufficiency is described. Growth hormone levels were increased in patients with severe diabetic ketosis but not in those with hyperosmolar non-ketotic diabetic coma.
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PMID:Plasma 11-hydroxycorticosteroid and growth hormone levels in acute medical illnesses. 579 69

Epinephrine (0.1 micrograms.kg-1.min-1) was infused with or without somatostatin (0.1 microgram.kg-1.min-1) in six depancreatized dogs, studied under normo- and hypoinsulinemia to determine whether the participation of glucagon in epinephrine-induced hepatic glucose overproduction is governed by the degree of metabolic control. When normoglycemia was achieved by basal intraportal insulin replacement, insulin levels remained constant during the epinephrine infusion, and there was a twofold increase in extrapancreatic immunoreactive glucagon (eIRG) and glucose production (Ra). Although eIRG increments were prevented by somatostatin, the increase in Ra was undiminished, indicating that epinephrine can act independently of glucagon as in normal animals. During subbasal intraportal insulin infusion in the depancreatized dogs, insulin levels remained 35% lower than with basal replacement, and the animals were hyperglycemic. Epinephrine induced a similar twofold increase in eIRG as during normoglycemia, and again this rise was prevented by somatostatin. There was a significantly greater, threefold increase in Ra with epinephrine when the animals were hyperglycemic. This exaggerated response to epinephrine was not seen during eIRG suppression by somatostatin, suggesting that glucagon participated in the epinephrine-induced hepatic glucose overproduction when the depancreatized dogs were in poor metabolic control, as seen previously in alloxan-diabetic dogs. However, in the depancreatized, unlike in the alloxan-diabetic dogs, epinephrine-induced glucagon release was small. Thus, hypoinsulinemia appears to sensitize the liver to eIRG during epinephrine infusion. The fact that epinephrine induces hyperglycemia both in physiology and diabetes could indicate an important role in enhancing glucose transport in insulin-insensitive tissues.
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PMID:State of metabolic control determines role of epinephrine-glucagon interaction in glucoregulation in diabetes. 612 26

Simultaneous treatment with antidiabetic drugs and beta-adrenoceptor blocking agents is frequent on account of the high incidence of diabetes and cardiovascular disease. The effects of oral doses of pindolol, metoprolol, and propranolol on the response to insulin-induced hypoglycemia and an oral glucose load were investigated. During hypoglycemia metoprolol and propranolol inhibited the clearance of insulin (2 p less than 0.01) and caused a delay of glucose nadirs. This was not observed after pindolol. Epinephrine secretion and the counterregulatory response of growth hormone, ACTH and cortisol during hypoglycemia was significantly increased following metoprolol and propranolol but not after pindolol. The hypoglycemic symptoms and signs showed a prevalence of sweating and prolonged changes in skin conductivity while palpitations were not observed during beta-blockade. Asymptomatic hypoglycemia did not occur.
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PMID:Beta-adrenoceptor blocking agents induce different counter-regulatory responses to insulin. 613 71

The effect of elevated plasma epinephrine concentrations (approximately equal to 800 pg/ml) on ketone body kinetics was determined in postabsorptive normal subjects using primed-continuous infusions of 3-14C-acetoacetate. Infusion of epinephrine (60 ng/kg/min) resulted in a transient increase in total ketone body production to a maximum of 2.5-fold the basal rate within 45 min (P less than 0.01 versus controls). Ketone body uptake increased with a delay, compared with production, causing a 2.8-fold increase in total ketone body concentrations (P less than 0.05 versus controls). Plasma free fatty acid (FFA) and blood glycerol concentrations increased transiently during epinephrine; their course was similar to that of ketone body production. Epinephrine administration resulted in hyperglycemia, hyperlactatemia, and a modest increase in plasma insulin and glucagon concentrations. To assess epinephrine's effect on ketone body kinetics during lack of insulin, and to avoid epinephrine-induced alterations in plasma insulin and glucagon concentrations, epinephrine was also infused combined with somatostatin (6.5 micrograms/kg/h). During somatostatin infusion, epinephrine administration resulted in an enhanced and sustained elevation of total ketone body production from 4.4 +/- 0.8 to 15.1 +/- 1.2 mumol/kg/min (P less than 0.01 versus somatostatin alone). Ketone body concentrations increased markedly from 310 +/- 63 to 1763 +/- 137 mumol/L (P less than 0.01 versus somatostatin alone); the ketonemic effect was enhanced due to a 40% decrease of the metabolic clearance rate associated with somatostatin infusion. The increase in plasma FFA and blood glycerol concentrations during somatostatin-induced insulin deficiency was transiently enhanced by epinephrine, such that they increased to 3.2- and 5.6-fold their basal values after 45 min, respectively (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1984 Aug
PMID:Effect of epinephrine and somatostatin-induced insulin deficiency on ketone body kinetics and lipolysis in man. 614 45

Previously we reported that the heart norepinephrine concentration was markedly increased in diabetic rats. To further study the relationship between a disturbance in the autonomic nervous system and catecholamine metabolism in diabetes mellitus, the plasma catecholamine response to stress and catecholamine concentration of heart and adrenals were measured. Wistar male rats were made diabetic by streptozotocin and kept for 13 weeks. A silicon catheter was placed in the superior V. cava 1 week prior to the experiment. Insulin was injected subcutaneously for 3 days once daily. After an overnight fast and without anesthesia, 1 ml of blood, a control sample, was obtained and then the animals were exsanguinated. The blood was mixed with 1 mM EGTA at a final concentration and centrifuged. The tissue was homogenized with 0.4 N perchloric acid containing 1 mM EGTA and centrifuged at 10,000 x g for 20 minutes. Catecholamines were determined by high performance liquid chromatography. Normal rats responded to blood withdrawal stress, and plasma catecholamines were markedly increased, but almost no increase or an actual decrease was observed in diabetic rats. These abnormal responses were improved by insulin treatment. Heart norepinephrine was increased significantly in the diabetic rats compared with the control rats and was reduced significantly by insulin injections. Adrenal epinephrine was also significantly increased in the diabetic rats compared with the control rats, but was not significantly reduced by insulin. These result suggest a possible disturbance of catecholamine secretion in the diabetic rats.
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PMID:Decreased response of plasma catecholamine to stress in diabetic rats. 622 22

Isolated perfused hearts from control Bio-Breeding/Worcester (BB/W) rats and spontaneously diabetic BB/W rats were studied to determine whether metabolic abnormalities that are expressed in alloxan-diabetic rats in the regulation of enzymes involved in glycogen metabolism could be observed in this non-chemically induced insulin-deficient rat. Perfusion of hearts from control rats with 10(-8) M insulin for 10 min resulted in activation of glycogen synthase (30% synthase I without insulin to 44% synthase I with insulin). Perfusion of hearts from BB/W diabetic rats demonstrated a lack of acute synthase activation with insulin and a 45% decrease in synthase phosphatase activity. Perfusion of hearts from BB/W diabetic rats with 0.28 microM epinephrine for 1 min resulted in a greater activation of phosphorylase (44% phosphorylase a) than that observed in BB/W control hearts (31% phosphorylase a) perfused under the same conditions. Epinephrine produced similar changes in cyclic AMP accumulation, protein kinase activation, and phosphorylase kinase activation in perfused hearts of BB/W control and diabetic rats. Further, phosphorylase phosphatase activities were not changed by epinephrine or insulin deficiency. These studies further document metabolic abnormalities in the BB/W diabetic rat that are attributable to insulin deficiency in a non-chemically induced model for insulin-dependent diabetes.
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PMID:Altered regulation of cardiac glycogen metabolism in spontaneously diabetic rats. 631 7


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