Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 12-year follow-up study of 610 persons (239 black and 371 white) in Evans County, Georgia, psychologic distress as measured by total score on the Health Opinion Survey, a 20-item questionnaire, was a predictor of mortality. The hazard ratio, comparing the 95th percentile score with the median, was 1.93 (97.5% confidence interval (CI) 1.42-2.62), controlling for age, race, and sex; there was no interaction with these variables. A purer measure of distress symptomatology, based on 18 of the questionnaire items, was also predictive of mortality. The hazard ratio was 1.94 (97.5% Cl 1.33-2.82), controlling for age, race, sex, and the item, "Do you have any sickness or illness problems at the present time?"; no interactions with the latter variables were found. This pattern was not affected in any major way by several modifications of the analyses: 1) controlling also for smoking, serum cholesterol, Quetelet index (weight (kg)/height (m)2), diastolic blood pressure, a social network index, and a social class index; 2) excluding persons with a diagnosis (in 1968) of chronic heart disease, angina pectoris, myocardial infarction, stroke, transient cerebral ischemic attach, or diabetes mellitus, or whose deaths were due to neoplastic disease; and 3) restricting the analyses to the last half of the follow-up period to explore the role of incipient or early physical illness in producing the association. With the restricted samples, confidence intervals included 1.00, which may be attributed to both the substantially smaller samples and the slightly reduced strength of the effect. The evidence is consistent with a causal role for psychologic distress, as measured by the Health Opinion Survey, in subsequent mortality rates.
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PMID:Psychologic distress as a predictor of mortality. 281 89

The effects of streptozotocin-induced diabetes on the retinal dopaminergic system have been examined in Long-Evans (pigmented) rats. Tyrosine hydroxylase activity was significantly decreased while dopamine-stimulated adenylate cyclase was increased in 2-month-diabetic rats. The observed increase in dopamine-stimulated adenylate cyclase activity in diabetic retinae may be related to neurotransmitter receptor changes because postreceptor activation of adenylate cyclase by guanylyl imidodiphosphate was not altered.
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PMID:Dopamine-stimulated adenylate cyclase and tyrosine hydroxylase in diabetic rat retina. 286 Sep 52

A single high dose of streptozotocin was found to cause a transient increase in islet capillary permeability 2-4 h after administration. Staining of areas of increased vascular permeability by Evans blue showed that islets, but not exocrine tissue, were affected. The permeability increase seems to involve vasoactive substances released by mast cells. A mast cell inhibitor (disodium cromoglycate) and a serotonin antagonist (methysergide) were found protective. Furthermore, administration of methysergide partially prevented the development of hyperglycaemia in streptozotocin-treated rats. In mice, almost full protection from diabetes development was reached by both methysergide and disodium cromoglycate. Our observations indicate an important role of mast cell controlled membrane permeability in this model of beta-cell destruction and diabetes development.
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PMID:Diabetogenic action of streptozotocin: essential role of membrane permeability. 294 74

The effects of streptozotocin (STZ)-induced diabetes on acetaminophen metabolism and hepatotoxicity in male Sprague-Dawley (SD) and Long Evans Hooded (LEH) rats were compared. In agreement with earlier studies, normal SD rats were more resistant to acetaminophen-induced hepatic necrosis than normal LEH rats. In contrast to LEH rats, the diabetic state did not protect SD rats from liver injury. Pharmacokinetic studies revealed that normal SD rats eliminated acetaminophen faster than normal LEH rats, and that the diabetic state further enhanced elimination in both strains of rats; however, the effect was much greater in LEH rats. Normal SD rats had a greater capacity to metabolize acetaminophen to nontoxic glucuronide and sulfate conjugates than normal LEH rats. In LEH rats, the diabetic state enhanced acetaminophen glucuronidation and sulfation, whereas in SD rats the diabetic state increased only sulfation; glucuronidation was unaffected. Additional studies revealed that the difference in the glucuronidation capacities between normal LEH and normal SD rats was not due to differences in either the amount of the enzyme, glucuronyl transferase, or basal hepatic levels of the cofactor, UDPGA. Similarly, the diabetes-induced enhancement of glucuronidation in LEH rats was not due to differences in predrug levels of either glucuronyl transferase or UDPGA. Thus, the major difference in susceptibility of the two strains of normal rats to acetaminophen hepatotoxicity appears to be due to the capacity to clear the drug through nontoxic pathways. The greater glucuronidation capacity seen in diabetic LEH rats and in normal and diabetic SD rats as compared to normal LEH rats, appears to be due to a greater ability to produce UDPGA in response to the metabolic demand.
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PMID:Strain differences in susceptibility of normal and diabetic rats to acetaminophen hepatotoxicity. 308 Oct 10

The hormonal milieu of the testis was examined in streptozocin-induced diabetic (STZ-D) adult male Wistar and Long-Evans rats. Serum testosterone, creatinine, and urea nitrogen (BUN) levels and blood glucose concentrations were determined in diabetic and control Wistar rats (experiment 1). These parameters plus luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were studied in experiments 2 and 3 with Long-Evans rats in untreated diabetic, control, insulin-treated diabetic, nondiabetic STZ-injected, and semistarved groups. Wistar diabetic rats had significantly decreased serum testosterone and increased blood glucose, BUN, and serum creatinine compared with controls. Several findings in Long-Evans rats suggested the existence of a primary Leydig cell defect in steroidogenesis during untreated diabetes that was completely or partially compensated for by increased pituitary gonadotropin secretion. Serum LH and FSH levels increased in Long-Evans diabetic rats. Serum testosterone was significantly reduced only in experiment 2. These hormonal alterations from control levels were not seen in insulin-treated diabetic animals. Semistarved animals, weight matched to the diabetic group in experiment 2, had significantly decreased serum testosterone and increased FSH levels. In addition, Long-Evans diabetic rat BUN and serum creatinine levels increased much less or were unchanged from control values compared with the increase noted in diabetic Wistar rats. In light of the hypogonadism that complicates clinical uremia, these findings suggest the more apt use of the Long-Evans strain rather than the Wistar strain in the study of STZ-D hypogonadal function.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1987 Oct
PMID:Primary hypoandrogenism in experimental diabetes in the Long-Evans rat. 311 51

Spontaneous diabetes was fully prevented in 65 BB/hooded (BB/h) highly diabetes-prone hybrid rats that were given five intraperitoneal injections (25 to 30 x 10(6) cells/injection) of fresh splenocytes or concanavalin A (ConA)-activated cultured splenocytes (blasts) from the diabetes-free Wistar-Furth or Long-Evans strains during the first 2 postnatal wk. Rats remained under observation for up to the age of 180-200 days. Of 70 littermate controls that received no cell injections, 63 developed overt diabetes before the age of 180 days. One intraperitoneal injection (25 x 10(6) cells) of splenocytes or blasts given during the first 36 h after birth was not as effective as multiple injections in preventing overt diabetes. Mild insulitis was present in 4 of 59 "protected" rats; small, discrete mononuclear infiltrates in periductular connective tissue and/or between pancreatic acini were observed in 27. Nondiabetic BB/h rats that were protected with splenocytes or blasts from diabetes-free strains had the same degree of lymphopenia in peripheral blood and spleen as age-matched, insulin-treated diabetic BB/h rats, but the level of islet cell surface antibodies in their serum was significantly lower. The same neonatal injections that protected rats from the development of spontaneous diabetes were completely ineffective in preventing the adoptive transfer of diabetes later in life by the injection of blasts from acutely diabetic BB/h rats.
Diabetes 1988 Aug
PMID:Prevention of spontaneous but not of adoptively transferred diabetes by injection of neonatal BB/hooded hybrid rats with splenocytes or concanavalin A blasts from diabetes-free strains. 339 42

The purpose of this study was to establish the correlation between the genetically determined rate of acetylation of certain drugs and the development of diabetic neuropathy. Acetylator phenotype was determined according to Evans in 100 healthy individuals and 160 diabetics including 80 patients with type I and 80 with type II diabetes. The diagnosis of diabetic neuropathy was based on clinical neurological examination. In addition, electrostimulation was carried out in 49 diabetics. Among the healthy controls, the fast acetylator phenotype was found in 44 cases (44%) and the slow one in 56 (56%). In type I diabetes these values were 51 (64%) and 29 (36%), in type II 46 (58%) and 34 (42%), respectively. The predominance of fast acetylators in type I diabetes was statistically significant (p less than 0.01) when compared to the healthy population of Warsaw. However, no significant correlation was found between diabetic neuropathy and the distribution of acetylator phenotype. Further prospective studies are necessary in order to ascertain whether the acetylator phenotype might be considered a genetic marker of type I diabetes.
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PMID:Acetylator phenotypes in diabetes mellitus. 340 76

Brattleboro rats lacking vasopressin have an elevated plasma osmolality and a stimulated renin-angiotensin system relative to Long-Evans rats (LE). The current studies were performed to elucidate the factors controlling water and salt intake in the Brattleboro rat with diabetes insipidus (DI). DI and LE rats were given the choice of water and saline solutions ranging from 0.1-1.0% to assess palatability, dialyzed with isotonic glucose to test for sodium appetite after sodium depletion, and infused intracranially with an angiotensin II analogue (saralasin) to assess the role of angiotensin II in spontaneous salt and water intake. DI rats exhibited spontaneous salt intake which was not significantly different from LE rats and increased their intake of 3.0% NaCl following sodium depletion, although less reliably than LE rats. A significant proportion of those DI rats not developing a sodium appetite showed attenuation of their diabetes following dialysis. No evidence for involvement of angiotensin II in spontaneous salt and water intake was found.
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PMID:Salt and water intake in Brattleboro rats with hypothalamic diabetes insipidus. 356 52

The purpose of the work was checking whether possible electrophysiological changes in peripheral nerves in diabetes were connected with acetylation phenotype. The authors determined the conduction velocity in peripheral nerves (medianus, peroneal, femoral, facial and sural) in 49 diabetics, divided into two groups depending on the acetylation phenotype determined by Evans method. The results failed to demonstrate differences in the frequency of neuropathy between both groups of acetylators.
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PMID:[Electrophysiologic changes in peripheral nerves in patients with 2 acetylation types of diabetes mellitus]. 360 Sep 72

The response to vasoactive agents of microvessels of the rat was tested in vivo by direct microscopic observation of the exteriorized mesentery and assessment of cutaneous vascular permeability changes with Evans blue. The constrictor response to a standard amount of noradrenaline in mesenteric microvessels was fully antagonized by acetylcholine in normal, diabetic, adrenalectomized and diabetic-adrenalectomized rats. In contrast, the minimum doses of histamine or bradykinin, effective in normal or adrenalectomized animals, had to be increased about 20 fold to be active in diabetic or diabetic-adrenalectomized animals. Topical application of insulin to mesenteric microvessels of diabetic animals, in amounts not causing any increase in serum insulin levels, improved or restored the capacity of the animals to respond to histamine or bradykinin, acting as antagonists of the vasoconstrictor response to noradrenaline. Topical insulin, however, was ineffective in normal animals given 2-deoxyglucose, the acute effects of which result from cellular glucopaenia unrelated to insulin deficiency. Vascular permeability responses to intracutaneous histamine or bradykinin were decreased in animals pretreated with 2-deoxyglucose as much as in diabetic animals. Pretreatment of normal animals with indomethacin produced no effect on the responses of these animals to histamine or bradykinin, tested as antagonists of noradrenaline on mesenteric microvessels, or as vascular permeability-increasing factors in the skin. Pretreatment of normal animals with chloroquine, mepacrine or dexamethasone had no effect on the reactivity of mesenteric microvessels to histamine and bradykinin, acting as antagonists to noradrenaline. 7 It is suggested that vasoactive substances, endowed with permeability-increasing properties, evoke relaxation of microvessels through an insulin-dependent action on endothelial cells, unrelated to the release of arachidonic acid metabolites. This action would lead to increased vascular permeability, with opening of interendothelial junctions, and temporary changes in composition of extravascular fluid, which in turn, would provide the basis for vasodilatation. Diabetes mellitus apparently impairs such responses as a result of the accompanying cellular glucopaenia. Adrenal corticosteroids are not involved in the impaired responses.
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PMID:Vascular reactivity in diabetes mellitus: possible role of insulin on the endothelial cell. 643 70


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