Hyperglycemia Pathophysiology
Mostrando 1-8 de 8 artigos, teses e dissertações.
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1. The effect of increase in blood glucose level on hearing loss
Abstract Objective: Previous studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic em
Brazilian Journal of Otorhinolaryngology. Publicado em: 2022
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2. Hyperglycemia during acute myocardial infarction: pathophysiology correlations / Hiperglicemia no infarto agudo do miocárdio: correlações fisiopatológicas
Introduction- Hyperglycemia (HG) is an important prognostic factor in acute myocardial infarction (AMI). However, the pathophysiology is poorly understood. So we proposed a simultaneous correlation between glycemia and biochemical markers of stress, glucose and lipid metabolism, coagulation and inflammation system. Methods- Eighty AMI patients were included
Publicado em: 2009
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3. Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS
To investigate the pathophysiology of cerebral edema occurring during treatment of diabetic coma, the effects of hyperglycemia and rapid lowering of plasma glucose were evaluated in normal rabbits. During 2 h of hyperglycemia (plasma glucose=61 mM), both brain (cerebral cortex) and muscle initially lost about 10% of water content. After 4 h of hyperglycemia,
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4. The pathophysiology of experimental insulin-deficient diabetes in the monkey. Implications for pancreatic transplantation.
In an 11-year study of experimental insulin-deficient diabetes (IDDM) induced in rhesus monkeys by streptozotocin or total pancreatectomy, the authors have found that pathophysiologic changes occur in eye and kidney, which closely resemble the early stages of human insulin deficient diabetes mellitus (IDDM). In addition, morphologic changes of thickening of
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5. Mechanism by which hyperglycemia inhibits hepatic glucose production in conscious rats. Implications for the pathophysiology of fasting hyperglycemia in diabetes.
To examine the relationship between the plasma glucose concentration (PG) and the pathways of hepatic glucose production (HGP), five groups of conscious rats were studied after a 6-h fast: (a) control rats (PG = 8.0 +/- 0.2 mM); (b) control rats (PG = 7.9 +/- 0.2 mM) with somatostatin and insulin replaced at the basal level; (c) control rats (PG = 18.1 +/- 0
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6. Genes and pathophysiology of type 2 diabetes: more than just the Randle cycle all over again
The Randle cycle, which has been invoked to explain the reciprocal relationship between fatty acid oxidation and glucose oxidation, has long been implicated as a potential mechanism for hyperglycemia and type 2 diabetes mellitus (T2DM). Now genetic, functional genomic, and transgenic approaches have identified PPARγ coactivators (PGC-1α and PGC-1β) as key
American Society for Clinical Investigation.
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7. Transgenic Expression of Insulin-Response Element Binding Protein-1 in β-Cells Reproduces Type 2 Diabetes
Recent evidence supports the idea that insulin signaling through the insulin receptor substrate/phosphatidyl-inositol 3-kinase/Akt pathway is involved in the maintenance of β-cell mass and function. We previously identified the insulin-response element binding protein-1 (IRE-BP1) as an effector of insulin-induced Akt signaling in the liver, and showed that
The Endocrine Society.
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8. Diabetes mellitus and genetic prediabetes. Decreased replicative capacity of cultured skin fibroblasts.
The idea that the gene(s) that cause diabetes mellitus can be expressed in extrapancreatic cells has been examined by tissue culture techniques. Skin biopsies were obtained from 25 normal subjects (N), 26 overt diabetics (D), 16 of juvenile onset (JOD) and 9 of maturity onset (MOD), and 21 subjects genetically predisposed to diabetes (P) on the basis of matu