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PedAM

Pediatric Disease Annotations & Medicines




Disease hyperglycemia
Symptom |diabetes
Sentences 382
PubMedID- 26355954 Due to hyperglycemia in diabetes, reducing sugars react non-enzymatically with free amino groups of protein to form a diverse group of protein-bound moieties known as ages (3).
PubMedID- 22611498 Endothelial dysfunction associated with insulin resistance appears to precede the development of overt hyperglycemia in patients with type 2 diabetes mellitus .
PubMedID- 22211582 Efficacy of protamine zinc recombinant human insulin for controlling hyperglycemia in dogs with diabetes mellitus.
PubMedID- 26287417 However, auc measurements for hypoglycemia (glucose <3.9 mmol/l) were not statistically significant.a ppb-r-203-based diet reduced postprandial hyperglycemia in patients with type 2 diabetes without increasing the risk of hypoglycemia or glucose excursion.
PubMedID- 24857350 Background: chorea is a common presenting feature of metabolic disorders, including nonketotic hyperglycemia in patients with type 2 diabetes mellitus, but rarely has been reported in diabetic ketoacidosis, hypothyroidism and vitamin b12 deficiency.
PubMedID- 25883713 Therefore, dpp-4 inhibitors may be useful in the management of hyperglycemia in patients with glucocorticoids-induced diabetes, which is characterized by normal or mild increase in fasting plasma glucose levels and a remarkable increase in postprandial glucose levels.
PubMedID- 22187476 Unexplained hyperglycemia in a patient with type 1 diabetes may suggest impending dka, and monitoring of ketones should therefore be performed.
PubMedID- 25847066 diabetes involves the state of chronic hyperglycemia caused by a range of genetic and environmental factors, and it is widely considered as one of the risk factors for periodontal disease (1).
PubMedID- 22332001 The hyperglycemia associated with type 2 diabetes also appears to impair gap junctional communication between astrocytes as shown in (1) cultured astrocytes harvested from 1-day-old wistar-hanover rats and exposed to high glucose, and (2) brain slices from 20-to-24-week-old stz rats .
PubMedID- 22973412 Chronic hyperglycemia exposes patients with type 1 diabetes to an increased risk for death if left untreated.
PubMedID- 21115768 Subjects who had at least one ogtt performed during the study period were identified as having normal glucose tolerance (ngt), igt, cystic fibrosis–related diabetes without fasting hyperglycemia (cfrd fh−) or cfrd with fasting hyperglycemia (cfrd fh+) by standard definitions (table 1).
PubMedID- 22911800 hyperglycemia in diabetes mellitus damages blood vessels and induces vascular complications in the retinal, renal, and cardiovascular tissues .
PubMedID- 25729706 The response of α-cell to hyperglycemia in diabetes is blunted or vanishing, and plasma glucagon remains inappropriately excessive at comparable blood glucose levels.
PubMedID- 22154739 We hypothesized that et-1-induced vasoconstriction is augmented in type 2 diabetes with hyperglycemia through an increment in advanced glycation end-products (ages).
PubMedID- 23670996 It is hoped that targeting therapy at the metabolic perturbations underlying hyperglycemia in patients with type 2 diabetes will have a similar benefit (27).
PubMedID- 24404519 While many studies have reported that psychiatric stress aggravates hyperglycemia in diabetes 3, the pattern and extent of hyperglycemia induced by psychiatric stress and the difference in the amount of psychiatric stress-induced hyperglycemia between normal and diabetic subjects remain unknown.
PubMedID- 25560829 hyperglycemia associated with type 1 diabetes is a consequence of immune-mediated destruction of insulin producing pancreatic beta-cells.
PubMedID- 21152193 The hyperglycemia associated with diabetes can lead to modifications of macromolecules, for example, ldl, by forming advanced glycation end products (age), which can bind to surface receptors, such as rage (receptor for ages) .
PubMedID- 24967064 Chronic hyperglycemia in diabetes stimulates reactive oxygen species (ros) production with development of microangiopathic complications such as diabetic retinopathy (dr) and diabetic nephropathy (dn) (1).
PubMedID- 26126619 In contrast to injection of stz to adult rats in a lower dose (60 mg/kg) that leads to type 1 diabetes with severe hyperglycemia , administration of stz to neonatal rats in a higher dose (90–100 mg/kg) leads to acute hyperglycemia within the first few days without resulting in complete loss of insulin production .
PubMedID- 23690866 In addition, high fructose consumption progresses to dietary model of type 2 diabetes that is associated with obesity, ir, hyperglycemia, and dyslipidemia 2.
PubMedID- 21354306 hyperglycemia in patients with type 2 diabetes causes multiple neuronal complications, e.g., diabetic polyneuropathy, cognitive decline, and embryonic neural crest defects due to increased apoptosis.
PubMedID- 24250607 Several drugs such as sulfonylureas and biguanides are presently available to reduce hyperglycemia in diabetes mellitus.
PubMedID- 22777596 Cortical location of the lesion, hemorrhagic transformation, and hyperglycemia in patients without diabetes are important predictors of es.
PubMedID- 22439599 hyperglycemia in patients with type 2 diabetes places them at significant risk for cardiovascular events and other diabetic complications .
PubMedID- 22187469 As retinopathy is estimated to take at least 5 years to develop after the onset of hyperglycemia, patients with type 1 diabetes should have an initial dilated and comprehensive eye examination within 5 years after the onset of diabetes.
PubMedID- 23209008 Finally, it attempts to integrate these mechanisms into the schema of pathophysiological factors that combine to produce hyperglycemia in patients with diabetes mellitus.
PubMedID- 23264286 At the onset, kpd often appears as type 1 diabetes with acute hyperglycemia and ketosis or ketoacidosis and the obvious need for insulin therapy but the signs of autoimmunity against islet β-cells are absent.
PubMedID- 21525431 These results suggest that hyperglycemia in diabetes downregulated trpc6 protein expression in mcs through a nadph oxidase nox4-ros-pkc pathway, proving a mechanism for impaired mc contraction in diabetes.
PubMedID- 24672797 The hyperglycemia in diabetes is associated with an increased risk for plasma hypercoagulability 3.
PubMedID- 25905210 The hyperglycemic hyperosmolar state (hhs) is a life-threatening metabolic decompensation of diabetes which presents with severe hyperglycemia and profound dehydration, typically accompanied by alteration in consciousness ranging from lethargy to coma.
PubMedID- 23378622 In early diabetes, before the onset of microalbuminuria, mild hyperglycemia and activation of the intrarenal renin-angiotensin-aldosterone system (raas) may lead to oxidative stress at the postglomerular capillary level (25,26).
PubMedID- 23737732 This mouse spontaneously exhibits type 2 diabetes, associated with mild hyperglycemia, mild glucose intolerance, mild hyperinsulinemia, mild obesity, and mild microalbuminuria.
PubMedID- 21266043 Chronic hyperglycemia in diabetes, through the nonenzymatic glycation of free amino groups in proteins by glucose, leads to the formation of labile schiff base intermediates that undergo amadori rearrangement, leading to the relatively stable early adducts ketoamine or fructosamine (so-called amadori products).
PubMedID- 26453314 However, hif-1 signaling is inhibited in diabetes due to hyperglycemia-induced hif-1alpha destabilization and functional repression.
PubMedID- 23264422 As retinopathy is estimated to take at least 5 years to develop after the onset of hyperglycemia, patients with type 1 diabetes should have an initial dilated and comprehensive eye examination within 5 years after the onset of diabetes.
PubMedID- 22224063 1 chronic hyperglycemia during diabetes causes glycation of body proteins that in turn leads to secondary complications disturbing eyes, kidneys, nerves, and arteries.
PubMedID- 22260979 Although hyperglycemia associated with diabetes mellitus is well known to enhance ros production in vascular endothelial cells, the effects of either acute or chronic high glucose environments on neurons and glial cells remain unclear.
PubMedID- 20876838 Managing hyperglycemia in patients with type 2 diabetes mellitus: rationale for the use of dipeptidyl peptidase-4 inhibitors in combination with other oral antidiabetic drugs.
PubMedID- 24454371 Our study showed that fasting hyperglycemia, mostly associated with type 2 diabetes, was the only significant predictor of vascular calcifications in esrd patients.
PubMedID- 24137241 This rat model successfully imitated human type ii diabetes, with moderate hyperglycemia, hypertension, dyslipidemia and insulin resistance.
PubMedID- 23087670 Persistent hyperglycemia in patients with diabetes may activate another lipogenic transcription factor, carbohydrate response element binding protein (chrebp; iizuka et al., 2004; dentin et al., 2006; ma et al., 2006; postic et al., 2007; davies et al., 2008).
PubMedID- 21896927 A history of type 1 diabetes manifestation with acute hyperglycemia and ketonuria; type 1 diabetes of <3 months duration; positive results for at least two of the three islet antibodies, glutamic acid decarboxylase, protein tyrosine phosphatase, or islet cell antibodies; and residual basal fasting c-peptide of >0.1 nmol/l (for two of the studies) and >0.2 nmol/l (for the other two studies) were required for subjects to be enrolled (11–13).
PubMedID- 24324393 While frank autonomic neuropathy almost certainly contributes to the altered vagal sensory and motor functions observed in chronic diabetes, the actions of acute hyperglycemia to modulate vagal afferent and efferent functions (macgregor et al., 1976; shi et al., 2003; takahashi et al., 2003; zhou et al., 2008) suggests that poor glycemic control per se also negatively impacts vagal reflex functions.
PubMedID- 21464443 The effects of leptin on hyperglycemia in mice with stz-induced diabetes are acute.
PubMedID- 20971966 Given that a lack of suppression of glucagon secretion contributes to hyperglycemia in individuals with type 2 diabetes (47), the development of a physiologically regulated human α-cell line may have significant utility as a screening tool for the identification of novel therapeutics that suppress glucagon secretion.
PubMedID- 26244639 Non-enzymatic glycation or maillard reaction is known to be a significant contributor to the onset of hyperglycemia-induced pathologies associated with diabetes, and perhaps the chronic pathologies associated with aging and neurodegeneration .
PubMedID- 26055217 Dipeptidyl peptidase-4 (dpp-4) inhibitors increase active glucagon-like peptide-1 (glp-1) and glucose-dependent insulinotropic polypeptide (gip) by inhibiting dpp-4 enzymatic activity, and improve hyperglycemia in patients with diabetes in a glucose-dependent manner by increasing insulin secretion 2.
PubMedID- 26015297 In addition to hyperglycemia, patients with type 2 diabetes have hyperinsulinemia as a result of insulin-resistance.
PubMedID- 22580727 The pathogenesis of nafld remains obscure, but it has been hypothesized that hepatic fat accumulation in type 1 diabetes may be due to lipoprotein abnormalities, hyperglycemia-induced activation of the transcription factors carbohydrate response element-binding protein (chrebp) and sterol regulatory element-binding protein 1c (srebp-1c), upregulation of glucose transporter 2 (glut2) with subsequent intrahepatic fat synthesis, or a combination of these mechanisms.

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