Disease relevance of Diabetes Mellitus, Experimental

• Effect of insulin-like growth factor I infusion on renal hypertrophy in experimental diabetes mellitus in rats [1].
• The presence of genetic hypertension stimulates early renal accumulation of fibronectin in experimental diabetes mellitus [2].
• Histologically, the testes with the highest weights appeared normal, those with the lowest weights atrophic with few degenerating Leydig cells. these hypothalamic-hypophyseal changes are probably responsible for the testicular lesions found in experimental diabetes mellitus and may have relevance to the problem of infertility in human diabetes [3].
• Endogenous levels of nerve growth factor (NGF) are altered in experimental diabetes mellitus: a possible role for NGF in the pathogenesis of diabetic neuropathy [4].
• In conclusion, our results demonstrate that the antihypertensive drug urapidil has no detrimental effect on hyperglycemia compared with the angiotensin-converting enzyme inhibitor ramipril in experimental diabetes mellitus despite its 5-HT1A receptor agonistic properties [5].

High impact information on Diabetes Mellitus, Experimental

• After 19-d maternal insulinopenic diabetes (streptozotocin), placental GLUT3 mRNA and protein levels were increased four-to-fivefold compared to nondiabetic rats, whereas GLUT1 mRNA and protein levels remained unmodified [6].
• Levels increased in STZ-induced (streptozotocin) diabetes and were suppressed to normal with insulin treatment [7].
• Differential tissue regulation of insulin-like growth factor binding proteins in experimental diabetes mellitus in the rat [8].
• To study the effect of glucagon neutralization on urea synthesis in diabetic rats, animals with newly induced (75 mg/kg streptozocin) experimental diabetes mellitus were divided into two groups [9].
• Alloxan exhibits the most potent diabetogenicity and has been used for induction of experimental diabetes mellitus [10].

Chemical compound and disease context of Diabetes Mellitus, Experimental

• Effects of polyol-pathway inhibition and dietary myo-inositol on glomerular hemodynamic function in experimental diabetes mellitus in rats [11].
• Streptozocin (STZ) and alloxan (ALX) exhibit the most potent diabetogenicity and are used for induction of experimental diabetes mellitus [12].
• Absent or delayed preovulatory luteinizing hormone surge in experimental diabetes mellitus [13].
• Experimental diabetes mellitus inhibits prostacyclin synthesis by the rat penis: pathological implications [14].
• Aminoguanidine treatment reduces the increase in collagen stability of rats with experimental diabetes mellitus [15].

Biological context of Diabetes Mellitus, Experimental

• The former was performed by incubating commercially available hemoglobin with 5 and 20 mmol/l glucose and the latter through experimentally induced (streptozotocin) diabetes in an animal model (male Wistar rats) to identify the new fluorophore formed due to the nonenzymatic glycosylation of hemoglobin [16].
• Renin and angiotensinogen gene expression in experimental diabetes mellitus [17].
• However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental diabetes mellitus is only partly related to the increased diuresis [18].
• Reversal, by treatment with an aldose reductase inhibitor, of impaired axonal transport and motor nerve conduction velocity in experimental diabetes mellitus [19].
• Altered dose-to-effect of propofol due to pharmacokinetics in rats with experimental diabetes mellitus [20].

Anatomical context of Diabetes Mellitus, Experimental

• It was concluded that, in experimental diabetes mellitus in the rat, there is an accumulation of substances in the glomerular basement membrane and mesangium with an affinity for wheat germ agglutinin, most probably N-acetyl glucosamine, and this is partially prevented by insulin treatment [21].
• Blood-brain barrier glucose transporter mRNA is increased in experimental diabetes mellitus [22].
• This study was designed to explore effects of experimental diabetes mellitus on expression of substance P in the trigeminal ganglion and of nerve growth factor (NGF) in the iris [23].
• Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus [24].
• Reactivity of tracheal smooth muscles in albino rats with experimental diabetes mellitus treated with a new complex compound of oxovanadium (IV) and isonicotinic acid hydrazide [25].

Gene context of Diabetes Mellitus, Experimental

• We have recently shown that experimental diabetes mellitus is associated with an increase in glomerular expression of the cyclin kinase inhibitor p21WAF1/CIP1 (p21) [26].
• In experimental diabetes mellitus, several reports describe overexpression of TGF-beta or TGF-beta type II receptor in the glomerular and tubulointerstitial compartments [27].
• Despite the clear memory-correlated alterations in IR signaling pathways, insulin deficits in experimental diabetes mellitus (DM) rats induced by intraperitoneal injections of streptozotocin resulted in only minor memory impairments [28].
• It has been shown that experimental diabetes mellitus increases renal ET-1 gene transcription [2] [29].
• The data suggest that the nephroprotective actions of the ACE inhibitor lisinopril in experimental diabetes mellitus were associated with and thus could be mediated in part by inhibition of diabetes-induced activation of PKC beta isoenzymes in the renal cortex [30].

Analytical, diagnostic and therapeutic context of Diabetes Mellitus, Experimental

• Fluorophotometry was used to evaluate the integrity of the blood-ocular barriers to fluorescein in experimental diabetes mellitus in rats [31].
• 1. The effect of experimental diabetes mellitus (DM; hyperglycaemic, non-ketototic; 2 months duration) in the rat on receptor-linked prostacyclin (PGI2) synthesis (measured as 6-oxo-PGF1 alpha by radioimmunoassay) was studied in the aorta and urinary bladder using adrenaline, angiotensin II (AII) and acetylcholine (ACh) [32].
• The concentration of CA-III in the liver, muscles and serum of rats with experimental diabetes mellitus was measured by the method of enzyme-immunoassay [33].
• METHODS--One year after induction of experimental (streptozotocin) diabetes in rats, six diabetic animals together with six age-matched control animals were sacrificed and the retinas fixed for transmission electron microscopy (TEM) [34].
• Dietary self-selection and circulating metabolic fuels (glucose, free fatty acids, ketones) were examined in three forms of experimental diabetes mellitus in rats: pancreatectomy and streptozotocin treatment in adult and neonatal rats [35].

References