Disease relevance of C12285

• In TNF inhibitor recipients, mucosal permeability to sucralose was similar to that in nonirradiated control mice and significantly less than in recipients of the control adenovirus [1].
• During test meals with sucralose, one episode of symptomatic hypoglycemia occurred in each of three IDDM patients, but these episodes were not considered the result of sucralose administration [2].
• Sucralose, as a sole carbon source, was unable to support growth of ten strains of oral bacteria and dental plaque [3].
• Four groups of 12 Sprague-Dawley rats were infected with Streptococcus mutans (sobrinus), caged in a König-Höfer programmed feeding machine, and fed diet 2000 or modified diet to contain sucralose at various concentrations instead of sucrose [4].
• The incorporation of 126 mmol/L sucralose into glucose agar medium caused total inhibition of growth of Streptococcus sobrinus 6715-17, Streptococcus sanguis 10904, Streptococcus sanguis Challis, Streptococcus salivarius, and Actinomyces viscosus WVU627 [3].

Psychiatry related information on C12285

• There were marked individual differences in sucralose preferences: about half the rats preferred sucralose to water at some concentrations while most remaining rats avoided sucralose [5].

High impact information on C12285

• Mucosal permeability to sucralose and colonic histology were assessed 14 and 25 days after transplantation [1].
• In the United States, four potently sweet artificial sweeteners are approved, namely, saccharin, aspartame, acesulfame potassium, and sucralose [6].
• OBJECTIVE: To examine the effect of a single high oral dose of the novel noncaloric sweetener sucralose on short-term glucose homeostasis in patients with IDDM or NIDDM [2].
• Sugarcane ShSUT1: analysis of sucrose transport activity and inhibition by sucralose [7].
• Sucralose had no effect on IPS production [3].

Chemical compound and disease context of C12285

• Sucralose is the active compound of the most commonly sold sweetener in the United States. Different than aspartame, sucralose is not considered to be a migraine trigger [8].

Biological context of C12285

• Sucralose metabolism and pharmacokinetics in man [9].
• Sucralose: lack of effects on sperm glycolysis and reproduction in the rat [10].
• Neurotoxicity studies on sucralose and its hydrolysis products with special reference to histopathologic and ultrastructural changes [11].
• Quantification of AUC in the various groups showed that sucralose with coffee had no statistically significant impact on plaque acidogenesis [12].
• The teratogenic potential of sucralose was examined following gavage administration to pregnant rats and rabbits during organogenesis [13].

Anatomical context of C12285

• A minisensor for the rapid screening of sucralose based on surface-stabilized bilayer lipid membranes [14].
• Subsequent studies specifically designed to investigate the potential for adverse immune system effects of sucralose ([McNeil,]) showed no adverse effects [10].
• No changes were detected in the central nervous system by light or electron microscopy in either of the species that received sucralose or its hydrolysis products [11].
• The non-nutritive sweeteners acesulfame-K, aspartame, cyclamate, saccharin and sucralose were tested for DNA damaging activity in the rat hepatocyte/DNA repair assay [15].

Associations of C12285 with other chemical compounds

• This work describes an electrochemical technique that is suitable for the rapid and sensitive screening of the sweetener sucralose based on surface-stabilized bilayer lipid membranes (s-BLMs) composed of egg phosphatidylcholine [14].
• 51Cr-EDTA and lactulose correlated in basal 0-6 h permeability testing (r = 0.529, P < 0.0001), as did 6-24 h excretion of 51Cr-EDTA and sucralose (r = 0.474, P < 0.001); 97% and 90% of the subjects had a permeability increase after indomethacin intake for 0-6 h and 6-24 h excretion of Cr-EDTA, respectively [16].
• One urinary metabolite was detected after both intravenous and oral doses and was identified by mass spectrometry as a glucuronic acid conjugate of sucralose [17].
• Additional information can be gained when sucralose is administered in combination with lactulose and a monosaccharide such as L-rhamnose in the form of a 'triple sugar test.' We describe a simple assay for urinary sucralose by HPLC with refractive index detection (HPLC-RI) [18].
• The %Delta in FC were compared to %Delta in BWG after 52 weeks on study in one saccharin (825 rats), two sucralose (480 rats), two neotame (630 rats), and five dietary restriction (>1000 rats) studies [19].

Gene context of C12285

• Our earlier work demonstrated that the sweetener sucralose, C12 H19 CI3 O8, mixed with water had no effect on intraoral plaque pH [12].

Analytical, diagnostic and therapeutic context of C12285

• These studies establish that sucralose is non-toxic in rodents following acute oral administration [20].
• The metabolic and pharmacokinetic profile of sucralose was studied in human volunteers [9].
• These teratology studies in both pregnant rodent and non-rodent animal models demonstrate that maternal consumption of high levels of sucralose during the period of organogenesis has no effect on normal foetal development in the rat or rabbit [13].
• Determination of the artificial sweetener Sucralose by capillary electrophoresis [21].
• Similarly, haematology, serum biochemistry, urinalysis and EKG tracings were unaffected by sucralose administration [22].

References