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While indicating that diabetogenic mechanism effects of iAs exposure is different from the mechanism associated with traditional risk factors -reduced type 2 diabetes, Insulin resistance it’s interesting that iAs exposure could improve the insulin sensitivity on the basis of the insulin lerance testing by glucose activation ‘uptakerelated’ genes and enzymes in normal and diabetic anybody. Even though iAs exposure did not change glucose lerance in normal mice, it caused the pancreatic βcell dysfunction and increased gluconeogenesis and oxidative damages in liver. Our data suggested that iAs exposure could cause pre diabetic effects by altering the lipid metabolism, gluconeogenesis and insulin secretion in normal individual, and worsen diabetic effects in diabetes individual by these processes. In this study, we compared inorganic influences arsenic on normal and diabetic mice by systems xicology approaches.
IAs exposure worsened the glucose lerance in diabetic mice, that might be since increased gluconeogenesis and impairment of pancreatic βcell function. Arsenic roles on development of diabetes are unclear.
The type 2 diabetes makes up more than 90percent of all diabetes casesEstablished risk factors for T2D, similar to genetics, diet and lifestyle, do not fully explain the increase in this disease.
Certainly, So there’s considerable interest in understanding nontraditional contribution risk factors to the diabetes epidemic, including environmental pollutants3, Among these environmental pollutants, arsenic exposure is paid much attentionAs is an ubiquitous xic metalloid in the environment. 500 µg/L3, Although some other researches concluded that the existing data were insufficient in support of an association between As and T2D10, data from human studies support an association between As and diabetes in population with arsenic ‘drinkingwater’ levels of gt. Needless to say, epidemiological studies carried out in Bangladesh6, Taiwan7, Mexico8, and United States9 have shown a strong diabetogenic effect of As in human populations mainly through As contaminated drinking water.
The mice were exposed to iAs or deionized water for 16 weeks.
Seven week old male C57BKS/Leprdb mice were purchased from Model Animal Research Center of Nanjing University. You must take this seriously. Considering the above said. Oxidative stress and damage, enzyme activities, gene expression profiles, and metabolic profiles in mice were determined. Following acclimation for one week, 16 db/db mice were randomly assigned to two groups. Certainly, all mice were housed in ‘stainlesssteel’ cages under controlled conditions with 25 ± 3°C, 50 ± 5percent humidity and 12/12 h light/dark cycle. With all that said… The diabetes related endpoints, including blood glucose levels, glucose tolerance, and insulin lerance were analyzed. It’s a well c57BLKS/J db/m mice were chosen as normal control mice. It is with all that said. A well-known fact that is. The sodium arsenite solution was prepared every week to minimize oxidation of As to As. One group was fed with deionized water, and another group with 3 mg/L sodium arsenite solution. Sodium arsenite was obtained from National Standard Material Center. Also, the gluconeogenesis, lipid metabolism, insulin resistance and function of ‘βcell’ were also analyzed. Notice that body weights were determined almost any two weeks. Exposure duration was 16 weeks. Besides, the metabolic profiles in db/db mice exposed to iAs had higher similarity with those in db/db control mice, that were different with those in db/m mice with or without iAs exposure -reduced type 2 diabetes. Besides, the protocol was approved by the Committee on Animal Ethics Nanjing Experiments Military General Hospital. With all that said. Daily water consumption was measured in all exposure groups. Anyway, As roles on diabetes development were characterized, depending on above information. Anyways, all experimental processes were in accordance with NIH Guide for the Care and Use of Laboratory Animals.
Blood glucose was measured as described for the OGTT.
Now let me tell you something. Glucose was dissolved in diH2O and orally administered to the fasted mice. The ITT was conducted by intraperitoneal injection of 5 U/kg body weight insulin. Actually, blood samples were collected from tail to measure the glucose levels before and 15, 30, 60, 90, and 120 min after glucose administration. Nevertheless, urine and feces samples were collected each two weeks and kept at −80° High performance liquid chromatography coupled with inductively coupled plasma mass spectrometry methods described by Van de Wiele et al50 were applied to detect and quantify iAs, iAs, MMA and DMA in urine and feces.