المؤلفون: YUCHI ZHANG, DONGWEI HAN, PENGYANG YU, QIJING HUANG, PENGLING GE

المصدر: Experimental & Therapeutic Medicine; Mar2017, Vol. 13 Issue 3, p1044-1050, 7p

مصطلحات موضوعية: DIABETES, OBESITY, MICE, MESSENGER RNA, GENE expression, MEDICAL research

مستخلص: Diabetes mellitus is one of the primary diseases that pose a threat to human health. The focus of the present study is type II diabetes (T2D), which is caused by obesity and is the most prevalent type of diabetes. However, genome-scale transcriptional analysis of diabetic liver in the development process of T2D is yet to be further elucidated. Microassays were performed on liver tissue samples from three-, six- and nine-week-old db/db mice with diabetes and db/m mice to investigate differentially expressed mRNA. Based on the results of genome-scale transcriptional analysis, five genes were screened in the present study: chromobox 8 (CBX8), de-etiolated homolog 1 and damage specific DNA binding protein 1 associated 1 (DDA1), Phosphoinositide-3-kinase regulatory subunit 6 (PIK3R6), WD repeat domain 41 (WDR41) and Glycine Amidinotransferase (GATM). At three weeks of age, no significant differences in levels or ratios of expression were observed. However, at six and nine weeks, expression of CBX8, DDA1, PIK3R6 and WDR41 was significantly upregulated (P<0.05) in the db/db model group compared with the control group, whereas GATM expression was significantly downregulated (P<0.05). These results suggest that T2D-related differential expression of genes becomes more marked with age, which was confirmed via reverse transcription-quantitative polymerase chain reaction. Genome-scale transcriptional analysis in diabetic mice provided a novel insight into the molecular. events associated with the role of mRNAs in T2D development, with specific emphasis upon CBX8, DDA1, PIK3R6, GATM and WDR41. The results of the present study may provide rationale for the investigation of the target genes of these mRNAs in future studies. [ABSTRACT FROM AUTHOR]

: Copyright of Experimental & Therapeutic Medicine is the property of Spandidos Publications UK Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: JIAMING XIE, YUAN JIANG, YUNA KAN, JING ZHAO, HAIXUE KUANG, PENGLING GE

المصدر: Molecular Medicine Reports; 2015, Vol. 12 Issue 2, p2043-2048, 6p

مصطلحات موضوعية: CALCIUM, LABORATORY rats, INSULIN resistance, HIGH-calcium diet, ADIPOSE tissues

مستخلص: A high-fat diet not only leads to obesity, but also leads to a predisposition towards insulin resistance (IR), which is characterized by hyperinsulinemia and reduced glucose tolerance. However, the etiology of IR remains to be fully elucidated. The present study investigated whether calcium-sensing receptor (CaSR) is involved in the development of IR in rats fed a high-fat diet. IR was induced in the rats by feeding with a fat emulsion via gavage for 2, 4, 6 or 8 weeks. Reverse transcription-quantitative polymerase chain reaction (RT-q-PCR) and western blot analysis were performed to investigate whether CaSR-associated proteins were affected. The gavage of fat emulsion for 8 weeks induced a notable decline in the insulin sensitivity index (ISI) between -4.98 and -5.60. With 6 weeks of gavage, a significant difference in the ISI was observed between the IR and control groups. The results of the RT-qPCR and western blot analysis demonstrated that phosphatidylinositol 3-kinase/Akt pathway, which is a pathway closely associated with the CaSR signaling pathway, was significantly inhibited in the rats with IR. The results of the present study provided evidence that CaSR is associated with the development of IR in rats fed a high-fat diet and suggested that CaSR may be important in the pathogenesis of diabetes. [ABSTRACT FROM AUTHOR]

: Copyright of Molecular Medicine Reports is the property of Spandidos Publications UK Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)