Role of microRNAs in the treatment of type 2 diabetes mellitus with Roux-en-Y gastric bypass

The aim of this study was to investigate the effect of Roux-en-Y gastric bypass (RYGB) on the peripheral blood microRNAs (miRNAs) of patients with type 2 diabetes mellitus (T2DM). miRNAs are small 20- to 22-nucleotide (nt) noncoding RNAs. They constitute a novel class of gene regulators that negatively regulate gene expression at the post-transcriptional level. miRNAs play an important role in several biological processes. Twelve patients with T2DM who were scheduled to undergo laparoscopic RYGB surgery were separated into two groups, using a body mass index of 30 kg/m2 as a cut-off point. Venous blood was collected before operation and 12 months after operation. A significant change was observed in the peripheral blood miRNA expression profile of both groups after RYGB surgery compared with those before operation. The expression levels of hsa-miR-29a-3p, hsa-miR-122-5p, hsa-miR-124-3p, and hsa-miR-320a were downregulated. The methylation state of the CpG sites within an approximately 400-bp genomic DNA fragment of each of the four miRNA genes, including about 200 bp upstream and 100 bp downstream of the pre-miRNA, did not vary after RYGB surgery. With remission of T2DM in both groups, RYGB could modulate the expression level of many peripheral blood miRNAs associated with lipid metabolism, insulin secretion, beta-cell function, and insulin resistance. The expression level of peripheral blood diabetes-related miRNA varied in patients with T2DM after receiving RYGB surgery, laying a strong foundation for future studies on this subject. The molecular mechanisms underlying RYGB surgery that can cause aberrant expression of miRNA remains to be determined.

Structure characterization of human cytomegalovirus UL131A, UL130 and UL128 genes in clinical strains in China.

Human cytomegalovirus (HCMV) genetic determinants of endothelial cell tropism, leukocytes and dendritic cells have been identified in the genes UL131A, UL130, and UL128. We examined the structure of these three genes in HCMV. Eighteen low-passage clinical isolates and five non-passage strains from congenitally HCMV-infected infants in China were used to assess the structures of the UL131A, UL130, and UL128 genes and to find possible relationships between sequence polymorphism and different signs of HCMV disease. Comparisons were made between the UL131A, UL130, and UL128 genes of clinical strains and published sequences of Towne and Merlin strains. The UL131A coding region in the clinical strains was similar to that of Towne and Merlin strains, while UL130, and UL128 coding regions in the clinical strains were parallel with those of Towne and Merlin, respectively. Sequence comparison indicated that the UL130, and UL128 genes encode chemokine-like proteins in the clinical strain; the transmembrane regions of UL131A, and UL130 were conserved in all clinical and reference strains. The three genes of clinical strains from infants with different signs of HCMV disease had similar structure characterization. We conclude that the UL131A, UL130, and UL128 genes are highly conserved in these clinical strains. No correlation was found between the structure of the three genes and variations in HCMV disease. The finding of chemokine-like domains in UL130, and UL128 putative proteins suggests that the predicted products play a role in HCMV infectivity.