MiR-146b is a regulator of human visceral preadipocyte proliferation and differentiation and its expression is altered in human obesity.

Visceral obesity is an independent risk factor for metabolic syndrome, and abnormal fat accumulation is linked to increases in the number and size of adipocytes. MiR-146b was a miRNA highly expressed in mature adipocytes while very lowly expressed in human mesenchymal stem cells (hMSCs) and human visceral preadipocytes (vHPA). In this paper, we mainly focused on the roles of miR-146b in adipogenesis. We found miR-146b could inhibit the proliferation of visceral preadipocytes and promote their differentiation. MiR-146b in human visceral adipocytes inhibited the expression of KLF7, a member of the Kruppel-like transcription factors, as demonstrated by a firefly luciferase reporter assay, indicating that KLF7 is a direct target of the endogenous miR-146b. MiR-146b expression was significantly altered in visceral and subcutaneous adipose tissues in human overweight and obese subjects, and in the epididymal fat tissues and brown fat tissues of diet-induced obese mice. Our data indicates that miR-146b may be a new therapeutic target against human visceral obesity and metabolic dysfunction.

Metformin prevents LYRM1-induced insulin resistance in 3T3-L1 adipocytes via a mitochondrial-dependent mechanism.

We previously proposed that LYR motif containing 1 (LYRM1)-induced mitochondrial reactive oxygen species (ROS) production contributes to obesity-related insulin resistance. Metformin inhibits ROS production and promotes mitochondrial biogenesis in specific tissues. We assessed the effects of metformin on insulin resistance in LYRM1-over-expressing 3T3-L1 adipocytes. Metformin enhanced basal and insulin-stimulated glucose uptake and GLUT4 translocation, reduced IRS-1 and Akt phosphorylation and ROS levels, and affected the expression of regulators of mitochondrial biogenesis in LYRM1-over-expressing adipocytes. Metformin may ameliorate LYRM1-induced insulin resistance and mitochondrial dysfunction in part via a direct antioxidant effect and in part by activating the adenosine monophosphate-activated protein kinase (AMPK)-PGC1/NRFs pathway.

Knockdown of LYRM1 rescues insulin resistance and mitochondrial dysfunction induced by FCCP in 3T3-L1 adipocytes.

LYR motif-containing 1 (LYRM1) was recently discovered to be involved in adipose tissue homeostasis and obesity-associated insulin resistance. We previously demonstrated that LYRM1 overexpression might contribute to insulin resistance and mitochondrial dysfunction. Additionally, knockdown of LYRM1 enhanced insulin sensitivity and mitochondrial function in 3T3-L1 adipocytes. We investigated whether knockdown of LYRM1 in 3T3-L1 adipocytes could rescue insulin resistance and mitochondrial dysfunction induced by the cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP), a mitochondrion uncoupler, to further ascertain the mechanism by which LYRM1 is involved in obesity-associated insulin resistance. Incubation of 3T3-L1 adipocytes with 1 µM FCCP for 12 h decreased insulin-stimulated glucose uptake, reduced intracellular ATP synthesis, increased intracellular reactive oxygen species (ROS) production, impaired insulin-stimulated Glucose transporter type 4 (GLUT4) translocation, and diminished insulin-stimulated tyrosine phosphorylation of Insulin receptor substrate-1 (IRS-1) and serine phosphorylation of Protein Kinase B (Akt). Knockdown of LYRM1 restored insulin-stimulated glucose uptake, rescued intracellular ATP synthesis, reduced intracellular ROS production, restored insulin-stimulated GLUT4 translocation, and rescued insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt in FCCP-treated 3T3-L1 adipocytes. This study indicates that FCCP-induced mitochondrial dysfunction and insulin resistance are ameliorated by knockdown of LYRM1.

Untangling the transcriptome from fungus-infected plant tissues.

The development of sequencing technology allows low-cost generation of sequence data. The huge amount of raw sequence data now available has introduced many challenges associated with analysis of these large-scale data banks. For example, it is very important to distinguish materials of plant and fungal origin in fungus-infected plant tissue. The origin of transcripts that were sequenced from Library 895-M6 (poplar tissue infected by Marssonina brunnea) on Illumina/Solexa GA IIx was determined by combining three methods: (1) based on the taxonomic information of homologous sequences; (2) based on the reference genome sequence; (3) based on the transcriptome sequence of the host and its pathogen obtained from Library 895 (poplar) and Library M6 (M. brunnea) as well as Library 895-M6 (mixture of poplar and M. brunnea). We idenified accurately the origin of 80,978 (99.5%) contigs in the mixed poplar and M. brunnea sample (Library 895-M6) by integrating the results from the three methods. The results of this study demonstrate that a combination of these three approaches described here is an effective strategy for determining the origin of sequences in a mixed pool, and provides a basis for further transcriptome analysis of the mixed sample.

[Study of the correlation between the colorectal cancer Chinese medicine syndrome types and (excision repair cross-complementing 1, ERCC1) gene polymorphisms].

OBJECTIVE: To explore the correlation between excision repair cross-complementing 1 (ERCC1) C8092A and C19007T gene polymorphisms and different Chinese medicine (CM) syndrome types of colorectal cancer (CC). METHODS: Ninety-nine patients with CC were syndrome typed as dampness-heat accumulation syndrome, qi stagnation with blood stasis syndrome, Pi-Shen yang deficiency syndrome, and Gan-Shen yin deficiency syndrome. The gene polymorphisms of excision repair cross-complementing 1 (ERCC1) C8092A and C19007T in different CM syndrome types of CC were examined by polymorphisms chain reaction amplification and direct sequencing, and analyzed statistically. RESULTS: The frequencies of C8092A genotype and allele in different CM syndrome types had no statistical difference (P > 0.05). The frequencies of C19007T genotype and allele in different CM syndrome types had statistical difference (P < 0.05). Of them, there was no statistical difference in the frequencies between dampness-heat accumulation syndrome and qi stagnation with blood stasis syndrome, or between Pi-Shen yang deficiency syndrome and Gan-Shen yin deficiency syndrome (P > 0.05). There was statistical difference between dampness-heat accumulation syndrome and Pi-Shen yang deficiency syndrome as well as Gan-Shen yin deficiency syndrome (P < 0.05). There was statistical difference between qi stagnation with blood stasis syndrome and Pi-Shen yang deficiency syndrome as well as Gan-Shen yin deficiency syndrome (P < 0.05). CONCLUSION: ERCC1 C19007T gene polymorphisms might be associated with CM syndrome types of CC, which needed to be further studied.