Estrogen restores disordered lipid metabolism in visceral fat of prediabetic mice

BACKGROUND Visceral obesity is increasingly prevalent among adolescents and young adults and is commonly recognized as a risk factor for type 2 diabetes.Estrogen[17β-estradiol(E2)]is known to offer protection against obesity via diverse me-chanisms,while its specific effects on visceral adipose tissue(VAT)remain to be fully elucidated.AIM To investigate the impact of E2 on the gene expression profile within VAT of a mouse model of prediabetes.METHODS Metabolic parameters were collected,encompassing body weight,weights of visceral and subcutaneous adipose tissues(VAT and SAT),random blood glucose levels,glucose tolerance,insulin tolerance,and overall body composition.The gene expression profiles of VAT were quantified utilizing the Whole Mouse Genome Oligo Microarray and subsequently analyzed through Agilent Feature Extraction software.Functional and pathway analyses were conducted employing Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses,respectively.RESULTS Feeding a high-fat diet(HFD)moderately increased the weights of both VAT and SAT,but this increase was mitigated by the protective effect of endogenous E2.Conversely,ovariectomy(OVX)led to a significant increase in VAT weight and the VAT/SAT weight ratio,and this increase was also reversed with E2 treatment.Notably,OVX diminished the expression of genes involved in lipid metabolism compared to HFD feeding alone,signaling a widespread reduction in lipid metabolic activity,which was completely counteracted by E2 adminis-tration.This study provides a comprehensive insight into E2's local and direct protective effects against visceral adiposity in VAT at the gene level.CONCLUSION In conclusion,the present study demonstrated that the HFD-induced over-nutritional challenge disrupted the gene expression profile of visceral fat,leading to a universally decreased lipid metabolic status in E2 deficient mice.E2 treatment effectively reversed this condition,shedding light on the mechanistic role and therapeutic potential of E2 in combating visceral obesity.

11β-hydroxysteroid dehydrogenase types 1 and 2. in postnatal development of rat testis： gene express,on, localization and regulation by luteinizing hormone and androgens

11β-hydroxysteroid dehydrogenase type 1 （11β-HSD1） and type 2 （11β-HSD2） are expressed in rat testis, where they regulate the local concentrations of glucocorticoids. Here, we investigated the expression and localization of 11β-HSD in rat testis during postnatal development, and the regulation of these genes by luteinizing hormone （LH） and androgens, mRNA and protein levels were analyzed by quantitative real-time-polymerase chain reaction and western blotting, respectively, in testes collected from rats at postnatal day （PND） 7, 14, 21, 35, and 90, and from rats treated with LH, 7α.methyl-19-nortestosterone （MENT） and testosterone at PND 21 and PND 90. Immunohistochemical staining was used to identify the localization of the 11β-HSD in rat testis at PND 7, 14, and 90. We found that 11β-HSD1 expression was restricted to the interstitial areas, and that its levels increased during rat testis development. In contrast, whereas 11β-HSD2 was expressed in both the interstitial areas and seminiferous tubules at PND 7, it was present only in the interstitial areas at PND 90, and its levels declined during testicular development. Moreover, 11β-HSD1 mRNA was induced by LH in both the PND 21 and 90 testes and by MENT at PND 21, whereas 11β-HSD2 mRNA was induced by testosterone and MENT in the PND 21 testis and by LH in the PND 90 testis. In conclusion, our study indicates that the 11β-HSD1 and 11β-HSD2 genes have distinct patterns of spatiotemporal expression and hormonal regulation during postnatal development of the rat testis.

Effect of miR-184 and miR-205 on the tumorigenesis of conjunctival mucosa associated lymphoid tissue lymphoma through regulating RasL10B and TNFAIP8

AIM:To explore the effect of miR-184 and miR-205 on the proliferation and metastasis of conjunctival mucosa associated lymphoid tissue(MALT)lymphoma.METHODS:Tissue of tumor and adjacent normal control from 5 patients with conjunctival MALT was included.RPMI8226 cell line was selected to verify the effect of mi RNAs in B cells.The function of micro RNA on the RPMI8226 cell apoptosis,migration and invasion was evaluated by apoptosis assay and Transwell assay.The m RNA and protein expression were examined by quantitative RT-PCR and Western blotting.The effect of micro RNA on regulation of downstream gene expression was evaluated by luciferase report assay.RESULTS:A decreased level of miR-184 and miR-205 was observed in MALT lymphoma tissue.Exogenous miR-184 and miR-205 analogues promoted apoptosis,and inhibited the survival,migration,and invasion of RPMI8226 cells.miR-184 and miR-205 inhibitor reversed the process.The RNA and protein level of Ras L10 B and TNFAIP8 were downregulated in MALT lymphoma tissue.The exogenous of miR-184 and miR-205 promoted the expression of Ras L10 B and TNFAIP8.Meanwhile,inhibition of miR-184 and miR-205 repressed the expression of target gene,Ras L10 B and TNFAIP8.CONCLUSION:miR-184 and miR-205 suppresses the tumorigenesis of conjunctival MALT lymphoma through regulating Ras L10 B and TNFAIP8.

Human PRV Infection in China: An Alarm to Accelerate Eradication of PRV in Domestic Pigs

Pseudorabies,also known as Aujeszky's disease,is one of the most economically important viral diseases in pigs and is lethal to other susceptible animals(Ren et al.2020).The causative agent,pseudorabies virus(PRV),is an enveloped virus with a large double-stranded DNA genome encoding at least 70 proteins(Wong et al.2019).PRV belongs to the family Herpesviridae,subfamily Alphaherpesvirinae,genus Varicellovirus and infects multiple animals,such as pigs,dogs,cats,rabbits,cattle,sheep,goats,minks.

Identification of a novel mutation in the SRD5A2 gene of one patient with 46,XY disorder of sex development

Dear Editor, 46,XY disorder of sex development （DSD） is characterized by a female phenotype in an individual with a normal 46,XY karyotype.1 The clinical phenotTpe of 46,XY DSD is characterized by bilateral undescended testes and a normal female appearance, including breasts, female external genitalia, and other secondary sex characteristics, but the absence of a uterus or ovaries.2 Development of the male external genitalia in the fetal period depends on the biosynthesis of testosterone （T）, the conversion ofT into dihydrotestosterone （DHT） by steroid 5α-reductase type 2 （SRD5A2）, and the response of functionally active androgen receptors in genital tissues） The disruption of any of these stages will block the differentiation of internal and external genitalia and cause 46,XY DSD.