Background Promoting the thermogenic remodeling of white adipose tissue (WAT) is a promising strategy to combat obesity. Lipophagy degrades lipid droplets to supply free fatty acids that fuel thermogenesis in beige adipocytes. GDP dissociation inhibitor 2 (GDI2) is a negative regulator of Rab GTPases implicated in adipocyte lipid storage, but its role in lipophagy-mediated WAT browning has not been explored. This study aimed to characterize GDI2 as a novel regulator of lipophagy and beige fat thermogenesis. Methods The metabolic relevance of GDI2 was profiled in differentiated adipocytes, obese mouse models, thermogenic mouse models, and human subjects. Subcellular localization was determined by confocal microscopy and immunogold electron microscopy. Adipocyte-specific Gdi2 knockout mice were generated and subjected to cold exposure or β3-adrenergic stimulation, and assess thermogenic capacity. Stimulated lipolysis was evaluated in primary adipocytes, Gdi2 -knockout C3H10T1/2 cells, and ex vivo WAT explants. The lipophagy stage at which GDI2 acts was defined by immunoblotting, confocal imaging of lipid droplets with LC3B, autophagic inhibitor treatments, mCherry-EGFP-LC3B reporter, and transmission electron microscopy. RNA-seq was employed to profile downstream transcriptional adaptations. High-fat diet feeding was used to determine whether Gdi2 deficiency confers resistance to obesity and associated metabolic disorders. Results GDI2 expression is positively correlated with BMI in humans and is upregulated in the adipose tissue of obese mice, while it is suppressed by cold exposure. Adipocyte-specific deletion of Gdi2 in mice promotes cold-induced WAT browning and energy expenditure, and confers resistance to diet-induced obesity, insulin resistance, and hepatic steatosis. Mechanistically, GDI2 acts as a molecular brake on lipophagy by inhibiting the late-stage fusion of autophagosomes with lysosomes independently of the canonical neutral lipolysis pathway. Gdi2 deficiency releases this brake, accelerating the lipophagic degradation of lipid droplets and generating a robust supply of free fatty acids. These fatty acids serve as signaling ligands to activate a PPARα/PGC1α-dependent transcriptional program, driving thermogenic and mitochondrial oxidative phosphorylation gene expression to channel lipid flux into energy dissipation. Conclusions GDI2 functions as a key inhibitor of adipocyte lipophagy that restrains beige fat thermogenesis, positioning it as a potential therapeutic target to combat obesity and related metabolic disorders.

The biosensors based on metasurfaces have attracted significant attention for biological detection in the terahertz (THz) band due to the characteristics of rapid, label-free, and nondestructive. Benefiting from the low-loss characteristics of the electromagnetically induced transparency (EIT), we propose two single-band EIT meta-biosensors and a dual-band EIT meta-biosensor through various combinations of three designed T-shaped resonators that act as bright modes. By utilizing the excellent biocompatibility of gold nanoparticles (AuNPs), the proposed meta-biosensors modified with carcinoembryonic antigen (CEA) antibody-conjugated AuNPs achieve the specific detection of CEA within mixed tumor markers in the THz band, which indicates that the frequency shifts of the transparent peaks increase only with increasing CEA concentration, as the CEA antibody-conjugated AuNPs specifically capture the target antigens. Furthermore, we employ a mutual information feature extraction algorithm integrated with a support vector machine (SVM) to verify the discrimination of transmission spectra samples with different CEA concentrations, and the classification results show high intraclass consistency and clear interclass distinction. This work paves the way for the development of novel meta-biosensors with high sensitivity and specific target antigen recognition, which would provide technical support for cancer screening and disease diagnosis.

Background:Obesity, a prevalent metabolic disorder, is linked to perturbations in the balance of gene expression regulation. Noncoding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), play pivotal roles in regulating gene expression. The aim of this study was to identify additional ncRNA candidates that are implicated in obesity, elucidating their potential as key regulators of the pathogenesis of obesity. Methods:We identified distinct ncRNA expression profiles in omental adipose tissue in obese and healthy subjects through comprehensive whole-transcriptome sequencing. Subsequent analyses included functional annotation with GO and KEGG pathway mapping, validation via real-time quantitative polymerase chain reaction (qRT‒PCR), the exploration of protein‒protein interactions (PPIs), and the identification of key regulatory genes through network analysis. Results:The results indicated that, compared with those in healthy individuals, various lncRNAs, circRNAs, and miRNAs were significantly differentially expressed in obese subjects. Further verifications of top changed gene expressions proved the most genes' consistence with RNA-sequencing including 11 lncRNAs and 4 circRNAs. Gene network analysis highlighted the most significant features associated with metabolic pathways, specifically ENST00000605862, ENST00000558885, and ENST00000686149. Collectively, our findings suggest potential ncRNA therapeutic targets for obesity, including ENST00000605862, ENST00000558885, and ENST00000686149.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that several instances of duplicated data existed within several of the figures in this article; specifically: i) two pairs of data panels in the four‑panel Fig. 2B (so affecting all the panels in this figure part, which showed the results from migration and invasion assay experiments) were overlapping; ii) a pair of data panels for the fluorescence experiments shown in Fig. 4 were also found to be overlapping; and iii) one set of protein bands in the western blots featured in Fig. 5 (for the caspase‑3 data) had also been included in a paper submitted to and published in Oncology Reports a few months earlier, with the author Tao Sun held in common between these papers. Owing to the number of cases of data duplication that were identified in this paper, the Editor of Oncology Reports has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 2984‑2990, 2016; DOI: 10.3892/or.2016.4678].

IntroductionThe aim of this work is to investigate the inhibitory effect of aloperin (Alo) on hepatocyte apoptosis in non-alcoholic fatty liver disease, and the underlying mechanism.Material and methodsRats in the Alo groups were fed a high-fat + high-sugar diet for eight weeks and then treated with low-, moderate-, and high-dose Alo for another eight weeks via gavage. Oxidative stress indices were tested by a colourimetric method, and pathological changes were observed by haematoxylin–eosin staining. Apoptosis was detected by TUNEL staining. TLR4, TRIF, and NF-B(p65) mRNA and protein expressions were detected by RT-qPCR, Western blot assay and immunohistochemistry. In the in vitro study, L02 cells were treated with FFA (free fatty acid) for 24 h to establish a non-alcoholic steatohepatitis (NASH) model. Inhibition of cell proliferation was measured by the MTT method, and cell apoptosis was evaluated by flow cytometry. Finally, the nuclear import volume of NF-B(p65) was evaluated by cellular immunofluorescence.ResultsCell apoptosis significantly decreased in the Alo-treatment groups in a dose-dependent manner (p < 0.05). TLR4, TRIF, and NF-B(p65) expression in the Alo-treatment groups was significantly downregulated compared with model group (p < 0.05). The cell proliferation rate significantly increased, cell apoptosis significantly decreased (p < 0.05), and the TLR4/TRIF/NF-B pathway was significantly inhibited (p < 0.05) in the Alo-treatment groups. The nuclear import volume of NF-B(p65) in the Alo-treatment groups was significantly decreased compared with that in the model group in a dose-dependent manger (p < 0.05).ConclusionsAlo could improve NASH via the TLR4/TRIF/NF-B pathway.

Absent in melanoma 2 (AIM2) is a protein encoded by the AIM2 gene located on human chromosomes, AIM2 can recognize and bind to double stranded DNA (dsDNA), leading to the assembly of the AIM2 inflammasome. The AIM2 inflammasome plays important proinflammation role in many diseases, and can induce pyroptotic cell death. It has also been closely linked to the development and progression of metabolic diseases and can be activated in obesity, diabetes, nonalcoholic fatty liver disease, and atherosclerosis. In this article, we mainly review the role of AIM2 in glucose metabolism, especially in obesity-related disorders of glucose and lipid metabolism, and provide insights to better understand the role of AIM2 in the pathogenesis, and clinical treatment of metabolic disease.

Previous studies have demonstrated the regulatory roles of Transmembrane protein 147 (TMEM147) in various diseases, including cancer. However, systematic pan-cancer analyses investigating the role of TMEM147 in diagnosis, prognosis, and immunological prediction are lacking. An analysis of data from The Cancer Genome Atlas (TCGA) revealed differential TMEM147 expression across various types of cancer as well as within immune and molecular cancer subtypes. Moreover, high TMEM147 expression was associated with poor disease-specific survival (DSS), overall survival (OS), and progression-free interval (PFI) across cancers, suggesting its potential as a prognostic biomarker. Our study further revealed a significant correlation between TMEM147 expression and T helper cell and Tcm cell infiltration in most cancer types. In the case of liver hepatocellular carcinoma (LIHC), the effect of TMEM147 on prognosis varied among different clinical subtypes. Additionally, functional enrichment analysis revealed an association between TMEM147 and metabolic pathways. Finally, experiments on the MIHA cell line and four LIHC cell lines confirmed the role of TMEM147 in promoting liver cancer cell proliferation, further confirming the clinical value of TMEM147 in liver cancer diagnosis. Our findings suggest that TMEM147 may serve as a diagnostic and prognostic biomarker across cancers while also playing a significant role in LIHC.

Obesity has become a major global problem that significantly confers an increased risk of developing life-threatening complications, including type 2 diabetes mellitus, fatty liver disease and cardiovascular diseases. Protein arginine methyltransferases (PRMTs) are enzymes that catalyse the methylation of target proteins. They are ubiquitous in eukaryotes and regulate transcription, splicing, cell metabolism and RNA biology. As a key, epigenetically modified enzyme, protein arginine methyltransferase 1 (PRMT1) is involved in obesity-related metabolic processes, such as lipid metabolism, the insulin signalling pathway, energy balance and inflammation, and plays an important role in the pathology of obesity-related metabolic disorders. This review summarizes recent research on the role of PRMT1 in obesity-related metabolic disorders. The primary objective was to comprehensively elucidate the functional role and regulatory mechanisms of PRMT1. Moreover, this study attempts to review the pathogenesis of PRMT1-mediated obesity-related metabolic disorders, thereby offering pivotal information for further studies and clinical treatment.

Metabolic syndromes are characterized by various complications caused by disrupted glucose and lipid metabolism, which are major factors affecting the health of a population. However, existing diagnostic and treatment strategies have limitations, such as the lack of early diagnostic and therapeutic approaches, variability in patient responses to treatment, and cost-effectiveness. Therefore, developing alternative solutions for metabolic syndromes is crucial. N6-methyladenosine (m6A) is one of the most abundant modifications that determine the fate of RNA. m6A modifications are closely associated with metabolic syndrome development and present novel prospects for clinical applications. Aberrant m6A modifications have been detected during inflammatory infiltration, apoptosis, autophagy, iron sagging, necrosis, and scorching during metabolic syndrome pathogenesis and progression. However, few reviews have systematically described the correlation between m6A modifications and these factors concerning metabolic syndrome pathogenesis and progression. This study summarizes the m6A methylation regulators and their roles in metabolic syndrome development, highlighting the potential of m6A modification as a biomarker in metabolic disorders.

Objective·To detect the differences in m6A methylation modification and gene expression of liver tissue mRNA in high-fat diet-induced mouse models of non-alcoholic fatty liver disease (NAFLD) using microarray technology.Methods·The NAFLD models were established in 6-8 weeks old male C57BL/6J mice fed with high-fat chow for 16 weeks (high-fat group, n=10). The basal group (n=10) was given 10% fat diet. Hematoxylin-eosin (H-E) staining was used to assess the histopathological changes in liver tissue and to determine the success of the NAFLD models. The changes of mRNA m6A methylation and expression levels in the liver tissues of the two groups were detected by using methylated RNA immunoprecipitation (MeRIP) and microarray expression profiling.Results·The livers of the mice in the basal group were bright red with few fat deposits, while the livers of the mice in the high-fat group were yellowish with diffuse infiltration and fusion of lipid droplets in the hepatocytes by H-E staining, suggesting that the high-fat diet-induced NAFLD models were successfully constructed. The results of the MeRIP-microarray showed that the m6A methylation levels of 320 genes in the livers of mice in the high-fat group were significantly altered compared with those in the basal group (P<0.05 and fold change>1.5), of which 108 genes were up-regulated and 212 genes were down-regulated. Genes with significant differences in m6A methylation levels between the two groups were intersected with those with differentially expressed mRNAs, and 163 genes were found to have significant differences in both m6A methylation level and mRNA expression level.Conclusion·The change in m6A modification of liver tissue mRNA in the high-fat diet-induced mouse models of NAFLD is significant and the change is associated with the gene expression of mRNA.

Metabolic diseases have become a major threat to human health worldwide as a result of changing lifestyles. The exploration of the underlying molecular mechanisms of metabolic diseases and the development of improved therapeutic methods have been hindered by the lack of appropriate human experimental models. Organoids are three-dimensional in vitro models of self-renewing cells that spontaneously self-organize into structures similar to the corresponding in vivo tissues, recapitulating the original tissue function. Off-body organoid technology has been successfully applied to disease modelling, developmental biology, regenerative medicine, and tumour precision medicine. This new generation of biological models has received widespread attention. This article focuses on the construction process and research progress with regard to organoids related to metabolic diseases in recent years, and looks forward to their prospective applications.

The detection of circulating tumor microRNAs (miRNAs) holds great promise for the noninvasive and early-stage diagnosis of cancer. However, the low abundance of lung cancer-related miRNAs and the false-positive results of single miRNA detection limited the development of strip-based point-of-care testing methods in clinic. We developed a duplex-specific nuclease (DSN)-mediated and dual-AND logic gate-based triple-line lateral flow strip detection system for the rapid and simultaneous detection of four miRNAs of lung cancer in a single strip test. This system combines DSN-mediated signal amplification with AND logic gate-based simple signal output. Meanwhile, the limit of detection of this platform was calculated to be 26.51 fM. Furthermore, this assay was used to detect lung cancer-related miRNAs from serum in a homogeneous and separation-free format, which could discriminate lung cancer patients from healthy individuals with an accuracy of 100%. Our approach provides a simple and easy-to-handle method for the diagnosis of lung cancer in clinic.

Background Insulin resistance (IR) in hepatocytes endangers human health, and frequently results in the development of non-alcoholic fatty liver disease (NAFLD). Research on m(6)A methylation of RNA molecules has gained popularity in recent years; however, the molecular mechanisms regulating the processes of m(6)A modification and IR are not known. The cytochrome P450 (CYP450) enzyme system, which is mainly found in the liver, is associated with the pathogenesis of NAFLD. However, few studies have been conducted on CYP450 related m(6)A methylation. Here, we investigated the role of the methyltransferase METTL3 in exacerbating IR in hepatocytes, mainly focusing on the regulation of m(6)A modifications in CYP2B6.Methods and results Analysis using dot blot and epitranscriptomic chips revealed that the m(6)A modification pattern of the transcriptome in high-fat diet (HFD)-induced fatty liver and free fatty acid (FFA)-induced fatty hepatocytes showed significant changes. CYP450 family members, especially Cyp2b10, whose homolog in humans is CYP2B6, led to a noticeable increase in m(6)A levels in HFD-induced mice livers. Application of the METTL3 methyltransferase inhibitor, STM2457, increased the level of insulin sensitivity in hepatocytes. We then analyzed the role of METTL3 in regulating m(6)A modification of CYP2B6 in hepatocytes. METTL3 regulated the m(6)A modification of CYP2B6, and a positive correlation was found between the levels of CYP2B6 translation and m(6)A modifications. Furthermore, interference with METTL3 expression and exposure to STM2457 inhibited METTL3 activity, which in turn interfered with the phosphorylated insulin receptor substrate (pIRS)-glucose transporter 2 (GLUT2) insulin signaling pathway; overexpression of CYP2B6 hindered IRS phosphorylation and translocation of GLUT2 to membranes, which ultimately exacerbated IR.Conclusion These findings offer unique insights into the role that METTL3-mediated m(6)A modifications of CYP2B6 play in regulating insulin sensitivity in hepatocytes and provide key information for the development of strategies to induce m(6)A modifications for the clinical treatment of NAFLD.

Dynamic monitoring of tumor markers is an important way to the diagnosis of malignant tumor, evaluate the therapeutic effect of tumor and analyze the prognosis of cancer patients. As a tumor marker of digestive tract, CA242 is often used to Assess the therapeutic effect of colorectal cancer and pancreatic cancer. In this study, immunosensor technology was used to detect CA242. PdAgPt nanocomposites, which have great advantages in biocompatibility, electrical conductivity and catalytic properties, were prepared by hydrothermal synthesis method. The prepared PdAgPt nanocomposites were loaded onto the surface of molybdenum disulfide (MoS2) with large surface area, and the new nanocomposites were synthesized. Using PdAgPt/MoS2 as signal amplification platform, the label-free CA242 electrochemical immunosensor has a wide detection range that extends from 1*10−4 U/ml to 1*102 U/ml and a low detection limit (LOD, 3.43*10−5 U/ml) after optimization of experimental conditions. In addition, the CA242 immunosensor designed in this study also performed well in the evaluation of repeatability, selectivity and stability, and was successfully used for the detection of CA242 in human serum sample. Therefore, the label-free electrochemical immunosensor constructed in this study has a broad application prospect in the detection of clinical biomarkers.

非酒精性脂肪性肝病是我国常见的慢性肝脏疾病,并且随着生活水平的日渐提升其发病率逐年升高,严重影响人类健康.细胞色素P450是一种含血红素的酶,主要表达于肝脏,负责大多数药物的代谢,与代谢性疾病的发生、发展关系密切.该文旨在综述细胞色素P450家族基因的检测方法和细胞色素P450家族在非酒精性脂肪性肝病及其相关疾病中的作用及研究进展,为非酒精性脂肪性肝病及其相关疾病的发生和调控机制提供更多视角,并为细胞色素P450进一步的作用研究提供参考.

Objective: This meta-analysis comprehensively summarizes the current clinical research on compound glycyrrhizin (CG) treatment for liver cancer and protecting liver function to guide clinical treatment. Methods: Eighteen English-language articles were retrieved from PubMed, SinoMed, Cochrane, Embase, Web of Science, and three Chinese databases: The Wan Fang database, China National Knowledge Infrastructure (CNKI), and the VIP database. Results: CG treatment improved the patient's alanine aminotransferase (ALT) level (in the metastatic liver cancer group: mean deviation (MD) = −13.78, 95% confidence interval (CI) = [−17.29, 10.27]; in the primary liver cancer group: MD = −32.15, 95% CI = [−35.48, 28.81]); aspartate aminotransferase (AST) level (in the primary liver cancer group: MD = −21.63, 95% CI = [−24.29, 18.96]; in the metastatic liver cancer group: MD = −15.64, 95% CI = [−19.08, −12.20]); serum total bilirubin (TBIL) level (MD = −1.61, 95% CI = [−2.71, −0.51]); and serum albumin (ALB) level (MD = 2.80, 95% CI = [1.85, 3.74]). CG treatment was efficient than the control (relative risk [RR] = 1.66, 95% CI = [1.35, 2.04]). Although adverse reactions, including fever, were higher than in the control group (RR = 1.13, 95% CI = [0.89, 1.43]), they were controllable. Conclusion: CG affects liver preservation in treating liver cancer, which can reduce ALT, AST, and TBIL levels in patients; increase the ALB level; and protect liver cells. The CG-treated group showed improvement compared with the control group; although adverse reactions occurred in the treated group, the duration was shortened.

目的 探讨乙型肝炎(以下简称乙肝)患者干扰素(IFN)治疗效果与机体肥胖程度的关系,以及肥胖致IFN治疗乙肝不敏感的分子机制与炎症细胞因子的关系.方法 以肥胖作为唯一影响因素,通过文献检索,筛选并提取文献数据,经过RevMan软件作图分析,分析肥胖和IFN治疗乙肝敏感性的关系.选取2017-2021年于该院行IFN治疗的乙肝患者91例为研究对象,根据体质量指数(BMI)将其分为对照组(BMI≤25 kg/m2,61例)和肥胖组(BMI≥28 kg/m2,30例).跟踪IFN治疗48周,比较两组谷氨酸氨基转移酶(ALT)和乙肝表面抗原(HBsAg)水平.收集不同肥胖程度的健康查体人群血浆,分为A(BMI≤25 kg/m2)、B(BMI≥28 kg/m2)两组,借助流式细胞术检测炎症细胞因子[白细胞介素(IL)-2、IL-4、IL-6、IL-10、IL-12p70、IL-17、肿瘤坏死因子(TNF)-α、IFN-γ]水平,寻找A、B两组中差异有统计学意义的炎症细胞因子.体外培养稳定转染人HBV基因组的HepG 2.2.15细胞,IFNα2b与筛选出的差异细胞因子单独或联合作用.收集细胞培养上清液,检测HBsAg、乙型肝炎e抗原(HBeAg)、HBV-DNA水平,并检测IFN信号转导通路JAK-STAT和抗病毒蛋白IFITM1、MX1、OAS1、PKR水平.结果 与对照组比较,肥胖组ALT、HBsAg水平升高(P<0.05).B组IL-2、IL-6、IL-10、IL-17水平明显高于A组,差异有统计学意义(P<0.05).IFNα2b单独或者与IL联合作用下,JAK1、STAT1、STAT2发生不同程度的磷酸化,JAK-STAT信号通路被激活,其中IL-6、IL-10降低JAK1-STAT磷酸化的程度尤其明显.IFN单独作用下,抗病毒蛋白IFITM1、MX1、OAS1、PKR水平升高,与IL-6、IL-10联合作用下,上述指标水平升高更加明显(P<0.05).结论 肥胖降低乙肝患者IFN治疗的敏感性,但是其机制并不与IL-2、IL-6、IL-10、IL-17水平升高直接有关.IL-2、IL-6、IL-10、IL-17可以上调抗病毒蛋白IF-ITM1、MX1、OAS1、PKR水平.

肥胖作为一种慢性疾病严重影响着人类的生活以及健康,近些年来,伴随肥胖发生的相关疾病例如胰岛素抵抗(IR)在人群中的患病数也在逐年增长,健康问题日益严峻,且找不到确定有效的根治方法.肥胖与IR之间存在特定的联系,2型糖尿病(T2DM)也与IR密不可分.表观遗传是近些年人类研究疾病在基因表达方面的突破点,在人类疾病发生和疾病进展中有重要的作用.该文着眼于表观遗传与肥胖,胰岛素抵抗的发生发展进行综述,把近年关于肥胖,胰岛素抵抗和表观遗传相关的研究进行阐述,了解最新的进展,为以后的研究提供思路.

Tigecycline serves as one of the last-resort antibiotics to treat severe infections caused by carbapenem-resistant Enterobacterales. Recently, a novel plasmid-mediated resistance-nodulation-division (RND)-type efflux pump gene cluster, TmexCD1-ToprJ1, and its variants, TmexCD2-ToprJ2 and TmexCD3-ToprJ3, encoding tetracyclines and tigecycline resistance, were revealed. In this study, we reported three TmexCD2-ToprJ2-harboring Klebsiella species strains, collected from two teaching tertiary hospitals in China, including one K. quasipneumoniae, one K. variicola, and one K. michiganensis. The three strains were characterized by antimicrobial susceptibility testing (AST), conjugation assay, WGS, and bioinformatics analysis. AST showed that K. variicola and K. quasipneumoniae strains were resistant to tigecycline with MIC values of 4μg/ml, whereas the K. michiganensis was susceptible to tigecycline with an MIC value of 1μg/ml. The TmexCD2-ToprJ2 clusters were located on three similar IncHI1B plasmids, of which two co-harbored the metallo-β-lactamase gene blaNDM-1. Conjugation experiments showed that all three plasmids were capable of self-transfer via conjugation. Our results showed, for the first time, that this novel plasmid-mediated tigecycline resistance mechanism TmexCD2-ToprJ2 has spread into different Klebsiella species, and clinical susceptibility testing may fail to detect. The co-occurrence of blaNDM-1 and TmexCD2-ToprJ2 in the same plasmid is of particular public health concern as the convergence of “mosaic” plasmids can confer both tigecycline and carbapenem resistance. Its further spread into other clinical high-risk Klebsiella clones will likely exacerbate the antimicrobial resistance crisis. A close monitoring of the dissemination of TmexCD-ToprJ encoding resistance should be considered.

目的:探讨两种不同的高脂饲料在C57/BL6J小鼠肥胖和胰岛素抵抗(IR)模型制备过程中的效果差别,以期为更好的制备C57/BL6J小鼠肥胖和IR模型提供理论指导.方法:以雄性C57/BL6小鼠为实验材料,随机分为三组,分别为基础组,喂食国内A公司啮齿动物基础饲料;模型1组,喂食国内A公司生产的啮齿动物高脂饲料(HFD-A组);模型2组,喂食美国ResearchDiets生产的啮齿动物高脂饲料(HFD-R组).至饲养12周比较组间体重、血脂指标,腹腔注射葡萄糖耐量(IPGTT)和胰岛素耐量(IPITT)等指标的差异.结果:随着饲养时间的延长三组动物体重均逐渐上升,至饲养12周基础组平均体重为(31.78±1.36)g,HFD-A组为(41.56±1.67)g,HFD-R组为(46.38±1.98)g,差异显著(P<0.05);至饲养12周时,HFD-A组和HFD-R组肥胖模型成功率均为100％(12/12),无统计学差异(P>0.05);与基础组比较,HFD-R组葡萄糖(Glu),甘油三酯(TG),胆固醇(CHOL),高密度脂蛋白(HDL),低密度脂蛋白(LDL)和游离脂肪酸(NEFA)等多项指标显著改变,差异有统计学意义(P<0.05),而HFD-A组仅Glu和LDL升高显著(P<0.05).与基础组比较,HFD-R组的IPGTT和IPITT检测结果均显著升高(P<0.05),而HFD-A组虽有升高趋势但是差异无统计学意义(P>0.05).结论:两种高脂饲料均能够在饲养12周时成功制备C57/BL6J小鼠肥胖模型,但是只有HFD-R组达到了IR模型的标准.