Glucagon-like peptide-1 (GLP-1) is a 30-amino acid peptide hormone that is mainly expressed in the intestine and hypothalamus. In recent years, basic and clinical studies have shown that GLP-1 is closely related to lipid metabolism, and it can participate in lipid metabolism by inhibiting fat synthesis, promoting fat differentiation, enhancing cholesterol metabolism, and promoting adipose browning. GLP-1 plays a key role in the occurrence and development of metabolic diseases such as obesity, nonalcoholic fatty liver disease, and atherosclerosis by regulating lipid metabolism. It is expected to become a new target for the treatment of metabolic disorders. The effects of GLP-1 and dual agonists on lipid metabolism also provide a more complete treatment plan for metabolic diseases. This article reviews the recent research progress of GLP-1 in lipid metabolism.

Glucagon-like peptide-1 (GLP-1) is a 30-amino acid peptide hormone that is mainly expressed in the intestine and hypothalamus. In recent years, basic and clinical studies have shown that GLP-1 is closely related to lipid metabolism, and it can participate in lipid metabolism by inhibiting fat synthesis, promoting fat differentiation, enhancing cholesterol metabolism, and promoting adipose browning. GLP-1 plays a key role in the occurrence and development of metabolic diseases such as obesity, nonalcoholic fatty liver disease, and atherosclerosis by regulating lipid metabolism. It is expected to become a new target for the treatment of metabolic disorders. The effects of GLP-1 and dual agonists on lipid metabolism also provide a more complete treatment plan for metabolic diseases. This article reviews the recent research progress of GLP-1 in lipid metabolism.

Glucagon-like peptide-1 (GLP-1) is a 30-amino acid peptide hormone that is mainly expressed in the intestine and hypothalamus. In recent years, basic and clinical studies have shown that GLP-1 is closely related to lipid metabolism, and it can participate in lipid metabolism by inhibiting fat synthesis, promoting fat differentiation, enhancing cholesterol metabolism, and promoting adipose browning. GLP-1 plays a key role in the occurrence and development of metabolic diseases such as obesity, nonalcoholic fatty liver disease, and atherosclerosis by regulating lipid metabolism. It is expected to become a new target for the treatment of metabolic disorders. The effects of GLP-1 and dual agonists on lipid metabolism also provide a more complete treatment plan for metabolic diseases. This article reviews the recent research progress of GLP-1 in lipid metabolism.

OBJECTIVETo identify the ETV6 gene rearrangement in patients with myelodysplastic syndromes (MDS) and explore its relationship with prognosis and disease stages.

METHODSETV6 rearrangement in 58 MDS cases were detected by conventional cytogenetics and Split-signal FISH. RT-PCR was used to detect 9p24-12p13 balance translocation with special designed primers ETV6F1/F2 and JAK2R1/R2. The relationship between ETV6 rearrangement and prognosis and disease staging in MDS patients was analyzed.

RESULTSETV6 rearrangement were found in 4 (6.9%) of 58 cases, among which ETV6/JAK2 fusion was identified by RT-PCR in 1 (1.7%) case. The mean follow-up duration was 12 months. All 4 patients (100%) with rearrangement transformed into acute leukemia, with a median survival time (MS) of 7 months; while 10 patients (17%) in the non-translocation group transformed to acute leukemia, with a MS of 28 months. In addition, all 4 patients (100%) with rearrangement were in advanced stage of MDS( RAEB), while 17 cases (31.5%) in non-rearrangement group were in that stage.

CONCLUSIONSETV6 rearrangement has higher expression rate (6.9%), and is closely associated with disease stage and prognosis in MDS.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Female ; Gene Rearrangement ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Middle Aged ; Myelodysplastic Syndromes ; genetics ; pathology ; Neoplasm Staging ; Prognosis ; Proto-Oncogene Proteins c-ets ; genetics ; Repressor Proteins ; genetics

BACKGROUND: Until now, there is no effective treatment for peripheral neuropathy caused by acrylamide. Therefore, it is necessary to explore new treatment methods. OBJECTIVE: To explore the protection role and its mechanism of bone marrow mesenchymal stem cells (BMSCs) against acrylamide-induced intoxication in the spinal cords of rats. METHODS: BMSCs were cultured by the whole bone marrow adherence method and identified by morphological observation and flow cytometry detection. Thirty Sprague-Dawley rats, clean grade, were randomly divided into three groups (n=10 for each group): normal control group, acrylamide group and BMSCs transplantation group. The latter two groups received acrylamide by gavage, 50 mg/(kg?d), 5 days per week, for 2 weeks with an interval of 2 days. Then, in the BMSCs transplantation group, 3×106BMSCs were transplanted by the caudal vein, 5 days per week, for 3 consecutive weeks. Hematoxylin-eosin staining was utilized to observe the morphological changes of the spinal cord. Tunel assay was used to detect cell apoptosis. Western blot assay was adopted to detect the expression levels of Bcl-2 and Bax. RESULTS AND CONCLUSION: In the acrylamide-exposed rats, the damage to the structure was found in the spinal cords by morphological observation, which was significantly alleviated after BMSCs transplantation. The disturbed expression levels of Bax and Bcl-2 were also significantly inversed after BMSCs transplantation (P < 0.05). These results suggest that BMSCs transplantation can inhibit cell apoptosis in the spinal cords of acrylamide-intoxicated rats, probably by up-regulating expression of Bcl-2 and down-regulating expression of Bax.

Equine interferon-gamma (eIFN-gamma) expressed both in E. coli and baculovirus were evaluated for antiviral activity against recombinant Vesicular Stomatits Virus expressing green fluorescence protein (rVSV-GFP) in EFK-78 cells. The assays were conducted in 96-well plate. Virus infectivity was measured by quantifying GFP-positive cells, instead of quantifying the CPE reduction. Prior to infection of EFK-78 cells with rVSV-GFP, the cells were incubated with eIFN-gamma. The GFP expression in the EFK-78 cells dramatically decreased in the cells treated with eIFN-gamma in a dose-dependent manner, comparing with the mock-treated cells. The titers of antiviral activity were 1 x 10(3) AU/mL and 1 x 10(5) AU/mL of eIFN-gamma expressed from E. coli and baculovirus, respectively. The antiviral activities of the recombinant eIFN-gamma were highly efficient and specific, as it was blocked by mAbs against eIFN-gamma.
Animals ; Antibodies, Monoclonal ; immunology ; Antiviral Agents ; metabolism ; pharmacology ; Baculoviridae ; genetics ; metabolism ; Escherichia coli ; genetics ; metabolism ; Green Fluorescent Proteins ; metabolism ; Horses ; Interferon-gamma ; biosynthesis ; genetics ; pharmacology ; Recombinant Proteins ; Vesicular stomatitis Indiana virus ; drug effects ; metabolism

OBJECTIVETo investigate the effect of up-regulated expression of tumor suppressor gene p14(ARF) on apoptosis of chronic myeloid leukemia (CML) cells and its interaction with imatinib.

METHODSTumor suppressor gene p14(ARF) was transduced into K562 (K562-p14(ARF)) and 4 blast crisis primary CML cells (CML-BC 1-4) using vesicular stomatitis virus glycoprotein (VSV-G) pseudotyped lentiviral vector with cells transduced by empty vector as control. Fluorescence microscopy and flow cytometry were applied to measure transduction efficiency, and Western blotting assay was used to detect p14(ARF) protein of K562 cells. WST-8 method was used to determine cell growth inhibition rate of K562 cells transduced by the target gene under different concentrations of imatinib (0, 0.015, 0.062, 0.125, 0.25, 0.5, 1.0, 2.0 μmol/L). Cell apoptosis and leukemic cellular colony-forming ability were detected by Annexin V-FITC/PI dyeing using flow cytometry (FCM) and semi-solid culture method respectively.

RESULTSFluorescence microscopy and FCM showed that transduction efficiency (GFP positive cells) of K562-p14(ARF), K562-VSV and CML-BC1 cells were close to 100%, and CML-BC 2-4 cells were 80% to 90% on average. Results of Western blotting showed that the levels of ARF protein expression of K562 cells transduced by p14(ARF) were significantly higher than of untransduced cells; the apoptosis rate of K562-p14(ARF) was 20%; the mean apoptosis rate of 4 primary leukemic cells transduced by the p14(ARF) [(71.1±22.4)%] was significantly higher than of control group [(12.4±6.2)%] (P<0.05). Imatinib significantly inhibited the proliferation of K562-p14(ARF) cells in a dose-dependent manner. The mean leukemic cellular colony-forming unit of 4 primary leukemic cells transduced by the p14(ARF) (41.5±13.2) was significantly lower than of the control group (88.5±7.9) (P<0.05).

CONCLUSIONIncreased p14(ARF) gene expression could induce apoptosis of CML cells; Moreover, it could enhance inhibitory effect on cell proliferation when combined with imatinib.

Apoptosis ; Gene Expression Regulation, Leukemic ; Genetic Vectors ; Humans ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; metabolism ; pathology ; Tumor Suppressor Protein p14ARF ; metabolism ; Up-Regulation

Zona Incerta ; Prefrontal Cortex ; Fear ; Neural Pathways