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6. Improvement of Adipose Macrophage Polarization in High Fat Diet-Induced Obese GHSR Knockout Mice

Author

Jing Zhao, Xinxin Xiang, Jian Ma, Fang Yuan, Yanhui Xu, Weizhen Zhang, He Lan, and Yin Li

Subjects
0301 basic medicine, medicine.medical_specialty, Article Subject, Growth hormone secretagogue receptor, Macrophage polarization, lcsh:Medicine, Mice, Obese, Adipokine, Adipose tissue, Diet, High-Fat, General Biochemistry, Genetics and Molecular Biology, Proinflammatory cytokine, Mice, 03 medical and health sciences, Insulin resistance, Internal medicine, medicine, Animals, Obesity, Receptors, Ghrelin, Inflammation, Mice, Knockout, General Immunology and Microbiology, Adiponectin, Chemistry, Macrophages, lcsh:R, digestive, oral, and skin physiology, General Medicine, medicine.disease, Rats, Mice, Inbred C57BL, 030104 developmental biology, Endocrinology, Adipose Tissue, Resistin, Rabbits, Insulin Resistance, Research Article
Abstract

Purpose. Adipose tissue inflammation is the key linking obesity to insulin resistance. Over 50% of the interstitial cells in adipose tissue are macrophages, which produce inflammatory cytokines and therefore play an important role in the progression of insulin resistance. Within this classification view, macrophage biology is driven by two polarization phenotypes, M1 (proinflammatory) and M2 (anti-inflammatory). The unique functional receptor of ghrelin, growth hormone secretagogue receptor (GHSR), is a classic seven-transmembrane G protein-coupled receptor that is linked to multiple intracellular signaling pathways. Knockout of GHSR improves the obesity and glucose metabolic disorders, suggesting a crucial role of ghrelin activity in insulin resistance. Here, we discussed whether macrophage polarization phenotypes in adipose tissue were changed in GHSR knockout (GHSR-/-) mice. Methods. GHSR-/- mice were fed with normal chow diet (NCD) or high fat diet (HFD). Markers of different macrophage polarization phenotypes were detected by real-time RT-PCR. Results. The size of adipocytes decreased and interstitial cells, especially infiltrated macrophages, reduced in epididymal adipose tissue of GHSR-/- mice fed with HFD. Compared with wild type mice, the mRNA levels of inflammatory adipokines such as resistin, IL-6, and PAI-1 were significantly lower in epididymal adipose tissue of GHSR-/- mice, whereas anti-inflammatory adipokine, adiponectin, was significantly higher. M1 markers, MCP-1, TNF-α, and iNOS, were significantly lower in epididymal adipose tissue of GHSR-/- mice, whereas M2 markers, Arg-1, Mgl-1, were Mrc1, were significantly higher. Conclusion. The GHSR-/- mice fed with HFD showed suppressed adipose inflammation, reduced macrophage infiltration, and enhanced M2 polarization of macrophages in adipose tissue, which improved insulin sensitivity.

Published
2018

11. MicroRNA-34a Promotes EMT and Liver Fibrosis in Primary Biliary Cholangitis by Regulating TGF- 1/smad Pathway.

Author

Pan, Ying, Wang, Jing, He, Lan, and Zhang, Fengchun

Subjects
CHOLANGITIS, FIBROSIS, P53 antioncogene, PROGNOSIS, LIVER, EPITHELIAL cells, TRANSFORMING growth factors
Abstract

Background and Aims: Primary biliary cholangitis (PBC) is an autoimmune cholestatic liver disease. We found microRNA-34a (miR-34a), as the downstream gene of p53, was overexpressed in some of fibrogenic diseases. In this study, we sought to explore whether miR-34a plays a role in the fibrosis of PBC.Methods: The peripheral blood of PBC patients and controls was collected to analyze the level of miR-34a. Human intrahepatic biliary epithelial cells (HIBEC) were cultured. The expression of miR-34a was regulated by miR-34a mimics and inhibitor. The biomarkers of epithelium-mesenchymal transition (EMT), fibrogenesis, inflammation, and transforming growth factor- (TGF-) β1/smad pathway were analyzed.Results: We found that miR-34a was overexpressed in the peripheral blood in PBC patients. In vitro, overexpressed miR-34a increased the EMT and fibrogenesis activity of HIBEC. Transforming growth factor-beta type 1 receptor (TβR1), TGF-β1, and p-smad2/3 were upregulated by miR-34a. Inflammatory factors such as IL-6 and IL-17 were also upregulated. Finally, we showed that miR-34a promoted EMT and liver fibrosis in PBC by targeting the TGF-β1/smad pathway antagonist transforming growth factor-beta-induced factor homeobox 2 (TGIF2).Conclusions: Our findings show that miR-34a plays an important role in the EMT and fibrosis of PBC through the TGF-β1/smad pathway by targeting TGIF2. This study suggests that miR-34a may be a new marker of fibrogenesis in PBC. Inhibition of miR-34a may be a promising strategy in treating PBC and improving the prognosis of the disease. [ABSTRACT FROM AUTHOR]

Published
2021
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18. Direct Comparison of 19F qNMR and 1H qNMR by Characterizing Atorvastatin Calcium Content.

Author

Liu, Yang, Liu, Zhaoxia, Yang, Huaxin, and He, Lan

Subjects
ATORVASTATIN, FLUORINE, COMPARATIVE studies, INDUSTRIAL contamination, NUCLEAR magnetic resonance spectroscopy
Abstract

Quantitative nuclear magnetic resonance (qNMR) is a powerful tool in measuring drug content because of its high speed, sensitivity, and precision. Most of the reports were based on proton qNMR (1H qNMR) and only a few fluorine qNMR (19F qNMR) were reported. No research has been conducted to directly compare the advantage and disadvantage between these two methods. In the present study, both 19F and 1H qNMR were performed to characterize the content of atorvastatin calcium with the same internal standard. Linearity, precision, and results from two methods were compared. Results showed that 19F qNMR has similar precision and sensitivity to 1H qNMR. Both methods generate similar results compared to mass balance method. Major advantage from 19F qNMR is that the analyte signal is with less or no interference from impurities. 19F qNMR is an excellent approach to quantify fluorine-containing analytes. [ABSTRACT FROM AUTHOR]

Published
2016
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19. Cardiomyocyte-Restricted Deletion of PPARβ/δin PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation

Author

Liu, Jian, primary, Wang, Peiyong, additional, He, Lan, additional, Li, Yuquan, additional, Luo, Jinwen, additional, Cheng, Lihong, additional, Qin, Qianhong, additional, Brako, Lawrence A., additional, Lo, Woo-kuen, additional, Lewis, William, additional, and Yang, Qinglin, additional

Published
2011
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