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      Expression of AdipoR1 and AdipoR2 and Serum Level of Adiponectin in Gastric Cancer

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          Abstract

          Background: Cancer is one of the major causes of death worldwide and the third leading cause of death in Iran. One of the proteins that are considered having anticancer effects is the adiponectin hormone. Adiponectin leads to programmed cell death, prevents cell growth and proliferation, and increases the expression levels of BCL2. Aim: The aim of this study was to assay the expression of adiponectin receptors ( AdipoR1 and AdipoR2) genes in gastric cancer patients. Materials and Methods: In this case-control study, 42 gastric cancer patients and 52 volunteers as healthy controls were enrolled. Total RNA was extracted. cDNA was synthesized by the reverse transcription method, and expression analysis was performed by real-time PCR. The serum level of adiponectin was also measured by ELISA. Results: The expression of both AdipoR1 and AdipoR2 was significantly higher than the control group ( p = 0.02). Serum adiponectin was significantly lower in gastric cancer cases when compared with normal controls ( p = 0.03). Conclusion: We found that expression level of AdipoR1 and AdipoR2 is strongly higher; however, the level of circulating adiponectin is lower in gastric cancer. Our study suggests that the expression of AdipoR1 and AdipoR2, besides the low level of adiponectin, may play an important role in the development and/or progression of gastric cancer.

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          Most cited references25

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          cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (AdiPose Most abundant Gene transcript 1).

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            Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages.

            We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming units-erythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor alpha. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (Blood. 2000;96:1723-1732)
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              Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys.

              Adiponectin is an adipose-specific plasma protein whose plasma concentrations are decreased in obese subjects and type 2 diabetic patients. This protein possesses putative antiatherogenic and anti-inflammatory properties. In the current study, we have analyzed the relationship between adiponectin and insulin resistance in rhesus monkeys (Macaca mulatta), which spontaneously develop obesity and which subsequently frequently progress to overt type 2 diabetes. The plasma levels of adiponectin were decreased in obese and diabetic monkeys as in humans. Prospective longitudinal studies revealed that the plasma levels of adiponectin declined at an early phase of obesity and remained decreased after the development of type 2 diabetes. Hyperinsulinemic-euglycemic clamp studies revealed that the obese monkeys with lower plasma adiponectin showed significantly lower insulin-stimulated peripheral glucose uptake (M rate). The plasma levels of adiponectin were significantly correlated to M rate (r = 0.66, P < 0.001). Longitudinally, the plasma adiponectin decreased in parallel to the progression of insulin resistance. No clear association was found between the plasma levels of adiponectin and its mRNA levels in adipose tissue. These results suggest that reduction in circulating adiponectin may be related to the development of insulin resistance.
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                Author and article information

                Journal
                GAT
                GAT
                10.1159/issn.2296-3774
                Gastrointestinal Tumors
                S. Karger AG
                2296-3774
                2296-3766
                2020
                October 2020
                16 September 2020
                : 7
                : 4
                : 103-109
                Affiliations
                [_a] aResearch Center for Cancer Screening and Epidemiology, AJA University of Medical Sciences, Tehran, Iran
                [_b] bMahak Hematology Oncology Research Center (Mahak-HORC), Mahak Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [_c] cDepartment of Bioengineering and Technology (GUIST), Gauhati University, Guwahati, India
                Author notes
                *Shahrokh Iravani, AJA Cancer Epidemiology Research and Treatment Center (AJA-CERTC), AJA University of Medical Sciences, Shahid Etemadzadeh St., Tehran 1411718541 (Iran), shahrokh.iravani1@gmail.com, Azim Mehrvar, Mahak Hematology Oncology Research Center (Mahak-HORC), Mahak Hospital, Tehran 1956993461 (Iran), DRAZIMMEHRVAR@yahoo.com
                Article
                510342 Gastrointest Tumors 2020;7:103–109
                10.1159/000510342
                b9c1cbde-7a75-485e-b1df-0d52b60c4316
                © 2020 The Author(s) Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 01 March 2020
                : 17 July 2020
                Page count
                Figures: 2, Tables: 2, Pages: 7
                Categories
                Research Article

                Oncology & Radiotherapy,Gastroenterology & Hepatology,Surgery,Nutrition & Dietetics,Internal medicine
                Gastric cancer,Adiponectin serum level, AdipoR2 , AdipoR1

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