CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD + -Sirt1-PGC1α signaling pathway

Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In t...

Full description

Saved in:
Bibliographic Details
Published in:Canadian journal of physiology and pharmacology 2023-07, Vol.101 (7), p.369-381
Main Authors: Ding, Qi, Wen, Ke, Li, Qian, Zhao, Qi-Hang, Zhao, Jia-Le, Xiao, Yun-Fei, Guan, Xiao-Hui, Jiang, Mei-Xiu, Zhang, Feng, Wang, Ling-Fang
Format: Article
Language:English
Subjects:
Adipose tissue (brown)
Body fat
CD38 antigen
Cell death
Energy expenditure
Energy metabolism
Homeostasis
Metabolic syndrome
Metabolites
mRNA
Musculoskeletal system
NAD
NAD(P)H oxidase
Obesity
Oxidative stress
Palmitic acid
Signal transduction
SIRT1 protein
Sirtuins
Skeletal muscle
Uncoupling protein 1
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3
cites cdi_FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3
container_end_page 381
container_issue 7
container_start_page 369
container_title Canadian journal of physiology and pharmacology
container_volume 101
creator Ding, Qi
Wen, Ke
Li, Qian
Zhao, Qi-Hang
Zhao, Jia-Le
Xiao, Yun-Fei
Guan, Xiao-Hui
Jiang, Mei-Xiu
Zhang, Feng
Wang, Ling-Fang
description Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation, and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NADPH oxidase 2 and FASN in mRNA level. We found that the expressions of Sirt1, Sirt3, and PGC1α were upregulated in CD38-deficient muscle tissue. In brown fat, the Sirt1-3, cell death inducing DFFA-like effector A, ELOVL3, and Dio2 expressions were increased in CD38-deficient mice. Our results showed the uncoupling protein 1 expression was upregulated. And NAD supplementation increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to the inhibition of oxidative stress and increasing energy expenditure via activating NAD /Sirtuins signaling pathways in muscle and brown fat.
doi_str_mv 10.1139/cjpp-2022-0454
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2814813362</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2831747265</sourcerecordid><originalsourceid>FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3</originalsourceid><addsrcrecordid>eNpdkUtuFDEQhq0IlExCtlkiS2yQIge_u3sZTSAgRRAJWLfcdnnGQ79iuwlzCA7DRXImupWEBatSqb76VaUPoTNGLxgT1Tu7G0fCKeeESiUP0IpxqkihJHuBVpTSkkjO-BE6Tmk3t7oU5SE6EgWruJLVCv1eX4kSO_DBBujtHo9x6IYMCacf0EI2Le6mZFvApne4icN9j40L45AA55DSBBh6iJs9hl8j9C7kKc6TbRymzRYbm8NPk0O_wZ8vr_A5Jl9DzIzcXq_Zwx-cwqY37TIdTd7em_0r9NKbNsHpUz1B3z-8_7b-SG6-XH9aX94QK7TIpKmo8LKRmjtdeV0wY1zJWWEMUKeoZkp756umVOCFlN40RWMKaz1VtrHgxAl6-5g7f3s3Qcp1F5KFtjU9DFOqeclkyYTQfEbf_IfuhinOZy-UYIUsuFYzdfFI2TikFMHXYwydifua0XoRVS-i6kVUvYiaF14_xU5NB-4f_mxG_AWh85F0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2831747265</pqid></control><display><type>article</type><title>CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD + -Sirt1-PGC1α signaling pathway</title><source>SPORTDiscus with Full Text</source><creator>Ding, Qi ; Wen, Ke ; Li, Qian ; Zhao, Qi-Hang ; Zhao, Jia-Le ; Xiao, Yun-Fei ; Guan, Xiao-Hui ; Jiang, Mei-Xiu ; Zhang, Feng ; Wang, Ling-Fang</creator><creatorcontrib>Ding, Qi ; Wen, Ke ; Li, Qian ; Zhao, Qi-Hang ; Zhao, Jia-Le ; Xiao, Yun-Fei ; Guan, Xiao-Hui ; Jiang, Mei-Xiu ; Zhang, Feng ; Wang, Ling-Fang</creatorcontrib><description>Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation, and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NADPH oxidase 2 and FASN in mRNA level. We found that the expressions of Sirt1, Sirt3, and PGC1α were upregulated in CD38-deficient muscle tissue. In brown fat, the Sirt1-3, cell death inducing DFFA-like effector A, ELOVL3, and Dio2 expressions were increased in CD38-deficient mice. Our results showed the uncoupling protein 1 expression was upregulated. And NAD supplementation increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to the inhibition of oxidative stress and increasing energy expenditure via activating NAD /Sirtuins signaling pathways in muscle and brown fat.</description><identifier>ISSN: 0008-4212</identifier><identifier>EISSN: 1205-7541</identifier><identifier>DOI: 10.1139/cjpp-2022-0454</identifier><identifier>PMID: 37192549</identifier><language>eng</language><publisher>Canada: Canadian Science Publishing NRC Research Press</publisher><subject>Adipose tissue (brown) ; Body fat ; CD38 antigen ; Cell death ; Energy expenditure ; Energy metabolism ; Homeostasis ; Metabolic syndrome ; Metabolites ; mRNA ; Musculoskeletal system ; NAD ; NAD(P)H oxidase ; Obesity ; Oxidative stress ; Palmitic acid ; Signal transduction ; SIRT1 protein ; Sirtuins ; Skeletal muscle ; Uncoupling protein 1</subject><ispartof>Canadian journal of physiology and pharmacology, 2023-07, Vol.101 (7), p.369-381</ispartof><rights>2023 Published by NRC Research Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3</citedby><cites>FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3</cites><orcidid>0000-0002-9002-3657</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37192549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ding, Qi</creatorcontrib><creatorcontrib>Wen, Ke</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Zhao, Qi-Hang</creatorcontrib><creatorcontrib>Zhao, Jia-Le</creatorcontrib><creatorcontrib>Xiao, Yun-Fei</creatorcontrib><creatorcontrib>Guan, Xiao-Hui</creatorcontrib><creatorcontrib>Jiang, Mei-Xiu</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Wang, Ling-Fang</creatorcontrib><title>CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD + -Sirt1-PGC1α signaling pathway</title><title>Canadian journal of physiology and pharmacology</title><addtitle>Can J Physiol Pharmacol</addtitle><description>Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation, and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NADPH oxidase 2 and FASN in mRNA level. We found that the expressions of Sirt1, Sirt3, and PGC1α were upregulated in CD38-deficient muscle tissue. In brown fat, the Sirt1-3, cell death inducing DFFA-like effector A, ELOVL3, and Dio2 expressions were increased in CD38-deficient mice. Our results showed the uncoupling protein 1 expression was upregulated. And NAD supplementation increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to the inhibition of oxidative stress and increasing energy expenditure via activating NAD /Sirtuins signaling pathways in muscle and brown fat.</description><subject>Adipose tissue (brown)</subject><subject>Body fat</subject><subject>CD38 antigen</subject><subject>Cell death</subject><subject>Energy expenditure</subject><subject>Energy metabolism</subject><subject>Homeostasis</subject><subject>Metabolic syndrome</subject><subject>Metabolites</subject><subject>mRNA</subject><subject>Musculoskeletal system</subject><subject>NAD</subject><subject>NAD(P)H oxidase</subject><subject>Obesity</subject><subject>Oxidative stress</subject><subject>Palmitic acid</subject><subject>Signal transduction</subject><subject>SIRT1 protein</subject><subject>Sirtuins</subject><subject>Skeletal muscle</subject><subject>Uncoupling protein 1</subject><issn>0008-4212</issn><issn>1205-7541</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpdkUtuFDEQhq0IlExCtlkiS2yQIge_u3sZTSAgRRAJWLfcdnnGQ79iuwlzCA7DRXImupWEBatSqb76VaUPoTNGLxgT1Tu7G0fCKeeESiUP0IpxqkihJHuBVpTSkkjO-BE6Tmk3t7oU5SE6EgWruJLVCv1eX4kSO_DBBujtHo9x6IYMCacf0EI2Le6mZFvApne4icN9j40L45AA55DSBBh6iJs9hl8j9C7kKc6TbRymzRYbm8NPk0O_wZ8vr_A5Jl9DzIzcXq_Zwx-cwqY37TIdTd7em_0r9NKbNsHpUz1B3z-8_7b-SG6-XH9aX94QK7TIpKmo8LKRmjtdeV0wY1zJWWEMUKeoZkp756umVOCFlN40RWMKaz1VtrHgxAl6-5g7f3s3Qcp1F5KFtjU9DFOqeclkyYTQfEbf_IfuhinOZy-UYIUsuFYzdfFI2TikFMHXYwydifua0XoRVS-i6kVUvYiaF14_xU5NB-4f_mxG_AWh85F0</recordid><startdate>20230701</startdate><enddate>20230701</enddate><creator>Ding, Qi</creator><creator>Wen, Ke</creator><creator>Li, Qian</creator><creator>Zhao, Qi-Hang</creator><creator>Zhao, Jia-Le</creator><creator>Xiao, Yun-Fei</creator><creator>Guan, Xiao-Hui</creator><creator>Jiang, Mei-Xiu</creator><creator>Zhang, Feng</creator><creator>Wang, Ling-Fang</creator><general>Canadian Science Publishing NRC Research Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9002-3657</orcidid></search><sort><creationdate>20230701</creationdate><title>CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD + -Sirt1-PGC1α signaling pathway</title><author>Ding, Qi ; Wen, Ke ; Li, Qian ; Zhao, Qi-Hang ; Zhao, Jia-Le ; Xiao, Yun-Fei ; Guan, Xiao-Hui ; Jiang, Mei-Xiu ; Zhang, Feng ; Wang, Ling-Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adipose tissue (brown)</topic><topic>Body fat</topic><topic>CD38 antigen</topic><topic>Cell death</topic><topic>Energy expenditure</topic><topic>Energy metabolism</topic><topic>Homeostasis</topic><topic>Metabolic syndrome</topic><topic>Metabolites</topic><topic>mRNA</topic><topic>Musculoskeletal system</topic><topic>NAD</topic><topic>NAD(P)H oxidase</topic><topic>Obesity</topic><topic>Oxidative stress</topic><topic>Palmitic acid</topic><topic>Signal transduction</topic><topic>SIRT1 protein</topic><topic>Sirtuins</topic><topic>Skeletal muscle</topic><topic>Uncoupling protein 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ding, Qi</creatorcontrib><creatorcontrib>Wen, Ke</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Zhao, Qi-Hang</creatorcontrib><creatorcontrib>Zhao, Jia-Le</creatorcontrib><creatorcontrib>Xiao, Yun-Fei</creatorcontrib><creatorcontrib>Guan, Xiao-Hui</creatorcontrib><creatorcontrib>Jiang, Mei-Xiu</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Wang, Ling-Fang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Canadian journal of physiology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ding, Qi</au><au>Wen, Ke</au><au>Li, Qian</au><au>Zhao, Qi-Hang</au><au>Zhao, Jia-Le</au><au>Xiao, Yun-Fei</au><au>Guan, Xiao-Hui</au><au>Jiang, Mei-Xiu</au><au>Zhang, Feng</au><au>Wang, Ling-Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD + -Sirt1-PGC1α signaling pathway</atitle><jtitle>Canadian journal of physiology and pharmacology</jtitle><addtitle>Can J Physiol Pharmacol</addtitle><date>2023-07-01</date><risdate>2023</risdate><volume>101</volume><issue>7</issue><spage>369</spage><epage>381</epage><pages>369-381</pages><issn>0008-4212</issn><eissn>1205-7541</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation, and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NADPH oxidase 2 and FASN in mRNA level. We found that the expressions of Sirt1, Sirt3, and PGC1α were upregulated in CD38-deficient muscle tissue. In brown fat, the Sirt1-3, cell death inducing DFFA-like effector A, ELOVL3, and Dio2 expressions were increased in CD38-deficient mice. Our results showed the uncoupling protein 1 expression was upregulated. And NAD supplementation increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to the inhibition of oxidative stress and increasing energy expenditure via activating NAD /Sirtuins signaling pathways in muscle and brown fat.</abstract><cop>Canada</cop><pub>Canadian Science Publishing NRC Research Press</pub><pmid>37192549</pmid><doi>10.1139/cjpp-2022-0454</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-9002-3657</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0008-4212
ispartof Canadian journal of physiology and pharmacology, 2023-07, Vol.101 (7), p.369-381
issn 0008-4212
1205-7541
language eng
recordid cdi_proquest_miscellaneous_2814813362
source SPORTDiscus with Full Text
subjects Adipose tissue (brown)
Body fat
CD38 antigen
Cell death
Energy expenditure
Energy metabolism
Homeostasis
Metabolic syndrome
Metabolites
mRNA
Musculoskeletal system
NAD
NAD(P)H oxidase
Obesity
Oxidative stress
Palmitic acid
Signal transduction
SIRT1 protein
Sirtuins
Skeletal muscle
Uncoupling protein 1
title CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD + -Sirt1-PGC1α signaling pathway
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T15%3A32%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CD38%20deficiency%20promotes%20skeletal%20muscle%20and%20brown%20adipose%20tissue%20energy%20expenditure%20through%20activating%20NAD%20+%20-Sirt1-PGC1%CE%B1%20signaling%20pathway&rft.jtitle=Canadian%20journal%20of%20physiology%20and%20pharmacology&rft.au=Ding,%20Qi&rft.date=2023-07-01&rft.volume=101&rft.issue=7&rft.spage=369&rft.epage=381&rft.pages=369-381&rft.issn=0008-4212&rft.eissn=1205-7541&rft_id=info:doi/10.1139/cjpp-2022-0454&rft_dat=%3Cproquest_cross%3E2831747265%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c363t-b903f4b462d69f671aad8217aae0d506156fdf9b85ef344fab7ba7ccf05cbced3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2831747265&rft_id=info:pmid/37192549&rfr_iscdi=true