Differential effects of Calca-derived peptides in male mice with diet-induced obesity
Key metabolic hormones, such as insulin, leptin, and adiponectin, have been studied extensively in obesity, however the pathophysiologic relevance of the calcitonin family of peptides remains unclear. This family includes calcitonin (CT), its precursor procalcitonin (PCT), and alpha calcitonin-gene...
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| creator | Bartelt, Alexander Jeschke, Anke Müller, Brigitte Gaziano, Isabella Morales, Michelle Yorgan, Timur Heckt, Timo Heine, Markus Gagel, Robert F Emeson, Ronald B Amling, Michael Niemeier, Andreas Heeren, Jörg Schinke, Thorsten Keller, Johannes |
| description | Key metabolic hormones, such as insulin, leptin, and adiponectin, have been studied extensively in obesity, however the pathophysiologic relevance of the calcitonin family of peptides remains unclear. This family includes calcitonin (CT), its precursor procalcitonin (PCT), and alpha calcitonin-gene related peptide (αCGRP), which are all encoded by the gene Calca. Here, we studied the role of Calca-derived peptides in diet-induced obesity (DIO) by challenging Calcr-/- (encoding the calcitonin receptor, CTR), Calca-/-, and αCGRP-/- mice and their respective littermates with high-fat diet (HFD) feeding for 16 weeks. HFD-induced pathologies were assessed by glucose tolerance, plasma cytokine and lipid markers, expression studies and histology. We found that DIO in mice lacking the CTR resulted in impaired glucose tolerance, features of enhanced nonalcoholic steatohepatitis (NASH) and adipose tissue inflammation compared to wildtype littermates. Furthermore, CTR-deficient mice were characterized by dyslipidemia and elevated HDL levels. In contrast, mice lacking Calca were protected from DIO, NASH and adipose tissue inflammation, and displayed improved glucose tolerance. Mice exclusively lacking αCGRP displayed a significantly less improved DIO phenotype compared to Calca-deficient mice. In summary, we demonstrate that the CT/CTR axis is involved in regulating plasma cholesterol levels while Calca, presumably through PCT, seems to have a detrimental effect in the context of metabolic disease. Our study provides the first comparative analyses of the roles of Calca-derived peptides and the CTR in metabolic disease. |
| doi_str_mv | 10.1371/journal.pone.0180547 |
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This family includes calcitonin (CT), its precursor procalcitonin (PCT), and alpha calcitonin-gene related peptide (αCGRP), which are all encoded by the gene Calca. Here, we studied the role of Calca-derived peptides in diet-induced obesity (DIO) by challenging Calcr-/- (encoding the calcitonin receptor, CTR), Calca-/-, and αCGRP-/- mice and their respective littermates with high-fat diet (HFD) feeding for 16 weeks. HFD-induced pathologies were assessed by glucose tolerance, plasma cytokine and lipid markers, expression studies and histology. We found that DIO in mice lacking the CTR resulted in impaired glucose tolerance, features of enhanced nonalcoholic steatohepatitis (NASH) and adipose tissue inflammation compared to wildtype littermates. Furthermore, CTR-deficient mice were characterized by dyslipidemia and elevated HDL levels. In contrast, mice lacking Calca were protected from DIO, NASH and adipose tissue inflammation, and displayed improved glucose tolerance. Mice exclusively lacking αCGRP displayed a significantly less improved DIO phenotype compared to Calca-deficient mice. In summary, we demonstrate that the CT/CTR axis is involved in regulating plasma cholesterol levels while Calca, presumably through PCT, seems to have a detrimental effect in the context of metabolic disease. Our study provides the first comparative analyses of the roles of Calca-derived peptides and the CTR in metabolic disease.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0180547</identifier><identifier>PMID: 28666011</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adipocytes ; Adiponectin ; Adipose tissue ; Animals ; Biochemistry ; Biology ; Biology and Life Sciences ; Biomechanics ; Calcitonin ; Calcitonin gene-related peptide ; Calcitonin Gene-Related Peptide - chemistry ; Cholesterol ; Diet ; Diet, High-Fat ; Dosage and administration ; Dyslipidemia ; Feeding ; Gene expression ; Genetic aspects ; Genetically modified mice ; Glucose ; Glucose tolerance ; Health aspects ; High density lipoprotein ; High fat diet ; Histology ; Homeostasis ; Hormones ; Insulin ; Insulin resistance ; Leptin ; Lipids ; Male ; Markers ; Medicine and Health Sciences ; Metabolic diseases ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity ; Obesity - etiology ; Obesity - metabolism ; Orthopedics ; Peptides ; Peptides - physiology ; Physiology ; Polypeptides ; Procalcitonin ; Research and Analysis Methods ; Rodents ; Sepsis ; Weight control</subject><ispartof>PloS one, 2017-06, Vol.12 (6), p.e0180547-e0180547</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Bartelt et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Bartelt et al 2017 Bartelt et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-2b8265a16cb5685a3398d751d2d556b73b868582ebb91377065eb8b413e9740e3</citedby><cites>FETCH-LOGICAL-c692t-2b8265a16cb5685a3398d751d2d556b73b868582ebb91377065eb8b413e9740e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5493411/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5493411/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28666011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bartelt, Alexander</creatorcontrib><creatorcontrib>Jeschke, Anke</creatorcontrib><creatorcontrib>Müller, Brigitte</creatorcontrib><creatorcontrib>Gaziano, Isabella</creatorcontrib><creatorcontrib>Morales, Michelle</creatorcontrib><creatorcontrib>Yorgan, Timur</creatorcontrib><creatorcontrib>Heckt, Timo</creatorcontrib><creatorcontrib>Heine, Markus</creatorcontrib><creatorcontrib>Gagel, Robert F</creatorcontrib><creatorcontrib>Emeson, Ronald B</creatorcontrib><creatorcontrib>Amling, Michael</creatorcontrib><creatorcontrib>Niemeier, Andreas</creatorcontrib><creatorcontrib>Heeren, Jörg</creatorcontrib><creatorcontrib>Schinke, Thorsten</creatorcontrib><creatorcontrib>Keller, Johannes</creatorcontrib><title>Differential effects of Calca-derived peptides in male mice with diet-induced obesity</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Key metabolic hormones, such as insulin, leptin, and adiponectin, have been studied extensively in obesity, however the pathophysiologic relevance of the calcitonin family of peptides remains unclear. This family includes calcitonin (CT), its precursor procalcitonin (PCT), and alpha calcitonin-gene related peptide (αCGRP), which are all encoded by the gene Calca. Here, we studied the role of Calca-derived peptides in diet-induced obesity (DIO) by challenging Calcr-/- (encoding the calcitonin receptor, CTR), Calca-/-, and αCGRP-/- mice and their respective littermates with high-fat diet (HFD) feeding for 16 weeks. HFD-induced pathologies were assessed by glucose tolerance, plasma cytokine and lipid markers, expression studies and histology. We found that DIO in mice lacking the CTR resulted in impaired glucose tolerance, features of enhanced nonalcoholic steatohepatitis (NASH) and adipose tissue inflammation compared to wildtype littermates. Furthermore, CTR-deficient mice were characterized by dyslipidemia and elevated HDL levels. In contrast, mice lacking Calca were protected from DIO, NASH and adipose tissue inflammation, and displayed improved glucose tolerance. Mice exclusively lacking αCGRP displayed a significantly less improved DIO phenotype compared to Calca-deficient mice. In summary, we demonstrate that the CT/CTR axis is involved in regulating plasma cholesterol levels while Calca, presumably through PCT, seems to have a detrimental effect in the context of metabolic disease. Our study provides the first comparative analyses of the roles of Calca-derived peptides and the CTR in metabolic disease.</description><subject>Adipocytes</subject><subject>Adiponectin</subject><subject>Adipose tissue</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Biomechanics</subject><subject>Calcitonin</subject><subject>Calcitonin gene-related peptide</subject><subject>Calcitonin Gene-Related Peptide - chemistry</subject><subject>Cholesterol</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Dosage and administration</subject><subject>Dyslipidemia</subject><subject>Feeding</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genetically modified mice</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Health aspects</subject><subject>High density lipoprotein</subject><subject>High fat diet</subject><subject>Histology</subject><subject>Homeostasis</subject><subject>Hormones</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Leptin</subject><subject>Lipids</subject><subject>Male</subject><subject>Markers</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic diseases</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Obesity</subject><subject>Obesity - etiology</subject><subject>Obesity - metabolism</subject><subject>Orthopedics</subject><subject>Peptides</subject><subject>Peptides - physiology</subject><subject>Physiology</subject><subject>Polypeptides</subject><subject>Procalcitonin</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Sepsis</subject><subject>Weight 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Markus</au><au>Gagel, Robert F</au><au>Emeson, Ronald B</au><au>Amling, Michael</au><au>Niemeier, Andreas</au><au>Heeren, Jörg</au><au>Schinke, Thorsten</au><au>Keller, Johannes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential effects of Calca-derived peptides in male mice with diet-induced obesity</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-06-30</date><risdate>2017</risdate><volume>12</volume><issue>6</issue><spage>e0180547</spage><epage>e0180547</epage><pages>e0180547-e0180547</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Key metabolic hormones, such as insulin, leptin, and adiponectin, have been studied extensively in obesity, however the pathophysiologic relevance of the calcitonin family of peptides remains unclear. This family includes calcitonin (CT), its precursor procalcitonin (PCT), and alpha calcitonin-gene related peptide (αCGRP), which are all encoded by the gene Calca. Here, we studied the role of Calca-derived peptides in diet-induced obesity (DIO) by challenging Calcr-/- (encoding the calcitonin receptor, CTR), Calca-/-, and αCGRP-/- mice and their respective littermates with high-fat diet (HFD) feeding for 16 weeks. HFD-induced pathologies were assessed by glucose tolerance, plasma cytokine and lipid markers, expression studies and histology. We found that DIO in mice lacking the CTR resulted in impaired glucose tolerance, features of enhanced nonalcoholic steatohepatitis (NASH) and adipose tissue inflammation compared to wildtype littermates. Furthermore, CTR-deficient mice were characterized by dyslipidemia and elevated HDL levels. In contrast, mice lacking Calca were protected from DIO, NASH and adipose tissue inflammation, and displayed improved glucose tolerance. Mice exclusively lacking αCGRP displayed a significantly less improved DIO phenotype compared to Calca-deficient mice. In summary, we demonstrate that the CT/CTR axis is involved in regulating plasma cholesterol levels while Calca, presumably through PCT, seems to have a detrimental effect in the context of metabolic disease. Our study provides the first comparative analyses of the roles of Calca-derived peptides and the CTR in metabolic disease.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28666011</pmid><doi>10.1371/journal.pone.0180547</doi><tpages>e0180547</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1914989116 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adipocytes Adiponectin Adipose tissue Animals Biochemistry Biology Biology and Life Sciences Biomechanics Calcitonin Calcitonin gene-related peptide Calcitonin Gene-Related Peptide - chemistry Cholesterol Diet Diet, High-Fat Dosage and administration Dyslipidemia Feeding Gene expression Genetic aspects Genetically modified mice Glucose Glucose tolerance Health aspects High density lipoprotein High fat diet Histology Homeostasis Hormones Insulin Insulin resistance Leptin Lipids Male Markers Medicine and Health Sciences Metabolic diseases Metabolism Mice Mice, Inbred C57BL Mice, Knockout Obesity Obesity - etiology Obesity - metabolism Orthopedics Peptides Peptides - physiology Physiology Polypeptides Procalcitonin Research and Analysis Methods Rodents Sepsis Weight control |
| title | Differential effects of Calca-derived peptides in male mice with diet-induced obesity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-10T18%3A51%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Differential%20effects%20of%20Calca-derived%20peptides%20in%20male%20mice%20with%20diet-induced%20obesity&rft.jtitle=PloS%20one&rft.au=Bartelt,%20Alexander&rft.date=2017-06-30&rft.volume=12&rft.issue=6&rft.spage=e0180547&rft.epage=e0180547&rft.pages=e0180547-e0180547&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0180547&rft_dat=%3Cgale_plos_%3EA497491302%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1914989116&rft_id=info:pmid/28666011&rft_galeid=A497491302&rft_doaj_id=oai_doaj_org_article_ce6530ae24dc4ee8950d1f77f22b9c2e&rfr_iscdi=true |