Beta-Hydroxybutyrate Suppresses Hepatic Production of the Ghrelin Receptor Antagonist LEAP2
IntroductionLiver-expressed antimicrobial peptide-2 (LEAP2) is an endogenous ghrelin receptor antagonist, which is upregulated in the fed state and downregulated during fasting. We hypothesized that the ketone body beta-hydroxybutyrate (BHB) is involved in the downregulation of LEAP2 during conditio...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2022-06, Vol.163 (6), p.1 |
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| creator | Holm, Stephanie Husted, Anna S Skov, Louise J Morville, Thomas H Hagemann, Christoffer A Jorsal, Tina Dall, Morten Jakobsen, Alexander Klein, Anders B Treebak, Jonas T Knop, Filip K Schwartz, Thue W Clemmensen, Christoffer Holst, Birgitte |
| description | IntroductionLiver-expressed antimicrobial peptide-2 (LEAP2) is an endogenous ghrelin receptor antagonist, which is upregulated in the fed state and downregulated during fasting. We hypothesized that the ketone body beta-hydroxybutyrate (BHB) is involved in the downregulation of LEAP2 during conditions with high circulating levels of BHB.
MethodsHepatic and intestinal Leap2 expression were determined in 3 groups of mice with increasing circulating levels of BHB: prolonged fasting, prolonged ketogenic diet, and oral BHB treatment. LEAP2 levels were measured in lean and obese individuals, in human individuals following endurance exercise, and in mice after BHB treatment. Lastly, we investigated Leap2 expression in isolated murine hepatocytes challenged with BHB.
ResultsWe confirmed increased circulating LEAP2 levels in individuals with obesity compared to lean individuals. The recovery period after endurance exercise was associated with increased plasma levels of BHB levels and decreased LEAP2 levels in humans. Leap2 expression was selectively decreased in the liver after fasting and after exposure to a ketogenic diet for 3 weeks. Importantly, we found that oral administration of BHB increased circulating levels of BHB in mice and decreased Leap2 expression levels and circulating LEAP2 plasma levels, as did Leap2 expression after direct exposure to BHB in isolated murine hepatocytes.
ConclusionFrom our data, we suggest that LEAP2 is downregulated during different states of energy deprivation in both humans and rodents. Furthermore, we here provide evidence that the ketone body, BHB, which is highly upregulated during fasting metabolism, directly downregulates LEAP2 levels. This may be relevant in ghrelin receptor–induced hunger signaling during energy deprivation. |
| doi_str_mv | 10.1210/endocr/bqac038 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9119693</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A775893530</galeid><oup_id>10.1210/endocr/bqac038</oup_id><sourcerecordid>A775893530</sourcerecordid><originalsourceid>FETCH-LOGICAL-c519t-1dff0b93212757ee0621d88b1b231f121cddb93e16be7508f9493bc03f7fe8b83</originalsourceid><addsrcrecordid>eNqFks1rFDEYxoMotlavHmXAix6mzcdkMrkI21K7woLFj5OHkMm82U2ZTaZJRtz_3pRd6wcFySEk7-99wpP3QeglwaeEEnwGfggmnvW32mDWPULHRDa8FkTgx-gYY8JqQak4Qs9SuinHpmnYU3TEOOOluztG384h63q5G2L4sevnvIs6Q_V5nqYIKUGqljDp7Ex1HcMwm-yCr4Kt8gaqq02E0fnqExiYcojVwme9Dt6lXK0uF9f0OXpi9ZjgxWE_QV_fX365WNarj1cfLhar2nAic00Ga3EvGSVUcAGAW0qGrutJTxmxxaUZhlIG0vYgOO6sbCTri10rLHR9x07Qu73uNPdbGAz4HPWopui2Ou5U0E79XfFuo9bhu5KEyFayIvDmIBDD7Qwpq61LBsZRewhzUrRteCMIb2hBX_-D3oQ5-mJP0U6SljPWit_UWo-gnLehvGvuRNVCCN7JMgBcqNMHqLIG2DoTPFhX7h9qMDGkFMHeeyRY3cVB7eOgDnEoDa_-_Jl7_Nf8C_B2D4R5-p_YT7KvwIE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2891653367</pqid></control><display><type>article</type><title>Beta-Hydroxybutyrate Suppresses Hepatic Production of the Ghrelin Receptor Antagonist LEAP2</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Holm, Stephanie ; Husted, Anna S ; Skov, Louise J ; Morville, Thomas H ; Hagemann, Christoffer A ; Jorsal, Tina ; Dall, Morten ; Jakobsen, Alexander ; Klein, Anders B ; Treebak, Jonas T ; Knop, Filip K ; Schwartz, Thue W ; Clemmensen, Christoffer ; Holst, Birgitte</creator><creatorcontrib>Holm, Stephanie ; Husted, Anna S ; Skov, Louise J ; Morville, Thomas H ; Hagemann, Christoffer A ; Jorsal, Tina ; Dall, Morten ; Jakobsen, Alexander ; Klein, Anders B ; Treebak, Jonas T ; Knop, Filip K ; Schwartz, Thue W ; Clemmensen, Christoffer ; Holst, Birgitte</creatorcontrib><description>IntroductionLiver-expressed antimicrobial peptide-2 (LEAP2) is an endogenous ghrelin receptor antagonist, which is upregulated in the fed state and downregulated during fasting. We hypothesized that the ketone body beta-hydroxybutyrate (BHB) is involved in the downregulation of LEAP2 during conditions with high circulating levels of BHB.
MethodsHepatic and intestinal Leap2 expression were determined in 3 groups of mice with increasing circulating levels of BHB: prolonged fasting, prolonged ketogenic diet, and oral BHB treatment. LEAP2 levels were measured in lean and obese individuals, in human individuals following endurance exercise, and in mice after BHB treatment. Lastly, we investigated Leap2 expression in isolated murine hepatocytes challenged with BHB.
ResultsWe confirmed increased circulating LEAP2 levels in individuals with obesity compared to lean individuals. The recovery period after endurance exercise was associated with increased plasma levels of BHB levels and decreased LEAP2 levels in humans. Leap2 expression was selectively decreased in the liver after fasting and after exposure to a ketogenic diet for 3 weeks. Importantly, we found that oral administration of BHB increased circulating levels of BHB in mice and decreased Leap2 expression levels and circulating LEAP2 plasma levels, as did Leap2 expression after direct exposure to BHB in isolated murine hepatocytes.
ConclusionFrom our data, we suggest that LEAP2 is downregulated during different states of energy deprivation in both humans and rodents. Furthermore, we here provide evidence that the ketone body, BHB, which is highly upregulated during fasting metabolism, directly downregulates LEAP2 levels. This may be relevant in ghrelin receptor–induced hunger signaling during energy deprivation.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/endocr/bqac038</identifier><identifier>PMID: 35352108</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>3-Hydroxybutyric Acid - metabolism ; Animals ; Antimicrobial peptides ; Aprotinin ; Body weight ; Deprivation ; Diet ; Diet, Ketogenic ; Down-regulation ; Endocrinology ; Endurance ; Energy requirements ; Ethylenediaminetetraacetic acid ; Exercise ; Fasting ; Fatty acids ; Ghrelin ; Ghrelin - metabolism ; Hepatocytes ; High fat diet ; Hunger ; Ketogenesis ; Ketones ; Liver ; Liver - metabolism ; Low carbohydrate diet ; Metabolism ; Mice ; Obesity ; Obesity - metabolism ; Oral administration ; Peptides ; Physiological aspects ; Plasma levels ; Receptors ; Receptors, Ghrelin - metabolism ; Type 2 diabetes ; Tyrosine</subject><ispartof>Endocrinology (Philadelphia), 2022-06, Vol.163 (6), p.1</ispartof><rights>The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. 2022</rights><rights>The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society.</rights><rights>COPYRIGHT 2022 Oxford University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c519t-1dff0b93212757ee0621d88b1b231f121cddb93e16be7508f9493bc03f7fe8b83</citedby><cites>FETCH-LOGICAL-c519t-1dff0b93212757ee0621d88b1b231f121cddb93e16be7508f9493bc03f7fe8b83</cites><orcidid>0000-0002-9628-8285 ; 0000-0003-2456-9667 ; 0000-0001-7432-097X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35352108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Holm, Stephanie</creatorcontrib><creatorcontrib>Husted, Anna S</creatorcontrib><creatorcontrib>Skov, Louise J</creatorcontrib><creatorcontrib>Morville, Thomas H</creatorcontrib><creatorcontrib>Hagemann, Christoffer A</creatorcontrib><creatorcontrib>Jorsal, Tina</creatorcontrib><creatorcontrib>Dall, Morten</creatorcontrib><creatorcontrib>Jakobsen, Alexander</creatorcontrib><creatorcontrib>Klein, Anders B</creatorcontrib><creatorcontrib>Treebak, Jonas T</creatorcontrib><creatorcontrib>Knop, Filip K</creatorcontrib><creatorcontrib>Schwartz, Thue W</creatorcontrib><creatorcontrib>Clemmensen, Christoffer</creatorcontrib><creatorcontrib>Holst, Birgitte</creatorcontrib><title>Beta-Hydroxybutyrate Suppresses Hepatic Production of the Ghrelin Receptor Antagonist LEAP2</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>IntroductionLiver-expressed antimicrobial peptide-2 (LEAP2) is an endogenous ghrelin receptor antagonist, which is upregulated in the fed state and downregulated during fasting. We hypothesized that the ketone body beta-hydroxybutyrate (BHB) is involved in the downregulation of LEAP2 during conditions with high circulating levels of BHB.
MethodsHepatic and intestinal Leap2 expression were determined in 3 groups of mice with increasing circulating levels of BHB: prolonged fasting, prolonged ketogenic diet, and oral BHB treatment. LEAP2 levels were measured in lean and obese individuals, in human individuals following endurance exercise, and in mice after BHB treatment. Lastly, we investigated Leap2 expression in isolated murine hepatocytes challenged with BHB.
ResultsWe confirmed increased circulating LEAP2 levels in individuals with obesity compared to lean individuals. The recovery period after endurance exercise was associated with increased plasma levels of BHB levels and decreased LEAP2 levels in humans. Leap2 expression was selectively decreased in the liver after fasting and after exposure to a ketogenic diet for 3 weeks. Importantly, we found that oral administration of BHB increased circulating levels of BHB in mice and decreased Leap2 expression levels and circulating LEAP2 plasma levels, as did Leap2 expression after direct exposure to BHB in isolated murine hepatocytes.
ConclusionFrom our data, we suggest that LEAP2 is downregulated during different states of energy deprivation in both humans and rodents. Furthermore, we here provide evidence that the ketone body, BHB, which is highly upregulated during fasting metabolism, directly downregulates LEAP2 levels. This may be relevant in ghrelin receptor–induced hunger signaling during energy deprivation.</description><subject>3-Hydroxybutyric Acid - metabolism</subject><subject>Animals</subject><subject>Antimicrobial peptides</subject><subject>Aprotinin</subject><subject>Body weight</subject><subject>Deprivation</subject><subject>Diet</subject><subject>Diet, Ketogenic</subject><subject>Down-regulation</subject><subject>Endocrinology</subject><subject>Endurance</subject><subject>Energy requirements</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Exercise</subject><subject>Fasting</subject><subject>Fatty acids</subject><subject>Ghrelin</subject><subject>Ghrelin - metabolism</subject><subject>Hepatocytes</subject><subject>High fat diet</subject><subject>Hunger</subject><subject>Ketogenesis</subject><subject>Ketones</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Low carbohydrate diet</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Oral administration</subject><subject>Peptides</subject><subject>Physiological aspects</subject><subject>Plasma levels</subject><subject>Receptors</subject><subject>Receptors, Ghrelin - metabolism</subject><subject>Type 2 diabetes</subject><subject>Tyrosine</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNqFks1rFDEYxoMotlavHmXAix6mzcdkMrkI21K7woLFj5OHkMm82U2ZTaZJRtz_3pRd6wcFySEk7-99wpP3QeglwaeEEnwGfggmnvW32mDWPULHRDa8FkTgx-gYY8JqQak4Qs9SuinHpmnYU3TEOOOluztG384h63q5G2L4sevnvIs6Q_V5nqYIKUGqljDp7Ex1HcMwm-yCr4Kt8gaqq02E0fnqExiYcojVwme9Dt6lXK0uF9f0OXpi9ZjgxWE_QV_fX365WNarj1cfLhar2nAic00Ga3EvGSVUcAGAW0qGrutJTxmxxaUZhlIG0vYgOO6sbCTri10rLHR9x07Qu73uNPdbGAz4HPWopui2Ou5U0E79XfFuo9bhu5KEyFayIvDmIBDD7Qwpq61LBsZRewhzUrRteCMIb2hBX_-D3oQ5-mJP0U6SljPWit_UWo-gnLehvGvuRNVCCN7JMgBcqNMHqLIG2DoTPFhX7h9qMDGkFMHeeyRY3cVB7eOgDnEoDa_-_Jl7_Nf8C_B2D4R5-p_YT7KvwIE</recordid><startdate>20220601</startdate><enddate>20220601</enddate><creator>Holm, Stephanie</creator><creator>Husted, Anna S</creator><creator>Skov, Louise J</creator><creator>Morville, Thomas H</creator><creator>Hagemann, Christoffer A</creator><creator>Jorsal, Tina</creator><creator>Dall, Morten</creator><creator>Jakobsen, Alexander</creator><creator>Klein, Anders B</creator><creator>Treebak, Jonas T</creator><creator>Knop, Filip K</creator><creator>Schwartz, Thue W</creator><creator>Clemmensen, Christoffer</creator><creator>Holst, Birgitte</creator><general>Oxford University Press</general><scope>TOX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9628-8285</orcidid><orcidid>https://orcid.org/0000-0003-2456-9667</orcidid><orcidid>https://orcid.org/0000-0001-7432-097X</orcidid></search><sort><creationdate>20220601</creationdate><title>Beta-Hydroxybutyrate Suppresses Hepatic Production of the Ghrelin Receptor Antagonist LEAP2</title><author>Holm, Stephanie ; Husted, Anna S ; Skov, Louise J ; Morville, Thomas H ; Hagemann, Christoffer A ; Jorsal, Tina ; Dall, Morten ; Jakobsen, Alexander ; Klein, Anders B ; Treebak, Jonas T ; Knop, Filip K ; Schwartz, Thue W ; Clemmensen, Christoffer ; Holst, Birgitte</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c519t-1dff0b93212757ee0621d88b1b231f121cddb93e16be7508f9493bc03f7fe8b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3-Hydroxybutyric Acid - metabolism</topic><topic>Animals</topic><topic>Antimicrobial peptides</topic><topic>Aprotinin</topic><topic>Body weight</topic><topic>Deprivation</topic><topic>Diet</topic><topic>Diet, Ketogenic</topic><topic>Down-regulation</topic><topic>Endocrinology</topic><topic>Endurance</topic><topic>Energy requirements</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Exercise</topic><topic>Fasting</topic><topic>Fatty acids</topic><topic>Ghrelin</topic><topic>Ghrelin - metabolism</topic><topic>Hepatocytes</topic><topic>High fat diet</topic><topic>Hunger</topic><topic>Ketogenesis</topic><topic>Ketones</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Low carbohydrate diet</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Oral administration</topic><topic>Peptides</topic><topic>Physiological aspects</topic><topic>Plasma levels</topic><topic>Receptors</topic><topic>Receptors, Ghrelin - metabolism</topic><topic>Type 2 diabetes</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Holm, Stephanie</creatorcontrib><creatorcontrib>Husted, Anna S</creatorcontrib><creatorcontrib>Skov, Louise J</creatorcontrib><creatorcontrib>Morville, Thomas H</creatorcontrib><creatorcontrib>Hagemann, Christoffer A</creatorcontrib><creatorcontrib>Jorsal, Tina</creatorcontrib><creatorcontrib>Dall, Morten</creatorcontrib><creatorcontrib>Jakobsen, Alexander</creatorcontrib><creatorcontrib>Klein, Anders B</creatorcontrib><creatorcontrib>Treebak, Jonas T</creatorcontrib><creatorcontrib>Knop, Filip K</creatorcontrib><creatorcontrib>Schwartz, Thue W</creatorcontrib><creatorcontrib>Clemmensen, Christoffer</creatorcontrib><creatorcontrib>Holst, Birgitte</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Holm, Stephanie</au><au>Husted, Anna S</au><au>Skov, Louise J</au><au>Morville, Thomas H</au><au>Hagemann, Christoffer A</au><au>Jorsal, Tina</au><au>Dall, Morten</au><au>Jakobsen, Alexander</au><au>Klein, Anders B</au><au>Treebak, Jonas T</au><au>Knop, Filip K</au><au>Schwartz, Thue W</au><au>Clemmensen, Christoffer</au><au>Holst, Birgitte</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beta-Hydroxybutyrate Suppresses Hepatic Production of the Ghrelin Receptor Antagonist LEAP2</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2022-06-01</date><risdate>2022</risdate><volume>163</volume><issue>6</issue><spage>1</spage><pages>1-</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>IntroductionLiver-expressed antimicrobial peptide-2 (LEAP2) is an endogenous ghrelin receptor antagonist, which is upregulated in the fed state and downregulated during fasting. We hypothesized that the ketone body beta-hydroxybutyrate (BHB) is involved in the downregulation of LEAP2 during conditions with high circulating levels of BHB.
MethodsHepatic and intestinal Leap2 expression were determined in 3 groups of mice with increasing circulating levels of BHB: prolonged fasting, prolonged ketogenic diet, and oral BHB treatment. LEAP2 levels were measured in lean and obese individuals, in human individuals following endurance exercise, and in mice after BHB treatment. Lastly, we investigated Leap2 expression in isolated murine hepatocytes challenged with BHB.
ResultsWe confirmed increased circulating LEAP2 levels in individuals with obesity compared to lean individuals. The recovery period after endurance exercise was associated with increased plasma levels of BHB levels and decreased LEAP2 levels in humans. Leap2 expression was selectively decreased in the liver after fasting and after exposure to a ketogenic diet for 3 weeks. Importantly, we found that oral administration of BHB increased circulating levels of BHB in mice and decreased Leap2 expression levels and circulating LEAP2 plasma levels, as did Leap2 expression after direct exposure to BHB in isolated murine hepatocytes.
ConclusionFrom our data, we suggest that LEAP2 is downregulated during different states of energy deprivation in both humans and rodents. Furthermore, we here provide evidence that the ketone body, BHB, which is highly upregulated during fasting metabolism, directly downregulates LEAP2 levels. This may be relevant in ghrelin receptor–induced hunger signaling during energy deprivation.</abstract><cop>US</cop><pub>Oxford University Press</pub><pmid>35352108</pmid><doi>10.1210/endocr/bqac038</doi><orcidid>https://orcid.org/0000-0002-9628-8285</orcidid><orcidid>https://orcid.org/0000-0003-2456-9667</orcidid><orcidid>https://orcid.org/0000-0001-7432-097X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 3-Hydroxybutyric Acid - metabolism Animals Antimicrobial peptides Aprotinin Body weight Deprivation Diet Diet, Ketogenic Down-regulation Endocrinology Endurance Energy requirements Ethylenediaminetetraacetic acid Exercise Fasting Fatty acids Ghrelin Ghrelin - metabolism Hepatocytes High fat diet Hunger Ketogenesis Ketones Liver Liver - metabolism Low carbohydrate diet Metabolism Mice Obesity Obesity - metabolism Oral administration Peptides Physiological aspects Plasma levels Receptors Receptors, Ghrelin - metabolism Type 2 diabetes Tyrosine |
| title | Beta-Hydroxybutyrate Suppresses Hepatic Production of the Ghrelin Receptor Antagonist LEAP2 |
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