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Circulating ghrelin concentrations are modulated in response to nutritional status, but responses to ghrelin in altered metabolic states are poorly understood. We investigated the metabolic effects of ghrelin in obesity and early after\n                      <jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\n                      oux\u2010en\u2010\n                      <jats:styled-content style=\"fixed-case\">Y<\/jats:styled-content>\n                      gastric bypass (\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>\n                      We assessed central and peripheral metabolic responses to acyl ghrelin infusion (1\u2009pmol\u2009kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      \u2009min\n                      <jats:sup>\u22121<\/jats:sup>\n                      ) in healthy, lean subjects (n\u2009=\u20099) and non\u2010diabetic, obese subjects (n\u2009=\u20099) before and 2\u2009weeks after\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      . Central responses were assessed by\n                      <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                      and pancreatic polypeptide (surrogate for vagal activity) secretion. Peripheral responses were assessed by hepatic and skeletal muscle insulin sensitivity during a hyperinsulinaemic\u2010euglycaemic clamp.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ghrelin\u2010stimulated\n                      <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                      secretion was attenuated in obese subjects, but was restored by\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      to a response similar to that of lean subjects. The heightened pancreatic polypeptide response to ghrelin infusion in the obese was attenuated after\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      . Hepatic glucose production and hepatic insulin sensitivity were not altered by ghrelin infusion in\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      subjects. Skeletal muscle insulin sensitivity was impaired to a similar degree in lean, obese and post\u2010\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      individuals in response to ghrelin infusion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These data suggest that obesity is characterized by abnormal central, but not peripheral, responsiveness to ghrelin that can be restored early after\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      before significant weight loss. Further work is necessary to fully elucidate the role of ghrelin in the metabolic changes that occur in obesity and following\n                      <jats:styled-content style=\"fixed-case\">RYGB<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.12952","type":"journal-article","created":{"date-parts":[[2017,3,27]],"date-time":"2017-03-27T07:57:18Z","timestamp":1490601438000},"page":"1267-1275","source":"Crossref","is-referenced-by-count":29,"title":["Metabolic responses to exogenous ghrelin in obesity and early after\n                    <scp>R<\/scp>\n                    oux\u2010en\u2010\n                    <scp>Y<\/scp>\n                    gastric bypass in humans"],"prefix":"10.1111","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6398-935X","authenticated-orcid":false,"given":"Robyn A.","family":"Tamboli","sequence":"first","affiliation":[{"name":"Department of Surgery Vanderbilt 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Tennessee"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pam","family":"Marks\u2010Shulman","sequence":"additional","affiliation":[{"name":"Department of Surgery Vanderbilt University Medical Center  Nashville Tennessee"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce D.","family":"Gaylinn","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine University of Virginia  Charlottesville Virginia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brandon","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Surgery Vanderbilt University Medical Center  Nashville Tennessee"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald H.","family":"Clements","sequence":"additional","affiliation":[{"name":"Department of Surgery Vanderbilt University Medical Center  Nashville 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