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Metabolic responses to exogenous ghrelin in obesity and early after R oux‐en‐ Y gastric bypass in humans
Author(s) -
Tamboli Robyn A.,
Antoun Joseph,
Sidani Reem M.,
Clements Austin,
Harmata Emily E.,
MarksShulman Pam,
Gaylinn Bruce D.,
Williams Brandon,
Clements Ronald H.,
Albaugh Vance L.,
Abumrad Naji N.
Publication year - 2017
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.12952
Subject(s) - ghrelin , medicine , endocrinology , insulin , glucose homeostasis , carbohydrate metabolism , homeostasis , insulin resistance , hormone , metabolic syndrome , obesity
Aims Ghrelin is a gastric‐derived hormone that stimulates growth hormone ( GH ) secretion and has a multi‐faceted role in the regulation of energy homeostasis, including glucose metabolism. 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 R oux‐en‐ Y gastric bypass ( RYGB ). Materials and methods We assessed central and peripheral metabolic responses to acyl ghrelin infusion (1 pmol kg −1  min −1 ) in healthy, lean subjects (n = 9) and non‐diabetic, obese subjects (n = 9) before and 2 weeks after RYGB . Central responses were assessed by GH and pancreatic polypeptide (surrogate for vagal activity) secretion. Peripheral responses were assessed by hepatic and skeletal muscle insulin sensitivity during a hyperinsulinaemic‐euglycaemic clamp. Results Ghrelin‐stimulated GH secretion was attenuated in obese subjects, but was restored by RYGB to a response similar to that of lean subjects. The heightened pancreatic polypeptide response to ghrelin infusion in the obese was attenuated after RYGB . Hepatic glucose production and hepatic insulin sensitivity were not altered by ghrelin infusion in RYGB subjects. Skeletal muscle insulin sensitivity was impaired to a similar degree in lean, obese and post‐ RYGB individuals in response to ghrelin infusion. Conclusions These data suggest that obesity is characterized by abnormal central, but not peripheral, responsiveness to ghrelin that can be restored early after RYGB 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 RYGB .

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