Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response

Glucose-dependent insulinotropic polypeptide (GIP) beyond its insulinotropic effects may regulate postprandial lipid metabolism. Whereas the insulinotropic action of GIP is known to be impaired in type 2 diabetes mellitus (T2DM), its adipogenic effect is unknown. We hypothesized that GIP is anabolic...

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Autores: Thondam, Sravan K., Daousi, Christina, WIlding, John P., Holst, Jens J., Ameen, Gulizar Issa, Yang, Chenjing, Whitmore, Catherine, Mora Fayos, Sílvia, Cuthbertson, Daniel J.
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2017
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/175938
Acceso en línea:https://hdl.handle.net/2445/175938
Access Level:acceso abierto
Palabra clave:Diabetis
Teixit adipós
Diabetes
Adipose tissues
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spelling Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive responseThondam, Sravan K.Daousi, ChristinaWIlding, John P.Holst, Jens J.Ameen, Gulizar IssaYang, ChenjingWhitmore, CatherineMora Fayos, SílviaCuthbertson, Daniel J.DiabetisTeixit adipósDiabetesAdipose tissuesGlucose-dependent insulinotropic polypeptide (GIP) beyond its insulinotropic effects may regulate postprandial lipid metabolism. Whereas the insulinotropic action of GIP is known to be impaired in type 2 diabetes mellitus (T2DM), its adipogenic effect is unknown. We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Twenty-three subjects categorized into four groups, normoglycemic lean (n = 6), normoglycemic obese (n = 6), obese with impaired glucose regulation (IGR; n = 6), and obese T2DM (n = 5), participated in a double-blind, randomized, crossover study involving a hyperglycemic clamp with a 240-min GIP infusion (2 pmol·kg−1·min−1) or normal saline. Insulin, NEFA, SAT-TAG content, and gene expression of key lipogenic enzymes were determined before and immediately after GIP/saline infusions. GIP lowered NEFA concentrations in the obese T2DM group despite diminished insulinotropic activity (mean NEFA AUC0-4 h ± SE, 41,992 ± 9,843 µmol·l−1·min−1 vs. 71,468 ± 13,605 with placebo, P = 0.039, 95% CI: 0.31-0.95). Additionally, GIP increased SAT-TAG in obese T2DM (1.78 ± 0.4 vs 0.86 ± 0.1-fold with placebo, P = 0.043, 95% CI: 0.1-1.8). Such effect with GIP was not observed in other three groups despite greater insulinotropic activity. Reduction in NEFA concentration with GIP correlated with adipose tissue insulin resistance for all subjects (Pearson, r = 0.56, P = 0.005). There were no significant gene expression changes in key SAT lipid metabolism enzymes. In conclusion, GIP appears to promote fat accretion and thus may exacerbate obesity and insulin resistance in T2DM.American Physiological Society2021202120172021info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersion10 p.application/pdfapplication/pdfhttps://hdl.handle.net/2445/175938Articles publicats en revistes (Bioquímica i Biomedicina Molecular)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésVersió postprint del document publicat a: https://doi.org/10.1152/ajpendo.00347.2016American Journal of Physiology-Endocrinology and Metabolism, 2017, vol. 312, p. E224-E233https://doi.org/10.1152/ajpendo.00347.2016(c) American Physiological Society, 2017info:eu-repo/semantics/openAccessoai:recercat.cat:2445/1759382026-05-29T05:05:01Z
dc.title.none.fl_str_mv Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
title Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
spellingShingle Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
Thondam, Sravan K.
Diabetis
Teixit adipós
Diabetes
Adipose tissues
title_short Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
title_full Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
title_fullStr Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
title_full_unstemmed Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
title_sort Glucose-dependent insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese, type-2 diabetes patients: a maladaptive response
dc.creator.none.fl_str_mv Thondam, Sravan K.
Daousi, Christina
WIlding, John P.
Holst, Jens J.
Ameen, Gulizar Issa
Yang, Chenjing
Whitmore, Catherine
Mora Fayos, Sílvia
Cuthbertson, Daniel J.
author Thondam, Sravan K.
author_facet Thondam, Sravan K.
Daousi, Christina
WIlding, John P.
Holst, Jens J.
Ameen, Gulizar Issa
Yang, Chenjing
Whitmore, Catherine
Mora Fayos, Sílvia
Cuthbertson, Daniel J.
author_role author
author2 Daousi, Christina
WIlding, John P.
Holst, Jens J.
Ameen, Gulizar Issa
Yang, Chenjing
Whitmore, Catherine
Mora Fayos, Sílvia
Cuthbertson, Daniel J.
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Diabetis
Teixit adipós
Diabetes
Adipose tissues
topic Diabetis
Teixit adipós
Diabetes
Adipose tissues
description Glucose-dependent insulinotropic polypeptide (GIP) beyond its insulinotropic effects may regulate postprandial lipid metabolism. Whereas the insulinotropic action of GIP is known to be impaired in type 2 diabetes mellitus (T2DM), its adipogenic effect is unknown. We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Twenty-three subjects categorized into four groups, normoglycemic lean (n = 6), normoglycemic obese (n = 6), obese with impaired glucose regulation (IGR; n = 6), and obese T2DM (n = 5), participated in a double-blind, randomized, crossover study involving a hyperglycemic clamp with a 240-min GIP infusion (2 pmol·kg−1·min−1) or normal saline. Insulin, NEFA, SAT-TAG content, and gene expression of key lipogenic enzymes were determined before and immediately after GIP/saline infusions. GIP lowered NEFA concentrations in the obese T2DM group despite diminished insulinotropic activity (mean NEFA AUC0-4 h ± SE, 41,992 ± 9,843 µmol·l−1·min−1 vs. 71,468 ± 13,605 with placebo, P = 0.039, 95% CI: 0.31-0.95). Additionally, GIP increased SAT-TAG in obese T2DM (1.78 ± 0.4 vs 0.86 ± 0.1-fold with placebo, P = 0.043, 95% CI: 0.1-1.8). Such effect with GIP was not observed in other three groups despite greater insulinotropic activity. Reduction in NEFA concentration with GIP correlated with adipose tissue insulin resistance for all subjects (Pearson, r = 0.56, P = 0.005). There were no significant gene expression changes in key SAT lipid metabolism enzymes. In conclusion, GIP appears to promote fat accretion and thus may exacerbate obesity and insulin resistance in T2DM.
publishDate 2017
dc.date.none.fl_str_mv 2017
2021
2021
2021
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/175938
url https://hdl.handle.net/2445/175938
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: https://doi.org/10.1152/ajpendo.00347.2016
American Journal of Physiology-Endocrinology and Metabolism, 2017, vol. 312, p. E224-E233
https://doi.org/10.1152/ajpendo.00347.2016
dc.rights.none.fl_str_mv (c) American Physiological Society, 2017
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) American Physiological Society, 2017
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 10 p.
application/pdf
application/pdf
dc.publisher.none.fl_str_mv American Physiological Society
publisher.none.fl_str_mv American Physiological Society
dc.source.none.fl_str_mv Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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