Biliopancreatic Diversion Induces Greater Metabolic Improvement Than Roux-en-Y Gastric Bypass.
Bile Acids and Salts
/ metabolism
Biliopancreatic Diversion
/ methods
Blood Glucose
/ metabolism
Fatty Acids
/ metabolism
Follow-Up Studies
Gastric Bypass
/ methods
Humans
Insulin
/ blood
Insulin Resistance
Insulin-Secreting Cells
/ metabolism
Intestinal Absorption
Obesity, Morbid
/ metabolism
Postprandial Period
Treatment Outcome
Weight Loss
bariatric surgery
insulin sensitivity
obesity
Journal
Cell metabolism
ISSN: 1932-7420
Titre abrégé: Cell Metab
Pays: United States
ID NLM: 101233170
Informations de publication
Date de publication:
05 11 2019
05 11 2019
Historique:
received:
08
04
2019
revised:
03
07
2019
accepted:
03
09
2019
pubmed:
8
10
2019
medline:
10
9
2020
entrez:
8
10
2019
Statut:
ppublish
Résumé
Diabetes remission is greater after biliopancreatic diversion (BPD) than Roux-en-Y gastric bypass (RYGB) surgery. We used a mixed-meal test with ingested and infused glucose tracers and the hyperinsulinemic-euglycemic clamp procedure with glucose tracer infusion to assess the effect of 20% weight loss induced by either RYGB or BPD on glucoregulation in people with obesity (ClinicalTrials.gov number: NCT03111953). The rate of appearance of ingested glucose into the circulation was much slower, and the postprandial increases in plasma glucose and insulin concentrations were markedly blunted after BPD compared to after RYGB. Insulin sensitivity, assessed as glucose disposal rate during insulin infusion, was ∼45% greater after BPD than RYGB, whereas β cell function was not different between groups. These results demonstrate that compared with matched-percentage weight loss induced by RYGB, BPD has unique beneficial effects on glycemic control, manifested by slower postprandial glucose absorption, blunted postprandial plasma glucose and insulin excursions, and greater improvement in insulin sensitivity.
Identifiants
pubmed: 31588013
pii: S1550-4131(19)30503-0
doi: 10.1016/j.cmet.2019.09.002
pmc: PMC6876863
mid: NIHMS1543472
pii:
doi:
Substances chimiques
Bile Acids and Salts
0
Blood Glucose
0
Fatty Acids
0
Insulin
0
Banques de données
ClinicalTrials.gov
['NCT03111953']
Types de publication
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
855-864.e3Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK101578
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL130357
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES027595
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL020948
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK056341
Pays : United States
Organisme : NIH HHS
ID : S10 OD020025
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR002346
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000448
Pays : United States
Organisme : NIDDK NIH HHS
ID : P60 DK020579
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020579
Pays : United States
Organisme : NIDDK NIH HHS
ID : K01 DK116917
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002345
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR000450
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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