Long-Term Modulation of Appetitive Hormones and Sweet Cravings After Adjustable Gastric Banding and Roux-en-Y Gastric Bypass.
Adjustable gastric banding
Appetite
Bariatric surgery
Ghrelin
Glp-1
Insulin resistance
Metabolic surgery
PYY
Roux-en-Y gastric bypass
Sweet cravings
Journal
Obesity surgery
ISSN: 1708-0428
Titre abrégé: Obes Surg
Pays: United States
ID NLM: 9106714
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
pubmed:
4
8
2019
medline:
23
5
2020
entrez:
4
8
2019
Statut:
ppublish
Résumé
Roux-en-Y gastric bypass (RYGB) produces greater weight loss compared with a purely restrictive procedure such as laparoscopic adjustable gastric banding (LAGB). The objective of this study was to quantify changes in hormones that regulate energy homeostasis and appetitive sensations before and after LAGB (n = 18) and RYGB (n = 38) in order to better understand the mechanisms underlying the greater weight loss after RYGB. A standardized test meal was administered prior to surgery, at 6 months, and annually thereafter to year 2 after LAGB and year 4 after RYGB. Blood samples were obtained in the fasted state and 30, 60, 90, and 120 min post-meal. Progressive increases in fasting PYY were observed after RYGB together with increases in postprandial area under the curve (AUC) levels that were unchanged after LAGB. GLP-1 AUC increased only after RYGB. There was a weight loss-related increase in fasting ghrelin levels after LAGB that was unchanged 1 year after RYGB despite greater percentage weight loss; ghrelin subsequently increased at years 2-4 post-RYGB. HOMA-IR decreased after both procedures but correlated with weight loss only after LAGB, whereas leptin correlated with weight loss in both groups. Sweet cravings decreased after RYGB. A number of weight loss-independent changes in the gut hormonal milieu likely act in concert to promote a decrease in insulin resistance and greater weight loss efficacy after RYGB. A progressive change in hormone levels over time may reflect gut enteroplasticity after RYGB. A decrease in sweet cravings specific to RYGB may further promote superior weight loss outcomes.
Sections du résumé
BACKGROUND
Roux-en-Y gastric bypass (RYGB) produces greater weight loss compared with a purely restrictive procedure such as laparoscopic adjustable gastric banding (LAGB).
OBJECTIVE
The objective of this study was to quantify changes in hormones that regulate energy homeostasis and appetitive sensations before and after LAGB (n = 18) and RYGB (n = 38) in order to better understand the mechanisms underlying the greater weight loss after RYGB.
METHODS
A standardized test meal was administered prior to surgery, at 6 months, and annually thereafter to year 2 after LAGB and year 4 after RYGB. Blood samples were obtained in the fasted state and 30, 60, 90, and 120 min post-meal.
RESULTS
Progressive increases in fasting PYY were observed after RYGB together with increases in postprandial area under the curve (AUC) levels that were unchanged after LAGB. GLP-1 AUC increased only after RYGB. There was a weight loss-related increase in fasting ghrelin levels after LAGB that was unchanged 1 year after RYGB despite greater percentage weight loss; ghrelin subsequently increased at years 2-4 post-RYGB. HOMA-IR decreased after both procedures but correlated with weight loss only after LAGB, whereas leptin correlated with weight loss in both groups. Sweet cravings decreased after RYGB.
CONCLUSION
A number of weight loss-independent changes in the gut hormonal milieu likely act in concert to promote a decrease in insulin resistance and greater weight loss efficacy after RYGB. A progressive change in hormone levels over time may reflect gut enteroplasticity after RYGB. A decrease in sweet cravings specific to RYGB may further promote superior weight loss outcomes.
Identifiants
pubmed: 31376135
doi: 10.1007/s11695-019-04111-z
pii: 10.1007/s11695-019-04111-z
pmc: PMC6851479
mid: NIHMS1536489
doi:
Substances chimiques
Ghrelin
0
Insulin
0
Glucagon-Like Peptide 1
89750-14-1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
3698-3705Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK064819
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK072011
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007271
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR024156
Pays : United States
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