Impact of gastric emptying and small intestinal transit on blood glucose, intestinal hormones, glucose absorption in the morbidly obese

Objective: This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption Methods: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2...

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Published inInternational Journal of Obesity Vol. 42; no. 9; pp. 1556 - 1564
Main Authors Nguyen, Nam Q, Debreceni, Tamara L, Burgess, Jenna E, Bellon, Max, Wishart, Judith, Standfield, Scott, Malbert, Charles-Henri, Horowitz, Michael
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.09.2018
Nature Publishing Group
Subjects
101/47
631/45/776/198
692/699/1503/1702/393
82/16
9/10
Absorption
Adult
Blood
Blood glucose
Blood Glucose - metabolism
Emptying
Epidemiology
Female
Gastric emptying
Gastric Emptying - physiology
Gastrointestinal Hormones - metabolism
Gastrointestinal Transit - physiology
GIP protein
Glucagon
Glucagon-like peptide 1
Glucose
Health Promotion and Disease Prevention
Hormones
Humans
Insulin
Internal Medicine
Intestine
Intestine, Small - metabolism
Life Sciences
Male
Medical imaging
Medicine
Medicine & Public Health
Metabolic Diseases
Middle Aged
Obesity
Obesity, Morbid - metabolism
Obesity, Morbid - physiopathology
Public Health
Radionuclide Imaging
Scintigraphy
Transit
insulin sensitivity
weight-loss
glp-1 secretion
bariatric surgery
liqutest meal
high-fat
glucagon receptor
incretin hormones
type-2 diabetes-mellitus
gastrointestinal symptoms
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Abstract Objective: This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption Methods: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2.5 years; 13 F:9 M; BMI: 48.6 ± 1.8 kg/m 2 ) and 10 lean (38.6 ± 8.4 years; 5 F:5 M; BMI: 23.9 ± 0.7 kg/m 2 ) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantified Results: When compared with lean subjects, GE (t50: 60.7 ± 6.5 vs. 41.1 ± 7.3 min; P   = 0.04) and CAT (221.5 ± 9.8 vs. 148.0 ± 7.1 min; P  =  0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP ( P  = 0.001), insulin ( P   = 0.02), glucose ( P  = 0.03) and 3-O-methylglucose ( P  = 0.001) were less. Whereas GLP-1 increased at 45 mins post-prandially in lean subjects, there was no increase in the obese ( P   = 0.04). Both fasting ( P  = 0.045) and postprandial ( P  = 0.012) plasma glucagon concentrations were higher in the obese Conclusions: GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1
AbstractList This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption METHODS: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2.5 years; 13 F:9 M; BMI: 48.6 ± 1.8 kg/m2) and 10 lean (38.6 ± 8.4 years; 5 F:5 M; BMI: 23.9 ± 0.7 kg/m2) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantified RESULTS: When compared with lean subjects, GE (t50: 60.7 ± 6.5 vs. 41.1 ± 7.3 min; P  = 0.04) and CAT (221.5 ± 9.8 vs. 148.0 ± 7.1 min; P =  0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP (P = 0.001), insulin (P  = 0.02), glucose (P = 0.03) and 3-O-methylglucose (P = 0.001) were less. Whereas GLP-1 increased at 45 mins post-prandially in lean subjects, there was no increase in the obese (P  = 0.04). Both fasting (P = 0.045) and postprandial (P = 0.012) plasma glucagon concentrations were higher in the obese CONCLUSIONS: GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1.OBJECTIVEThis study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption METHODS: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2.5 years; 13 F:9 M; BMI: 48.6 ± 1.8 kg/m2) and 10 lean (38.6 ± 8.4 years; 5 F:5 M; BMI: 23.9 ± 0.7 kg/m2) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantified RESULTS: When compared with lean subjects, GE (t50: 60.7 ± 6.5 vs. 41.1 ± 7.3 min; P  = 0.04) and CAT (221.5 ± 9.8 vs. 148.0 ± 7.1 min; P =  0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP (P = 0.001), insulin (P  = 0.02), glucose (P = 0.03) and 3-O-methylglucose (P = 0.001) were less. Whereas GLP-1 increased at 45 mins post-prandially in lean subjects, there was no increase in the obese (P  = 0.04). Both fasting (P = 0.045) and postprandial (P = 0.012) plasma glucagon concentrations were higher in the obese CONCLUSIONS: GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1.
Objective: This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption Methods: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 +/- 2.5 years; 13 F:9 M; BMI: 48.6 +/- 1.8 kg/m(2)) and 10 lean (38.6 +/- 8.4 years; 5 F:5 M; BMI: 23.9 +/- 0.7 kg/m(2)) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantified Results: When compared with lean subjects, GE (t50: 60.7 +/- 6.5 vs. 41.1 +/- 7.3 min; P = 0.04) and CAT (221.5 +/- 9.8 vs. 148.0 +/- 7.1 min; P = 0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP (P = 0.001), insulin (P = 0.02), glucose (P = 0.03) and 3-O-methylglucose (P = 0.001) were less. Whereas GLP-1 increased at 45 mins postprandially in lean subjects, there was no increase in the obese (P = 0.04). Both fasting (P = 0.045) and postprandial (P = 0.012) plasma glucagon concentrations were higher in the obese Conclusions: GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1
Objective:This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorptionMethods:GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2.5 years; 13 F:9 M; BMI: 48.6 ± 1.8 kg/m2) and 10 lean (38.6 ± 8.4 years; 5 F:5 M; BMI: 23.9 ± 0.7 kg/m2) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantifiedResults:When compared with lean subjects, GE (t50: 60.7 ± 6.5 vs. 41.1 ± 7.3 min; P  = 0.04) and CAT (221.5 ± 9.8 vs. 148.0 ± 7.1 min; P =  0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP (P = 0.001), insulin (P  = 0.02), glucose (P = 0.03) and 3-O-methylglucose (P = 0.001) were less. Whereas GLP-1 increased at 45 mins post-prandially in lean subjects, there was no increase in the obese (P  = 0.04). Both fasting (P = 0.045) and postprandial (P = 0.012) plasma glucagon concentrations were higher in the obeseConclusions:GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1
Objective: This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption Methods: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2.5 years; 13 F:9 M; BMI: 48.6 ± 1.8 kg/m 2 ) and 10 lean (38.6 ± 8.4 years; 5 F:5 M; BMI: 23.9 ± 0.7 kg/m 2 ) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantified Results: When compared with lean subjects, GE (t50: 60.7 ± 6.5 vs. 41.1 ± 7.3 min; P   = 0.04) and CAT (221.5 ± 9.8 vs. 148.0 ± 7.1 min; P  =  0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP ( P  = 0.001), insulin ( P   = 0.02), glucose ( P  = 0.03) and 3-O-methylglucose ( P  = 0.001) were less. Whereas GLP-1 increased at 45 mins post-prandially in lean subjects, there was no increase in the obese ( P   = 0.04). Both fasting ( P  = 0.045) and postprandial ( P  = 0.012) plasma glucagon concentrations were higher in the obese Conclusions: GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1
This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin hormones, and glucose absorption METHODS: GE and caecal arrival time (CAT) of a mixed meal were assessed in 22 morbidly obese (50.2 ± 2.5 years; 13 F:9 M; BMI: 48.6 ± 1.8 kg/m ) and 10 lean (38.6 ± 8.4 years; 5 F:5 M; BMI: 23.9 ± 0.7 kg/m ) subjects, using scintigraphy. Blood glucose, plasma 3-O-methylglucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured. Insulin sensitivity and resistance were also quantified RESULTS: When compared with lean subjects, GE (t50: 60.7 ± 6.5 vs. 41.1 ± 7.3 min; P  = 0.04) and CAT (221.5 ± 9.8 vs. 148.0 ± 7.1 min; P =  0.001) of solids were prolonged in morbid obesity. Postprandial rises in GIP (P = 0.001), insulin (P  = 0.02), glucose (P = 0.03) and 3-O-methylglucose (P = 0.001) were less. Whereas GLP-1 increased at 45 mins post-prandially in lean subjects, there was no increase in the obese (P  = 0.04). Both fasting (P = 0.045) and postprandial (P = 0.012) plasma glucagon concentrations were higher in the obese CONCLUSIONS: GE and SI transit are slower in the morbidly obese, and associated with reductions in postprandial glucose absorption, and glycaemic excursions, as well as plasma GIP and GLP-1.
Author Malbert, Charles-Henri
Horowitz, Michael
Burgess, Jenna E
Nguyen, Nam Q
Wishart, Judith
Bellon, Max
Standfield, Scott
Debreceni, Tamara L
Author_xml – sequence: 1
  givenname: Nam Q
  surname: Nguyen
  fullname: Nguyen, Nam Q
  email: quoc.nguyen@health.sa.gov.au
  organization: Department of Gastroenterology and Hepatology, Level 7, Royal Adelaide Hospital, North Terrace, Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital
– sequence: 2
  givenname: Tamara L
  surname: Debreceni
  fullname: Debreceni, Tamara L
  organization: Department of Gastroenterology and Hepatology, Level 7, Royal Adelaide Hospital, North Terrace
– sequence: 3
  givenname: Jenna E
  surname: Burgess
  fullname: Burgess, Jenna E
  organization: Department of Gastroenterology and Hepatology, Level 7, Royal Adelaide Hospital, North Terrace
– sequence: 4
  givenname: Max
  surname: Bellon
  fullname: Bellon, Max
  organization: Nuclear Medicine, PET and Bone Densitometry, Royal Adelaide Hospital
– sequence: 5
  givenname: Judith
  surname: Wishart
  fullname: Wishart, Judith
  organization: Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital
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  givenname: Scott
  surname: Standfield
  fullname: Standfield, Scott
  organization: Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital
– sequence: 7
  givenname: Charles-Henri
  surname: Malbert
  fullname: Malbert, Charles-Henri
  organization: Department of GI Physiology, INRA
– sequence: 8
  givenname: Michael
  surname: Horowitz
  fullname: Horowitz, Michael
  organization: Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital
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ISSN 0307-0565
1476-5497
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IsPeerReviewed true
IsScholarly true
Issue 9
Keywords insulin sensitivity
weight-loss
glp-1 secretion
bariatric surgery
liqutest meal
high-fat
glucagon receptor
incretin hormones
type-2 diabetes-mellitus
gastrointestinal symptoms
Language English
License Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
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  text: 2018-09-01
  day: 01
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PublicationSubtitle Official journal of the International Association for the Study of Obesity
PublicationTitle International Journal of Obesity
PublicationTitleAbbrev Int J Obes
PublicationTitleAlternate Int J Obes (Lond)
PublicationYear 2018
Publisher Nature Publishing Group UK
Nature Publishing Group
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Snippet Objective: This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia,...
This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia, incretin...
Objective:This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia,...
Objective: This study evaluated gastric emptying (GE) and small intestinal (SI) transit in people with morbid obesity and their relationships to glycaemia,...
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StartPage 1556
SubjectTerms 101/47
631/45/776/198
692/699/1503/1702/393
82/16
9/10
Absorption
Adult
Blood
Blood glucose
Blood Glucose - metabolism
Emptying
Epidemiology
Female
Gastric emptying
Gastric Emptying - physiology
Gastrointestinal Hormones - metabolism
Gastrointestinal Transit - physiology
GIP protein
Glucagon
Glucagon-like peptide 1
Glucose
Health Promotion and Disease Prevention
Hormones
Humans
Insulin
Internal Medicine
Intestine
Intestine, Small - metabolism
Life Sciences
Male
Medical imaging
Medicine
Medicine & Public Health
Metabolic Diseases
Middle Aged
Obesity
Obesity, Morbid - metabolism
Obesity, Morbid - physiopathology
Public Health
Radionuclide Imaging
Scintigraphy
Transit
Title Impact of gastric emptying and small intestinal transit on blood glucose, intestinal hormones, glucose absorption in the morbidly obese
URI https://link.springer.com/article/10.1038/s41366-018-0012-6
https://www.ncbi.nlm.nih.gov/pubmed/29453463
https://www.proquest.com/docview/2113248958
https://www.proquest.com/docview/2003052036
https://hal.inrae.fr/hal-02622130
Volume 42
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