A Study to Examine Changes in GIP Plasma Levels Following Gastric Bypass Surgery in Obese Patients

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ClinicalTrials.gov Identifier: NCT00207389

Recruitment Status : Terminated (Insufficient funding)

First Posted : September 21, 2005

Last Update Posted : January 26, 2017

Sponsor:

Information provided by (Responsible Party):

Caroline Apovian, Boston Medical Center

Study Description

Brief Summary:

Obesity is a multinational epidemic. There is evidence that despite educational measures and increased public awareness, the number of obese individuals continues to increase. Of the numerous obesity-related comorbidities, type 2 diabetes remains one of the most significant in terms of mortality and health care costs. Gastric Bypass Surgery (GBS) not only offers an effective form of therapy for morbid obesity, but also amelioration of type 2 diabetes mellitus. The normalization of glucose levels in GBS patients occurs within days after surgery and has been shown in surgical literature to be independent of the weight loss after surgery. The proximal gut, the site of release of certain incretins, may play a role in glucose homeostasis in obese individuals with type 2 diabetes mellitus. One such incretin is GIP, which when released into the circulation during the immediate postprandial period, accentuates the insulin response to a glucose meal. It is hypothesized that overactivity of this enteroinsular axis in obese individuals produces cell resistance to insulin and subsequent type 2 diabetes mellitus. A previous study reported elevated fasting GIP levels, as well as an exaggerated GIP response to a glucose meal, in obese subjects, which was significantly reduced months after GBS following weight loss. This pilot study of obese patients scheduled for GBS will compare the serum levels of certain peptides, including GIP, following a glucose meal before and after GBS, before weight loss has occured. In order to reproduce the preoperative state, and therefore to demonstrate the physiologic change, a small group of subjects who undergo open surgery will undergo the same measurements after surgery, but using a model in which the meal traverses the stomach, duodenum and jejunum with the aid of a gastrostomy tube.

Condition or disease
Obesity Type 2 Diabetes Mellitus Insulin Resistance

Show Detailed Description

Study Design


Study Type :	Observational
Actual Enrollment :	5 participants
Observational Model:	Cohort
Time Perspective:	Prospective
Official Title:	A Pilot Study to Examine the Relationship Between Changes in Plasma GIP Levels and Other Gastrointestinal Peptides Following Gastric Bypass Surgery in Obese Patients
Study Start Date :	March 2004
Actual Primary Completion Date :	August 2006
Actual Study Completion Date :	August 2006

Resource links provided by the National Library of Medicine

Genetics Home Reference related topics: Type 2 diabetes

U.S. FDA Resources

Groups and Cohorts

Group/Cohort
Laparoscopic gastric bypass Patients undergoing Laparoscopic gastric bypass
Open gastric bypass Patients undergoing Open gastric bypass

Outcome Measures

Primary Outcome Measures :

GIP area under the curve after OGTT

Secondary Outcome Measures :

Other GI peptides and hormones after OGTT

Eligibility Criteria

Information from the National Library of Medicine

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Ages Eligible for Study:	21 Years to 64 Years (Adult)
Sexes Eligible for Study:	All
Accepts Healthy Volunteers:	No

Criteria

Inclusion Criteria:

Patients 21-64 years of age
Obese (defined as a body mass index, BMI, > or = 30)
Type 2 diabetes or impaired glucose tolerance
Have been selected and scheduled for gastric bypass surgery.

Exclusion Criteria:

Substance abuse
Consumption of more than two alcoholic drinks per day
Use of more than 20 units of insulin (any brand or type) per day
Fasting blood glucose >180mg/dl on screening bloodwork.

Contacts and Locations

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00207389

Locations


United States, Massachusetts
Boston University Medical Center
Boston, Massachusetts, United States, 02118

Sponsors and Collaborators

Boston Medical Center

Investigators


Principal Investigator:	Caroline Apovian, MD	Boston University Medical Cneter
Principal Investigator:	Michael Wolfe, MD	Boston University
Study Chair:	Marie Mcdonnell, MD	Boston University
Study Chair:	Harmony Allison, MD	Boston University

More Information

Publications:

MCINTYRE N, HOLDSWORTH CD, TURNER DS. NEW INTERPRETATION OF ORAL GLUCOSE TOLERANCE. Lancet. 1964 Jul 4;2(7349):20-1.

Miyawaki K, Yamada Y, Ban N, Ihara Y, Tsukiyama K, Zhou H, Fujimoto S, Oku A, Tsuda K, Toyokuni S, Hiai H, Mizunoya W, Fushiki T, Holst JJ, Makino M, Tashita A, Kobara Y, Tsubamoto Y, Jinnouchi T, Jomori T, Seino Y. Inhibition of gastric inhibitory polypeptide signaling prevents obesity. Nat Med. 2002 Jul;8(7):738-42. Epub 2002 Jun 17.

Bayliss WM, Starling EH. Croonian lecture. The chemical regulation of the secretory process. Proc R Soc Lond 1904(73):310-332.

GREGORY RA, TRACY HJ. THE CONSTITUTION AND PROPERTIES OF TWO GASTRINS EXTRACTED FROM HOG ANTRAL MUCOSA. Gut. 1964 Apr;5:103-14.

Jorpes E, Mutt V. Cholecystokinin and pancreozymin, one single hormone? Acta Physiol Scand. 1966 Jan-Feb;66(1):196-202.

Kosaka T, Lim RKS. Demonstration of the humoral agent in fat inhibited gastric secretion. Proc Soc Exp Biol Med 1930;27:890-891.

Brown JC, Pederson RA, Jorpes E, Mutt V. Preparation of highly active enterogastrone. Can J Physiol Pharmacol. 1969 Jan;47(1):113-4.

Cleator IG, Gourlay RH. Release of immunoreactive gastric inhibitory polypeptide (IR-GIP) by oral ingestion of food substances. Am J Surg. 1975 Aug;130(2):128-35.

Villar HV, Fender HR, Rayford PL, Bloom SR, Ramus NI, Thompson JC. Suppression of gastrin release and gastric secretion by gastric inhibitory polypeptide (GIP) and vasoactive intestinal polypeptide (VIP). Ann Surg. 1976 Jul;184(1):97-102.

Arnold R, Ebert R, Creutzfeldt W, H.D. B, Börger H. Inhibition of gastric acid secretion by gastric inhibitory polypeptide (GIP) in man. Scand J Gastroenterol 1978;13(Suppl 48):11.


Responsible Party:	Caroline Apovian, Principal Investigator, Boston Medical Center
ClinicalTrials.gov Identifier:	NCT00207389 History of Changes
Other Study ID Numbers:	H-22610
First Posted:	September 21, 2005 Key Record Dates
Last Update Posted:	January 26, 2017
Last Verified:	January 2017


Studies a U.S. FDA-regulated Drug Product:		No
Studies a U.S. FDA-regulated Device Product:		No

Keywords provided by Caroline Apovian, Boston Medical Center:


Incretins:GIP , GLP-1 Gastric bypass surgery Laparoscopic gastric bypass surgery Postprandial expression of GIP

Additional relevant MeSH terms:


Diabetes Mellitus Diabetes Mellitus, Type 2 Insulin Resistance Glucose Metabolism Disorders	Metabolic Diseases Endocrine System Diseases Hyperinsulinism

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