Mechanisms of glucose homeostasis after roux-en-y gastric bypass surgery in the obese, insulin-resistant zucker rat

Katia Meirelles, Tamer Ahmed, Derek M. Culnan, Christopher J. Lynch, Charles H. Lang, Robert N. Cooney

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

OBJECTIVE:: Obesity-related diabetes is caused by insulin resistance and 2-cell dysfunction. The current study examines changes in food intake, weight loss, body fat depots, oxygen consumption, insulin sensitivity, and incretin levels as potential mechanisms for improved glucose tolerance after Roux-en-Y gastric bypass (RYGB). METHODS:: Three groups of genetically obese Zucker rats were studied: RYGB, sham surgery pair-fed (PF), and sham surgery ad libitum (AL) fed rats. Changes in body weight, visceral and subcutaneous fat depots, oral glucose tolerance, insulin sensitivity, and the plasma concentrations of insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide, and peptide YY (PYY) were measured. RESULTS:: Body weight and subcutaneous fat were decreased after RYGB, compared with the PF and AL groups. The reduction in visceral fat after RYGB appeared largely because of food restriction. Glucose tolerance and insulin sensitivity were significantly improved in only the RYGB group (P < 0.05 vs. AL, PF). Euglycemic, hyperinsulinemic clamp studies indicated RYGB improved the ability of insulin to stimulate peripheral (eg, skeletal muscle) glucose uptake. Fasting total GLP-1, glucose-dependent insulinotropic peptide, and PYY levels were similar between the groups, whereas postprandial plasma levels of intact GLP-1 (7-36) amide, total GLP-1, and PYY were increased in the RYGB group compared with PF and AL controls. CONCLUSIONS:: Glucose homeostasis after RYGB is associated with decreased subcutaneous fat, increased postprandial PYY, GLP-1, and insulin, as well as improved insulin sensitivity/action. Changes in food intake and visceral fat do not seem to explain improvements in insulin action after RYGB in the Zucker rat model.

Original languageEnglish (US)
Pages (from-to)277-285
Number of pages9
JournalAnnals of surgery
Volume249
Issue number2
DOIs
StatePublished - Feb 1 2009

Fingerprint

Zucker Rats
Gastric Bypass
Homeostasis
Insulin
Glucose
Peptide YY
Glucagon-Like Peptide 1
Insulin Resistance
Intra-Abdominal Fat
Subcutaneous Fat
Gastric Inhibitory Polypeptide
Eating
Incretins
Body Weight Changes
Aptitude
Glucose Clamp Technique
Glucose Tolerance Test
Glucagon
Oxygen Consumption
Adipose Tissue

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Meirelles, Katia ; Ahmed, Tamer ; Culnan, Derek M. ; Lynch, Christopher J. ; Lang, Charles H. ; Cooney, Robert N. / Mechanisms of glucose homeostasis after roux-en-y gastric bypass surgery in the obese, insulin-resistant zucker rat. In: Annals of surgery. 2009 ; Vol. 249, No. 2. pp. 277-285.
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title = "Mechanisms of glucose homeostasis after roux-en-y gastric bypass surgery in the obese, insulin-resistant zucker rat",
abstract = "OBJECTIVE:: Obesity-related diabetes is caused by insulin resistance and 2-cell dysfunction. The current study examines changes in food intake, weight loss, body fat depots, oxygen consumption, insulin sensitivity, and incretin levels as potential mechanisms for improved glucose tolerance after Roux-en-Y gastric bypass (RYGB). METHODS:: Three groups of genetically obese Zucker rats were studied: RYGB, sham surgery pair-fed (PF), and sham surgery ad libitum (AL) fed rats. Changes in body weight, visceral and subcutaneous fat depots, oral glucose tolerance, insulin sensitivity, and the plasma concentrations of insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide, and peptide YY (PYY) were measured. RESULTS:: Body weight and subcutaneous fat were decreased after RYGB, compared with the PF and AL groups. The reduction in visceral fat after RYGB appeared largely because of food restriction. Glucose tolerance and insulin sensitivity were significantly improved in only the RYGB group (P < 0.05 vs. AL, PF). Euglycemic, hyperinsulinemic clamp studies indicated RYGB improved the ability of insulin to stimulate peripheral (eg, skeletal muscle) glucose uptake. Fasting total GLP-1, glucose-dependent insulinotropic peptide, and PYY levels were similar between the groups, whereas postprandial plasma levels of intact GLP-1 (7-36) amide, total GLP-1, and PYY were increased in the RYGB group compared with PF and AL controls. CONCLUSIONS:: Glucose homeostasis after RYGB is associated with decreased subcutaneous fat, increased postprandial PYY, GLP-1, and insulin, as well as improved insulin sensitivity/action. Changes in food intake and visceral fat do not seem to explain improvements in insulin action after RYGB in the Zucker rat model.",
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Mechanisms of glucose homeostasis after roux-en-y gastric bypass surgery in the obese, insulin-resistant zucker rat. / Meirelles, Katia; Ahmed, Tamer; Culnan, Derek M.; Lynch, Christopher J.; Lang, Charles H.; Cooney, Robert N.

In: Annals of surgery, Vol. 249, No. 2, 01.02.2009, p. 277-285.

Research output: Contribution to journalArticle

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T1 - Mechanisms of glucose homeostasis after roux-en-y gastric bypass surgery in the obese, insulin-resistant zucker rat

AU - Meirelles, Katia

AU - Ahmed, Tamer

AU - Culnan, Derek M.

AU - Lynch, Christopher J.

AU - Lang, Charles H.

AU - Cooney, Robert N.

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N2 - OBJECTIVE:: Obesity-related diabetes is caused by insulin resistance and 2-cell dysfunction. The current study examines changes in food intake, weight loss, body fat depots, oxygen consumption, insulin sensitivity, and incretin levels as potential mechanisms for improved glucose tolerance after Roux-en-Y gastric bypass (RYGB). METHODS:: Three groups of genetically obese Zucker rats were studied: RYGB, sham surgery pair-fed (PF), and sham surgery ad libitum (AL) fed rats. Changes in body weight, visceral and subcutaneous fat depots, oral glucose tolerance, insulin sensitivity, and the plasma concentrations of insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide, and peptide YY (PYY) were measured. RESULTS:: Body weight and subcutaneous fat were decreased after RYGB, compared with the PF and AL groups. The reduction in visceral fat after RYGB appeared largely because of food restriction. Glucose tolerance and insulin sensitivity were significantly improved in only the RYGB group (P < 0.05 vs. AL, PF). Euglycemic, hyperinsulinemic clamp studies indicated RYGB improved the ability of insulin to stimulate peripheral (eg, skeletal muscle) glucose uptake. Fasting total GLP-1, glucose-dependent insulinotropic peptide, and PYY levels were similar between the groups, whereas postprandial plasma levels of intact GLP-1 (7-36) amide, total GLP-1, and PYY were increased in the RYGB group compared with PF and AL controls. CONCLUSIONS:: Glucose homeostasis after RYGB is associated with decreased subcutaneous fat, increased postprandial PYY, GLP-1, and insulin, as well as improved insulin sensitivity/action. Changes in food intake and visceral fat do not seem to explain improvements in insulin action after RYGB in the Zucker rat model.

AB - OBJECTIVE:: Obesity-related diabetes is caused by insulin resistance and 2-cell dysfunction. The current study examines changes in food intake, weight loss, body fat depots, oxygen consumption, insulin sensitivity, and incretin levels as potential mechanisms for improved glucose tolerance after Roux-en-Y gastric bypass (RYGB). METHODS:: Three groups of genetically obese Zucker rats were studied: RYGB, sham surgery pair-fed (PF), and sham surgery ad libitum (AL) fed rats. Changes in body weight, visceral and subcutaneous fat depots, oral glucose tolerance, insulin sensitivity, and the plasma concentrations of insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide, and peptide YY (PYY) were measured. RESULTS:: Body weight and subcutaneous fat were decreased after RYGB, compared with the PF and AL groups. The reduction in visceral fat after RYGB appeared largely because of food restriction. Glucose tolerance and insulin sensitivity were significantly improved in only the RYGB group (P < 0.05 vs. AL, PF). Euglycemic, hyperinsulinemic clamp studies indicated RYGB improved the ability of insulin to stimulate peripheral (eg, skeletal muscle) glucose uptake. Fasting total GLP-1, glucose-dependent insulinotropic peptide, and PYY levels were similar between the groups, whereas postprandial plasma levels of intact GLP-1 (7-36) amide, total GLP-1, and PYY were increased in the RYGB group compared with PF and AL controls. CONCLUSIONS:: Glucose homeostasis after RYGB is associated with decreased subcutaneous fat, increased postprandial PYY, GLP-1, and insulin, as well as improved insulin sensitivity/action. Changes in food intake and visceral fat do not seem to explain improvements in insulin action after RYGB in the Zucker rat model.

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