Weight loss through ileal transposition is accompanied by increased ileal hormone secretion and synthesis in rats

被引:212
作者
Strader, AD
Vahl, TP
Jandacek, RJ
Woods, SC
D'Alessio, DA
Seeley, RJ
机构
[1] Univ Cincinnati, Lab Med, Div Endocrinol, Cincinnati, OH USA
[2] Univ Cincinnati, Dept Psychiat, Cincinnati, OH USA
[3] Univ Cincinnati, Dept Internal Med, Cincinnati, OH USA
[4] Univ Cincinnati, Dept Pathol, Cincinnati, OH USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2005年 / 288卷 / 02期
关键词
glucagon-like peptide-1; peptide YY; obesity surgery; ileum;
D O I
10.1152/ajpendo.00153.2004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Bariatric surgeries, such as gastric bypass, result in dramatic and sustained weight loss that is usually attributed to a combination of gastric volume restriction and intestinal malabsorption. However, studies parceling out the contribution of enhanced intestinal stimulation in the absence of these two mechanisms have received little attention. Previous studies have demonstrated that patients who received intestinal bypass or Roux-en-Y surgery have increased release of gastrointestinal hormones. One possible mechanism for this increase is the rapid transit of nutrients into the intestine after eating. To determine whether there is increased secretion of anorectic peptides produced in the distal small intestine when this portion of the gut is given greater exposure to nutrients, we preformed ileal transpositions ( IT) in rats. In this procedure, an isolated segment of ileum is transposed to the jejunum, resulting in an intestinal tract of normal length but an alteration in the normal distribution of endocrine cells along the gut. Rats with IT lost more weight ( P < 0.05) and consumed less food ( P < 0.05) than control rats with intestinal transections and reanastomosis without transposition. Weight loss in the IT rats was not due to malabsorption of nutrients. However, transposition of distal gut to a proximal location caused increased synthesis and release of the anorectic ileal hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY; P < 0.01). The association of weight loss with increased release of GLP-1 and PYY suggests that procedures that promote gastrointestinal endocrine function can reduce energy intake. These findings support the importance of evaluating the contribution of gastrointestinal hormones to the weight loss seen with bariatric surgery.
引用
收藏
页码:E447 / E453
页数:7
相关论文
共 51 条
[1]  
AHREN B, 1997, AM J PHYSIOL, V273, P113
[2]   Comparison of the postprandial release of peptide YY and proglucagon-derived peptides in the rat [J].
Anini, Y ;
Fu-Cheng, XM ;
Cuber, JC ;
Kervran, A ;
Chariot, J ;
Rozé, C .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1999, 438 (03) :299-306
[3]   ENERGY-BALANCE AND REGULATION OF BODY-WEIGHT AFTER INTESTINAL-BYPASS SURGERY IN RATS [J].
ATKINSON, RL ;
BRENT, EL ;
WAGNER, BS ;
WHIPPLE, JH .
AMERICAN JOURNAL OF PHYSIOLOGY, 1983, 245 (05) :R658-R663
[4]  
Barrow Cynthia J, 2002, AORN J, V76, P593, DOI 10.1016/S0001-2092(06)60934-4
[5]   Gut hormone PYY3-36 physiologically inhibits food intake [J].
Batterham, RL ;
Cowley, MA ;
Small, CJ ;
Herzog, H ;
Cohen, MA ;
Dakin, CL ;
Wren, AM ;
Brynes, AE ;
Low, MJ ;
Ghatei, MA ;
Cone, RD ;
Bloom, SR .
NATURE, 2002, 418 (6898) :650-654
[6]   Inhibition of food intake in obese subjects by peptide YY3-36 [J].
Batterham, RL ;
Cohen, MA ;
Ellis, SM ;
Le Roux, CW ;
Withers, DJ ;
Frost, GS ;
Ghatei, MA ;
Bloom, SR .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (10) :941-948
[7]  
BOOZER CN, 1990, INT J OBESITY, V14, P869
[8]   INTESTINAL-BYPASS SURGERY FOR OBESITY DECREASES FOOD-INTAKE AND TASTE PREFERENCES [J].
BRAY, GA ;
BARRY, RE ;
BENFIELD, JR ;
CASTELNUOVOTEDESCO, P ;
RODIN, J .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1976, 29 (07) :779-783
[9]   Malabsorptive gastric bypass in patients with superobesity [J].
Brolin, RE ;
LaMarca, LB ;
Kenler, HA ;
Cody, RP .
JOURNAL OF GASTROINTESTINAL SURGERY, 2002, 6 (02) :195-203
[10]   Bariatric surgery and long-term control of morbid obesity [J].
Brolin, RE .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2002, 288 (22) :2793-2796