The contribution of malabsorption to the reduction in net energy absorption after long-limb Roux-en-Y gastric bypass

Odstrcil, Elizabeth; Martı́nez, Juan Gabriel; Ana, Carol A. Santa; Xue, Beiqi; Schneider, Reva; Steffer, Karen J.; Porter, Jack L.; Asplin, John R.; Kuhn, Joseph A.; Fordtran, John S.

doi:10.3945/ajcn.2010.29870

Cited by 182 publications

(114 citation statements)

References 36 publications

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“…Despite the rapid pouch emptying, the overall absorption of glucose has been reported to be largely unaffected after RYGB at 1 year, and comparable with normal subjects (9). These observations attest to the importance of the "restrictive component" of RYGB in triggering and maintaining weight loss (6)(7)(8).…”

Section: Obesity Biology and Integrated Physiologysupporting

confidence: 55%

“…While the mechanisms underlying the effects of RYGB on body weight are incompletely understood, the anatomical alterations are thought to reduce oral intake via the restrictive gastric pouch, nutrient malabsorption and neurohormonal changes arising from the intestinal "short circuit" that favor weight loss, and improved glycemic control (3)(4)(5). It has been suggested that weight loss following RYGB is predominantly due to restricted food intake (79%) and malabsorption (11%), particularly malabsorption of fats (40% reduction) (6)(7)(8). Surprisingly, carbohydrate absorption is not significantly altered following RYGB in humans, despite accelerated emptying of the gastric pouch and accelerated intestinal transit (9), and the underlying reasons are unclear.…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption

Nguyen

Debreceni

Bambrick

et al. 2014

Obesity

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Objective: To determine the effect of Roux-en-Y gastric bypass (RYGB) on the expression of intestinal sweet taste receptors (STRs), glucose transporters (GTs), glucose absorption, and glycemia. Methods: Intestinal biopsies were collected for mRNA expression of STR (T1R2) and GTs (SGLT-1 and GLUT2) from 11 non-diabetic RYGB, 13 non-diabetic obese, and 11 healthy subjects, at baseline and following a 30 min small intestinal (SI) glucose infusion (30 g/150 ml water with 3 g 3-O-methyl-D-glucopyranose (3-OMG)). Blood glucose, plasma 3-OMG, and insulin were measured for 270 min. Results: In RYGB patients, expression of both GTs was 2-fold higher at baseline and after glucose infusion than those of morbidly obese or healthy subjects (P < 0.001). STR expressions were comparable amongst the groups. Peak plasma 3-OMG in both RYGB (r 5 0.69, P 5 0.01) and obese (r 5 0.72, P 5 0.005) correlated with baseline expression of SGLT-1, as was the case with peak blood glucose in RYGB subjects (r 5 0.69, P 5 0.02). Conclusions: The upregulated intestinal GTs in RYGB patients are associated with increased glucose absorption when glucose is delivered at a physiological rate, suggesting a molecular adaptation to prevent carbohydrate malabsorption from rapid intestinal transit after RYGB.

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Section: Obesity Biology and Integrated Physiologysupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption

Nguyen

Debreceni

Bambrick

et al. 2014

Obesity

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“…Extreme caloric restriction to the limit just tolerated in patients after surgery improved insulin resistance in obese subjects similarly as found in after the first week after RYGB (5). Of interest, the malabsorptive component of the RYGB procedure approximately accounts only for up to 11% of the total reduction in combustible energy absorption (6). Changes of adipokine-induced inflammation and insulin resistance (7) and reduction of branched-chain amino acids correlating with insulin resistance (8) have been proposed as further mechanisms operating after bariatric surgery complementing the sole weight loss.…”

mentioning

confidence: 93%

GLP-1—A Candidate Humoral Mediator for Glucose Control After Roux-en-Y Gastric Bypass

Schirra

Göke

2014

Diabetes

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The worldwide increase in obesity is associated with a higher prevalence of type 2 diabetes (T2D), and severe obesity occurs with the greatest risk (1). Bariatric surgery is currently the most effective treatment not only for weight loss but also for prevention or treatment of T2D in such patients (2). It leads to remission or improvement of T2D in the majority of morbidly obese (3,4). Roux-en-Y gastric bypass (RYGB) is one of the most frequently performed procedures. With RYGB, the stomach is reduced to a small proximal pouch (30-50 mL) and anastomosed to the jejunum, thereby bypassing the majority of the stomach and duodenum. After RYGB, T2D improves rapidly often before significant weight loss occurs. The mechanisms behind this phenomenon are not clearly resolved. Caloric restriction contributes. Extreme caloric restriction to the limit just tolerated in patients after surgery improved insulin resistance in obese subjects similarly as found in after the first week after RYGB (5). Of interest, the malabsorptive component of the RYGB procedure approximately accounts only for up to 11% of the total reduction in combustible energy absorption (6). Changes of adipokine-induced inflammation and insulin resistance (7) and reduction of branched-chain amino acids correlating with insulin resistance (8) have been proposed as further mechanisms operating after bariatric surgery complementing the sole weight loss.A popular hypothesis points to an antidiabetic effect after RYGB of postprandially exaggeratedly released gut peptides, such as glucagon-like peptide 1 (GLP-1), already starting early after surgery. The release of GLP-1 depends on gastric emptying (GE) velocity (9). It lowers postprandial glycemia by stimulation of insulin, inhibition of glucagon secretion, and delay of GE. For example, Laferrère et al. (10) reported a sixfold increase in GLP-1 plasma levels and a fivefold increase of the incretin effect in obese patients with T2D 1 month after RYGB. In this issue, Shah et al. (11) addressed the contribution of endogenous GLP-1 to the meal-induced glucose metabolism, islet secretion, and GE after RYGB in 12 nondiabetic obese patients 5 6 0.9 years after RYGB and 8 weightmatched control subjects twice using the GLP-1 receptor (GLP-1R) antagonist exendin(9-39). After ingestion of a 220 kcal mixed-meal, glucose metabolism was measured using the isotope dilution method. Indices of insulin action and b-cell glucose responsitivity and the resulting glucose disposition indices were calculated using the oral minimal model. GE was measured by scintigraphy. As expected, GE (gastric pouch in the post-RYGB subjects) was greatly accelerated, leading to a several-fold increase in postprandial GLP-1, insulin, and C-peptide responses after RYGB. The GLP-1R antagonist increased the postprandial glucose excursions in both groups. Exendin(9-39) decreased insulin and C-peptide concentrations in subjects post-RYGB by about 30% with no effect in control subjects. The calculated b-cell response to glucose was significantly reduced in b...

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“…The highly variable degree of secondary hyperoxaluria may be due to differences in protein, lipid, calcium, and oxalate intake from other studies. However, only a handful of studies have reported dietary patterns (8,9,11,35). The present pattern of low protein intake by post-BS patients, evidenced by the food recalls and the lower urea, uric acid, and creatinine excretion, may have interfered with our rates of hyperoxaluria (36,37).…”

Section: Discussionmentioning

confidence: 96%

Response to Dietary Oxalate after Bariatric Surgery

Froeder

Arasaki

Malheiros³

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Bariatric surgery (BS) may be associated with increased oxalate excretion and a higher risk of nephrolithiasis. This study aimed to investigate urinary abnormalities and responses to an acute oxalate load as an indirect assessment of the intestinal absorption of oxalate in this population.Design, setting, participants, & measurements Twenty-four-hour urine specimens were collected from 61 patients a median of 48 months after BS (post-BS) as well as from 30 morbidly obese (MO) participants; dietary information was obtained through 24-hour food recalls. An oral oxalate load test (OLT), consisting of 2-hour urine samples after overnight fasting and 2, 4, and 6 hours after consuming 375 mg of oxalate (spinach juice), was performed on 21 MO and 22 post-BS patients 12 months after BS. Ten post-BS patients also underwent OLT before surgery (pre-BS).Results There was a higher percentage of low urinary volume (,1.5 L/d) in post-BS versus MO (P,0.001). Hypocitraturia and hyperoxaluria (P=0.13 and P=0.36, respectively) were more frequent in BS versus MO patients. The OLT showed intragroup (P,0.001 for all periods versus baseline) and intergroup differences (P,0.001 for post-BS versus MO; P=0.03for post-BS versus pre-BS). The total mean increment in oxaluria after 6 hours of load, expressed as area under the curve, was higher in both post-BS versus MO and in post-BS versus pre-BS participants (P,0.001 for both).Conclusions The mean oxaluric response to an oxalate load is markedly elevated in post-bariatric surgery patients, suggesting that increased intestinal absorption of dietary oxalate is a predisposing mechanism for enteric hyperoxaluria.

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The contribution of malabsorption to the reduction in net energy absorption after long-limb Roux-en-Y gastric bypass

Cited by 182 publications

References 36 publications

Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption

Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption

GLP-1—A Candidate Humoral Mediator for Glucose Control After Roux-en-Y Gastric Bypass

Response to Dietary Oxalate after Bariatric Surgery

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