Alterations in Gastrointestinal Physiology after Roux-En-Y Gastric Bypass

Ponsky, Todd A.; Brody, Fred; Pucci, Edward

doi:10.1016/j.jamcollsurg.2005.03.021

Cited by 66 publications

(59 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The flow of undigested food, which has pleiotropic effects on the structure and metabolism of the intestinal wall (60,76) and may support postprandial ghrelin suppression (47,75,79), can trigger hyperosmotic episodes, as evidenced by the increased prevalence of discomfort and dumping syndrome after RYGB (58,80,87). Dietary recommendations for RYGB-treated patients are therefore to moderate consumption of high-sugar foods (22,71,81). Hyperosmolarity-related ghrelin suppression might be a novel, contributing factor to reduced appetite after RYGB, as well as a compromise of the normal compensatory increase in ghrelin levels that occurs with diverse mechanisms of weight loss, but typically not after RYGB (18,84).…”

Section: Discussionmentioning

confidence: 99%

Hyperosmolarity in the small intestine contributes to postprandial ghrelin suppression

Overduin

Tylee

Frayo

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Plasma levels of the orexigenic hormone ghrelin are suppressed by meals with an efficacy dependent on their macronutrient composition. We hypothesized that heterogeneity in osmolarity among macronutrient classes contributes to these differences. In three studies, the impact of small intestinal hyperosmolarity was examined in Sprague-Dawley rats. In study 1, isotonic, 2.5ϫ, and 5ϫ hypertonic solutions of several agents with diverse absorption and metabolism properties were infused duodenally at a physiological rate (3 ml/10 min). Jugular vein blood was sampled before and at 30,60,90, 120, 180, 240, and 300 min after infusion. Plasma ghrelin was suppressed dose dependently and most strongly by glucose. Hyperosmolar infusions of lactulose, which transits the small intestine unabsorbed, and 3-O-methylglucose (3-O-MG), which is absorbed like glucose but remains unmetabolized, also suppressed ghrelin. Glucose, but not lactulose or 3-O-MG, infusions increased plasma insulin. In study 2, intestinal infusions of hyperosmolar NaCl suppressed ghrelin, a response that was not attenuated by coinfusion with the neural blocker lidocaine. In study 3, we reconfirmed that the low-osmolar lipid emulsion Intralipid suppresses ghrelin more weakly than isocaloric (but hypertonic) glucose. Importantly, raising Intralipid's osmolarity to that of the glucose solution by nonabsorbable lactulose supplementation enhanced ghrelin suppression to that seen after glucose. Hyperosmolar ghrelin occurred particularly during the initial 3 postinfusion hours. We conclude that small intestinal hyperosmolarity 1) is sufficient to suppress ghrelin, 2) may combine with other postprandial mechanisms to suppress ghrelin, 3) might contribute to altered ghrelin regulation after gastric bypass surgery, and 4) may inform dietary modifications for metabolic health.ghrelin; intestinal osmolarity; 3-O-methylglucose; lactulose; satiation GHRELIN IS THE ONLY KNOWN appetite-stimulating gastrointestinal hormone in humans and other vertebrates. Exogenous administration of this 28-amino-acid peptide increases short-term hunger, food intake, and motivation to eat, as well as body weight (14,16,17,67). Circulating ghrelin levels correlate with energy balance, i.e., they increase with weight loss or during meal anticipation and decrease with weight gain or after food intake. Ghrelin's orexigenic effects lend practical importance to a detailed understanding of its regulation by diet.The mechanisms underlying postmeal ghrelin suppression are incompletely understood, although some factors have been elucidated. First, the magnitude of ghrelin suppression correlates with the total caloric content of ingested food (8). Second, the nutrient sensors that initiate postprandial ghrelin suppression are not located in the stomach, i.e., the site of most ghrelin-producing cells, but more distally in the gastrointestinal tract and/or at postabsorptive sites (69, 91). Third, the magnitude of ghrelin suppression depends on the macronutrient composition of meals; e.g., ingested carbohyd...

show abstract

Section: Discussionmentioning

confidence: 99%

Hyperosmolarity in the small intestine contributes to postprandial ghrelin suppression

Overduin

Tylee

Frayo

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…This bypass significantly delays the interaction between lipolytic enzymes and ingested materials. 44 This effect might delay the breakdown of SNEDDS in the intestine. Thus, the efficient dissolution and absorption by SNEDDS could be maintained for a longer time.…”

mentioning

confidence: 99%

Self-nanoemulsifying drug delivery systems ameliorate the oral delivery of silymarin in rats with Roux-en-Y gastric bypass surgery

Chen

Chang

Shih

et al. 2015

IJN

View full text Add to dashboard Cite

Roux-en-Y gastric bypass (RYGB) is a popular surgery to reduce the body weight of obese patients. Although food intake is restricted by RYGB, drug absorption is also decreased. The purpose of this study was to develop novel self-nanoemulsifying drug delivery systems (SNEDDS) for enhancing the oral delivery of silymarin, which has poor water solubility. The SNEDDS were characterized by size, zeta potential, droplet number, and morphology. A technique of RYGB was performed in Sprague-Dawley rats. SNEDDS were administered at a silymarin dose of 600 mg/kg in normal and RYGB rats for comparison with silymarin aqueous suspension and polyethylene glycol (PEG) 400 solution. Plasma silibinin, the main active ingredient in silymarin, was chosen for estimating the pharmacokinetic parameters. SNEDDS diluted in simulated gastric fluid exhibited a droplet size of 190 nm with a spherical shape. The nanocarriers promoted silibinin availability via oral ingestion in RYGB rats by 2.5-fold and 1.5-fold compared to the suspension and PEG 400 solution, respectively. A significant double-peak concentration of silibinin was detected for RYGB rats receiving SNEDDS. Fluorescence imaging showed a deeper and broader penetration of Nile red, the fluorescence dye, into the gastrointestinal mucosa from SNEDDS than from PEG 400 solution. Histological examination showed that SNEDDS caused more minor inflammation at the gastrointestinal membrane as compared with that caused by PEG 400 solution, indicating a shielding of direct silymarin contact with the mucosa by the nanodroplets. SNEDDS generally showed low-level or negligible irritation in the gastrointestinal tract. Silymarin-loaded SNEDDS were successfully developed to improve the dissolution, permeability, and oral bioavailability of silymarin. To the best of our knowledge, this is the first investigation reporting the usefulness of SNEDDS for improving drug malabsorption elicited by gastric bypass surgery.

show abstract

“…The majority of the protein absorption occurs in the duodenum and jejunum. 8 Lipids. Lipids ingested are divided into free fatty acids, triglycerides, cholesterol, and phospholipids.…”

Section: Macronutrientsmentioning

confidence: 99%