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Obesity Unit (R.M., V.M., A.M.L., S.D., J.V.) and Departments of Biological Diagnostics (M.M., J.L.M., R.C.) and Gastroenterology (S.N.), Hospital Clínic Universitari, 08036 Barcelona, Spain
Address all correspondence and requests for reprints to: Dr. Josep Vidal, Obesity Unit, Endocrinology and Diabetes Department, Hospital Clínic Universitari, Villarroel 170, 08036 Barcelona, Spain. E-mail: jovidal{at}clinic.ub.es.
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Abstract |
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Objective: The objective of the study was to assess the changes in active glucagon-like peptide 1 (GLP-1) and total peptide YY (PYY) after RYGBP and examine their relationship with changes in hunger and satiety.
Design: This was a prospective study on the changes in active GLP-1, PYY, hunger, and satiety in response to a standardized test meal in nine normal-glucose-tolerant obese subjects [body mass index (BMI) 47.4 ± 6.1 kg/m2] before and 6 wk after RYGBP.
Results: Before surgery, meal ingestion failed to stimulate GLP-1 and PYY secretion. Six weeks after surgery, despite subjects still being markedly obese (BMI 43.6 ± 7.8 kg/m2), the area under the curve0–120' of GLP-1 and of PYY in response to the standardized test meal were significantly elevated (P < 0.05 and P < 0.01, respectively). These hormonal responses were significantly larger (P < 0.01) than those observed in a group matched for the BMI attained 6 wk after surgery. The 2.9 ± 1.2- and 1.6 ± 1.9-fold increase, respectively, in the area under the curve0–120' of GLP-1 and PYY were accompanied by a significant decrease in fasting (P < 0.05) and postprandial hunger (P = 0.05) and a significant increase in satiety (P < 0.05) after meal intake. Nevertheless, a significant correlation between changes in the hormonal and eating behavior parameters was not found.
Conclusion: Our data show that RYGBP is associated with an improvement in the active GLP-1 and total PYY response to a liquid-meal intake. Moreover, we provide circumstantial evidence for a potential role of these gastrointestinal hormones on the decreased appetite after RYGBP.
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Introduction |
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Gut-derived hormones have important sensing and signaling roles in the regulation of energy homeostasis (10). Thus, it has been hypothesized that a putative critical factor to the efficacy of RYGBP is change in the gut-derived hormones known to influence appetite (2, 3). In recent years, numerous reports have evaluated the gastrointestinal endocrine changes associated with RYGBP. Of note, Cummings et al. (11) first reported that despite massive weight loss, plasma levels of the stomach-derived orexigenic hormone ghrelin were paradoxically suppressed in patients who had undergone RYGBP, suggesting that this hormone was critical in the suppressed appetite and weight reduction after gastric bypass surgery. Nevertheless, subsequent studies have shown mixed results, making it hard to sustain this hypothesis (12).
In sharp contrast with ghrelin, other gut hormones such as glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) act as appetite suppressant agents (10). GLP-1 and PYY are released in response to nutrient ingestion from endocrine L cells, most densely located in the distal ileum. GLP-1 is the result of posttranslational proteolytic processing of the preproglucagon gene in the gut. Under physiological conditions, GLP-1 acts primarily to augment insulin secretion after oral glucose or meal ingestion and also decelerates gastric emptying and intestinal transit time (13). PYY has also been implicated as a major component of the ileal brake (14). In addition, GLP-1 or PYY infusion reduces energy intake in both lean and overweight subjects (15, 16, 17). Notably, enteroglucagon levels (used in the past as a marker of intestinal peptides derived from proglucagon) are increased after RYGB (18). Moreover, GLP-1 and PYY plasma concentration in response to nutrient intake was enlarged in recent cross-sectional studies in RYGB-operated subjects (19, 20). Finally, both GLP-1 and PYY levels increase after surgeries that expedite nutrient delivery to the hindgut and are associated with weight loss such as in jeunoileal bypass surgery in humans (21) and ileal transposition in a rodent model (22). Therefore, it could be hypothesized that an accelerated gastrointestinal transit time in RYGBP-operated subjects may result in an increase in GLP-1 and PYY response to nutrient intake with these hormonal changes potentially contributing to reduced appetite after surgery.
In the present study, we aimed to further assess the changes in GLP-1 and PYY after RYGBP. Moreover, we examined the relationship between circulating GLP-1 and PYY and the changes in hunger and satiety. Finally, we assessed the potential role of changes in gastric emptying and intestinal transit time associated with RYGBP on the hormonal response to food intake. A prospective analysis of the GLP-1 and PYY response to food intake in RYGBP-operated patients has, to our knowledge, not previously been reported.
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Subjects and Methods |
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Nine obese Caucasian subjects [seven women and two men, aged 39.4 ± 10.7 yr, body mass index (BMI) 47.4 ± 6.1 kg/m2] about to undergo a standardized laparoscopic RYGBP (23) were recruited from the Obesity Unit at the Hospital Clínic Universitari of Barcelona. As assessed from an oral glucose tolerance test before surgery, all patients had normal glucose tolerance. Six normal-glucose-tolerant obese subjects matched with the experimental group for gender (four women and two men), age (41.0 ± 10.7 yr), and BMI 6 wk after surgery (43.6 ± 7.9 kg/m2) were also studied. Before baseline examination, the body weight of all the participants had been stable for at least 4 wk. The study was approved by the hospital ethics committee, and written informed consent was obtained from all participants.
Study protocol
All subjects were evaluated both within 8 wk before RYGBP and 6 wk after the surgical procedure. Subjects attended the Research Facility at 0800 h after overnight fasting. They were asked to avoid smoking from the night before and to refrain from strenuous exercise or alcohol in the 24 h preceding the study. One subject in the RYGBP group and none in the BMI-matched group was an active smoker, and his smoking status did not change throughout the study. Subjects were weighed and measured wearing light clothing, and a canula was then inserted into the distal forearm for blood sample collection. Blood was withdrawn for measurement of active GLP-1 (GLP-17–36 amide or GLP-17–37) and total PYY in the fasting state. Subjects consumed a 250-ml standard mixed liquid meal (Isosource Energy, Novartis, Basel, Switzerland) containing 398 kcal, with 50% calories as carbohydrates, 15% as protein, and 35% as fat. The liquid formula was well tolerated by all patients even after RYGBP. Additional blood samples for GLP-1 and PYY plasma concentration assessment were collected at 10, 30, 60, 90, and 120 min after meal ingestion. Serum samples were centrifuged immediately at +4 C and stored at –80 C until assayed. Samples from one individual obtained before and after RYGBP were assessed in the same assay.
Hormone measurements
Human active GLP-1 (i.e. GLP-17–36 amide or GLP-17–37) was measured after extraction of plasma with ethanol using a commercial RIA (GLP-active-RIA kit, Linco Research, Inc., St. Charles, MO). This assay uses 125I-labeled GLP-17–36 amide and a GLP-1 antibody, which binds specifically to the N terminus of active GLP-1 and does not react with total GLP-11–37, GLP-19–36, or GLP-19–37. The lowest level of active GLP-1 that can be detected by this assay is 3 pM. The intra- and interassay coefficients of variation were 31 and 34%, respectively.
Human plasma total PYY was measured with a commercially available RIA (human-PYY-total RIA kit, Linco Research). This assay uses 125I-labeled PYY and an antibody that recognizes both the 1–36 and 3–36 forms of human PYY. The lowest level of PYY that can be detected by this assay is 4 pmol/liter. The intra- and interassay coefficients of variation were both less than 10%.
Hunger and satiety ratings
Subjects completed a validated visual analog scale (VAS) at the same time points as blood was drawn for hormonal measurements (24). In brief, the VAS consisted of 100-mm lines, and subjects were asked to make a vertical mark across the line corresponding to their feelings from 0 (not at all) to 100 (most imaginable) hunger or satiety. Quantification was performed by measuring the distance from the left end of the line to the mark.
Gastric emptying (GE) and orocecal transit time (OCTT)
In a subset of six subjects among those undergoing RYGB, GE rate and OCTT were assessed before and 6 wk after surgery. GE was estimated by measuring paracetamol plasma concentration after the ingestion of 1.5 g paracetamol (24, 25). Plasma concentrations of paracetamol were measured at 0, 5, 10, 20, 30, 60, 90, and 120 min after the ingestion of the drug with the test meal. Plasma samples were stored at –80 C until the analysis of paracetamol by fluorescence immunoassay (Abbott Laboratories, Chicago, IL). The assay had an inter- and intraassay coefficient of variation of less than 5%. OCTT was estimated by means of a lactulose breath test (26). After an overnight fast, subjects ingested 10 g lactulose syrup (Inalco Spa, Milano, Italy, packaged by Xactdose Inc., South Beloit, IL) after a baseline breath sample had been obtained. Breath sampling then continued every 15 min for the first 45 min and every 30 min thereafter for a total of 210 min. All breath samples were analyzed immediately by a model DP Quintron gas chromatograph (Quintron Instrument Co., Milwaukee, WI). The concentration of hydrogen was measured in parts per million, and a threshold increment of 5 ppm in three consecutive readings was used to establish the OCTT (26). The assay had an inter- and intraassay coefficient of variation of 13 and 11%, respectively.
Statistical analysis
Data are expressed as mean ± SD of the mean (SD) unless stated otherwise. Values for the area under the curve (AUC) for GLP-1, PYY, hunger, and satiety after a standard mixed liquid meal were calculated using the trapezoidal method. General linear model analysis with repeated measures followed by post hoc analysis using Bonferroni was performed to evaluate the change in GLP-1 or PYY after meal intake before and after surgery in the group of subjects undergoing RYGBP and the BMI-matched group. The variance homogenesis was checked by means of the Mauchly sphericity test. The Kolmogorov-Smirnov (Lilliefors) test was used to assess the normal distribution of the residuals. Two-tailed nonparametric paired (Wilcoxon rank) or unpaired (Mann-Whitney U) tests were used to compare the hormonal response among groups. Correlations were determined by univariate linear regression (Spearman’s rank test). Statistical analysis was performed using SPSS 11.0 for PC (SPSS, Inc., Chicago, IL) with significance set at P < 0.05.
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Results |
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Before surgery, the ingestion of the standard liquid meal failed to induce a significant increase of either PYY or GLP-1 (Fig. 1
). Although the hormonal response to meal ingestion was larger for PYY, compared with GLP-1, it did not reach statistical significance (P = 0.08). Six weeks after surgery, patients had lost a significant amount of weight (15.4 ± 6.3 kg, P < 0.01) but were still markedly obese (BMI 41.6 ± 5.7 kg/m2). On that second evaluation, neither fasting GLP-1 nor fasting PYY was significantly increased, compared with presurgical hormonal levels (Fig. 1). Remarkably, however, general linear model analysis with repeated measures showed a significant increase in the GLP-1 and PYY response to meal ingestion (respectively, P < 0.05 and P < 0.01). GLP-1 plasma levels were significantly increased at 30 and 60 min after meal ingestion (Fig. 1). The AUC0–120' of the GLP-1 in response to the test meal was significantly larger compared with before surgery (pre-RYGB 1704 ± 1053 vs. post-RYGB 2627 ± 1224 pM/min, P < 0.05), with this increment occurring in all but one participant (Fig. 2). Likewise, 6 wk after surgery, plasma PYY increased promptly after food intake, reached its maximum at 60 min, and maintained similar values throughout the following hour (Fig. 1). Consistently the AUC0–120' of PYY in response to the test meal was significantly increased (pre-RYGB 3408 ± 774 vs. post-RYGB 9396 ± 3051 pmol·liter–1·min, P < 0.01), with that increment being observed in all the study subjects (Fig. 2).
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Hunger and satiety VAS scores
Six weeks after surgery, ratings of hunger in the fasting state (P < 0.05) and after meal ingestion (AUC0–120', P = 0.05; Fig. 3) were significantly decreased, compared with the initial evaluation. Similarly, a greater postprandial satiety was reported in the operated patients after meal intake (P < 0.05, Fig. 3). Six weeks after surgery, fasting GLP-1 (r = 0.69; P < 0.05) and AUC0–120' of GLP-1 (r = 0.75; P < 0.05) were significantly correlated with satiety VAS in the fasting state. In contrast, we failed to find a significant correlation between fasting PYY, the maximal PYY plasma concentration, or the AUC0–120' of PYY in response to meal ingestion and hunger and satiety VAS scores. Of note, the 1.6 ± 1.9-fold increase in the GLP-1 AUC0–120' and the 2.9 ± 1.2-fold increase in the PYY AUC0–120' after meal ingestion 6 wk after RYGBP were associated with a 45 ± 86% decrease in the hunger and a 123 ± 22% increase in the satiety AUC0–120' ratings. However, no significant correlation was found between the changes in the hormonal and behavioral parameters.
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RYGBP surgery was associated with an acceleration of GE (Fig. 4) and OCTT. After surgery, the time to maximal paracetamol plasma concentration was shortened (after RYGB 6.7 ± 2.6 vs. before RYGB 19.5 ± 6.8 min; P < 0.05), and the AUC0–60' of paracetamol significantly increased (after RYGB 1036 ± 275 vs. before RYGB 626 ± 246 pmol·ml–1·min; P < 0.05). Similarly, the maximal paracetamol concentration increased after surgery (before RYGB 19.5 ± 6.8 vs. after RYGB 29.6 ± 11.5 pmol/ml), although it did not reach statistical significance. Before surgery a significant increase in expiratory hydrogen concentration after lactulose intake was observed at 115.0 ± 22.4 min, whereas OCTT was shortened to 75.0 ± 24.7 min 6 wk after RYGBP (P < 0.05). Interestingly, after surgery the GLP-1 response to meal intake was associated with a larger AUC0–60' of paracetamol plasma concentration (r = 0.94, P < 0.01) but not with the OCCT. Lastly, we failed to find a significant correlation between measurements of PYY plasma concentration and GE or OCTT estimates at either of the two study time points.
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Discussion |
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Kellum et al. (18) and Meryn et al. (30) reported marked postprandial elevations in plasma enteroglucagon levels (a measure of intestinal peptides derived from proglucagon such as GLP-1) 6–9 months after RYGBP. Moreover, a recent cross-sectional study showed a marked increase in the GLP-1 after meal intake in weight-stable RYGBP-operated subjects (19). In sharp contrast, two recent studies (31, 32) failed to show a significant change in fasting GLP-1 shortly after RYGBP. Nonetheless, because only the basal hormonal level was tested in these two studies, significant effects of RYGBP on the meal-induced hormonal secretion might have been overlooked. Although dietary-induced weight loss in obese subjects has been associated with an increase in GLP-1 response (28), our data and that of others suggest that other mechanisms may account for the noticeable increase in the GLP-1 response after RYGBP. Although a significant amount of weight loss was associated with either RYGBP or vertical banded gastroplasty (VBG), enteroglucagon response 6 months after surgery was only slightly elevated in VBG-operated subjects, compared with those who underwent RYGBP (18). Similarly, postprandrial GLP-1 was larger in weight-stable RYGBP-operated subjects when compared with BMI-matched subjects who had undergone gastric banding (19).
Our data are consistent with previous studies showing that RYGBP is associated with a substantial increase in postpandrial PYY plasma concentration (19, 20). In cross-sectional studies, it was shown that in weight-stable obese subjects, the PYY response to a test meal was approximately 2- to 5-fold larger after RYGBP, compared with lean and BMI-matched controls. Our prospective study further supports these findings and shows that the increase in PYY response to meal ingestion occurs at an early stage after RYGBP. Despite significant weight loss, a blunted PYY response to meal intake has been reported after gastric banding (19). On the other hand, VBG and jejunoileal bypass have been associated with an increase in fasting but not postprandial PYY, respectively at 12 months and 20 yr after surgery (21, 33). In sharp contrast with these results, in our and previous studies (19, 20), fasting PYY was not different after RYGBP surgery. The reason for the differential PYY response among different bariatric techniques remains elusive. It has been shown that dietary-induced weight loss is associated with increased fasting PYY levels (29). However, whether weight loss is associated with changes in postprandrial PYY remains to be elucidated. A prospective comparison of the changes in PYY, either fasting or postpandrially, among different treatments for obesity is warranted.
The mechanisms by which RYGB is associated with a decrease in meal frequency (6, 7) are not well understood. We used VAS measurements to quantify feelings of hunger and satiety in the fasting state and throughout the standardized test meal. Our data showed that RYGBP is associated with a decreased feeling of hunger both in the fasting state and after meal intake as well as with an increased satiety after meal ingestion. These results somewhat disagree with those by Korner et al. (20) in which only a nonstatistically significant tendency toward greater satiety was found in RYGBP-operated subjects, compared with BMI-matched controls. Nonetheless, the prospective nature of our study reinforces the validity of our findings.
Different studies have demonstrated that GLP-1 and PYY may contribute to an early sense of satiety and the ability of an individual to reduce meal size. Peripherally administered GLP-1 and PYY elicit satiety in healthy (15, 16) and obese subjects (15, 17). In that context, it is reasonable to hypothesize that the success of weight loss and maintenance after RYGBP could be due to decreased hunger and increased satiety induced not just by volume restriction but also by an increased hindgut hormonal response to nutrients (2, 3). Consistently, the changes in GLP-1 and PYY plasma concentration after meal intake were well suited to the changes in hunger and satiety. In further support of this hypothesis, Strader et al. (22) recently showed in a rodent model that in the absence of either restriction or malabsorption ileal transposition resulted in an increase in GLP-1 and PYY plasma concentration that was associated with reduced food intake and weight loss.
Finally, we sought to address why GLP-1 and PYY are elevated after RYGBP in response to a standardized liquid meal. It has been suggested that, because the surgical procedure alters the physiological gastric emptying mechanism and the length of the small bowel is shortened, the change in the hormonal response could be due to an earlier contact between nutrients and the L cells located in the hindgut (2, 3, 19, 22). Noteworthy, the changes in gastric emptying after RYGBP surgery have seldom been reported, and, to the best of our knowledge, the OCTT in RYGBP-operated obese subjects has not previously been assessed. Naslund and Beckman (34) and Horowitz et al. (35) showed no change or a slowing in gastric emptying after the ingestion of a solid meal in RYGBP-operated subjects. However, in accordance with our findings, using a scintigraphic technique Horowitz et al. (35) showed that gastric liquid emptying occurred more rapidly after RYGBP. The significant correlation between the AUC0–60' of paracetamol and the AUC0–60' of GLP-1 after meal ingestion in our study supports the possible role of shortening in GE in the improvement of the hormonal response from the distal gut. However, the GE changes in our study should be interpreted cautiously because of the potentially different paracetamol pharmacokinetics between the two study time points (36). The concurrence of an increased hormonal response and a shortening of the OCTT 6 wk after surgery in our study could be interpreted as circumstantial evidence supporting that the early contact of ingested nutrients with the distal gut is associated with a marked increase in GLP-1 and PYY plasma concentrations. Our data support those by Strader et al. (22) in a rodent of ileal transposition. Likewise, plasma PYY levels were markedly augmented, compared with healthy controls, in patients in whom a resection of the small intestine had been performed (37).
Our study has several limitations. First, the small sample size may not allow definite conclusions on the consequences of the changes in GLP-1 and PYY plasma levels on eating patterns or its relationship with gastrointestinal motility to be drawn. Thus, further studies are needed to clarify these issues. Second, our study lacks a proper control group. In contrast with RYGBP-operated patients, the subjects in our BMI-matched group were weight-stable, nonoperated individuals. A head-to-head prospective comparison between RYGBP- and GB-operated subjects would have been necessary to discern whether weight loss or the RYGBP is critical for the changes in the hindgut hormones. Finally, interpretation of the results should be cautious because of the commercially available assays used. The GLP-1 assay had a very high coefficient of variation. The assay used to measure PYY relies on a polyclonal antibody that cross-reacts 100% with the two described circulating forms of PYY, namely PYY1–36 and PYY3–36. Therefore, we measured total PYY concentrations rather than discriminated between two molecular isoforms. Thus, because so far only PYY3–36 has been shown to inhibit food intake in humans (16, 17) and it is unclear which isoform contributed to the increased postprandial rise our patients, this may have confounded our analysis.
In summary, our data show that RYGBP is associated with a marked increase in GLP-1 and PYY plasma concentrations in response to a liquid meal. However, whether weight loss or the RYGBP was critical for the changes in the hindgut hormones remains to be elucidated because our study lacks the proper control group. Moreover, we provide circumstantial evidence supporting the possible effect of these hindgut hormonal secretions on the changes in hunger and satiety that occur after gastric bypass surgery. Finally, our data support the hypothesis that changes in GLP-1 and PYY after RYGBP could be accounted for, at least in part, by changes in gastrointestinal motility. Confirmation of these findings may lead to the development of new drugs, thereby providing less invasive therapies for obesity.
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Acknowledgments |
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Footnotes |
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The authors of this manuscript have no potential conflicts of interest to declare.
First Published Online February 14, 2006
Abbreviations: AUC, Area under the curve; BMI, body mass index; GE, gastric emptying; GLP, glucagon-like peptide; OCTT, orocecal transit time; PYY, peptide YY; RYGBP, Roux-en-Y gastric bypass; VAS, visual analog scale; VBG, vertical banded gastroplasty.
Received April 26, 2005.
Accepted February 6, 2006.
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