Download Medical and Surgical Treatments for Obesity Have Opposite Effects

ORIGINAL
ARTICLE
E n d o c r i n e
C a r e
Medical and Surgical Treatments for Obesity Have
Opposite Effects on Peptide YY and Appetite:
A Prospective Study Controlled for Weight Loss
Juan P. Valderas, Verónica Irribarra, Camilo Boza, Rolando de la Cruz,
Yessica Liberona, Ana Maria Acosta, Macarena Yolito, and Alberto Maiz
Departments of Nutrition, Diabetes, and Metabolism (J.P.V., V.I., Y.L., A.M.A., M.Y., A.M.), Digestive
Surgery (C.B.), and Public Health (R.d.l.C.), School of Medicine, Pontificia Universidad Católica de Chile,
6510260 Santiago, Chile
Context: The effects of medical and surgical treatments for obesity on peptide YY (PYY) levels, in
patients with similar weight loss, remain unclear.
Objective: The objective of the study was to assess PYY and appetite before and after Roux-en-Y
gastric bypass (RYGB), sleeve gastrectomy (SG), and medical treatment (MED).
Design: This was a prospective, controlled, nonrandomized study.
Setting: The study was conducted at the Departments of Nutrition and Digestive Surgery at a
university hospital.
Participants: Participants included three groups of eight patients with similar body mass indexes
(RYGB 37.8 ⫾ 0.8, SG 35.3 ⫾ 0.7, and MED 39.1 ⫾ 1.7 kg/m2, P ⫽ NS) and eight lean controls (body
mass index 21.7 ⫾ 0.7 kg/m2).
Main Outcome Measures: Total plasma PYY, hunger, and satiety visual analog scales in fasting and
after ingestion of a standard test meal were measured.
Results: At baseline there were no differences in the area under the curve (AUC) of PYY, hunger,
or satiety in obese groups. Two months after the interventions, RYGB, SG, and MED groups
achieved similar weight loss (17.7 ⫾ 3, 14.9 ⫾ 2.4, 16.6 ⫾ 4%, respectively, P ⫽ NS). PYY AUC
increased in RYGB (P ⬍ 0.001) and SG (P ⬍ 0.05) and did not change in MED. PYY levels decreased
at fasting, 30 min, and 180 min after a standard test meal in MED (P ⬍ 0.05). Hunger AUC decreased
in RYGB (P ⬍ 0.05). Satiety AUC increased in RYGB (P ⬍ 0.05) and SG (P ⬍ 0.05). Appetite did not
change in MED. PYY AUC correlated with satiety AUC (r ⫽ 0.35, P ⬍ 0.05).
Conclusion: RYGB and SG increased PYY and reduced appetite. MED failed to produce changes. Different effects occur despite similar weight loss. This suggests that the weight-loss effects of these procedures are enhanced by an increase in PYY and satiety. (J Clin Endocrinol Metab 95: 1069–1075, 2010)
ver the last 30 yr, the prevalence of obesity has increased worldwide, becoming one of the world’s
most important public health problems and resulting in
great efforts toward the development of strategies to treat
this condition (1). However, medical interventions for
O
obesity, including diet, physical activity, behavioral therapy, and weight loss drugs, are associated with poor
weight reduction and are difficult to sustain in the long
term (2). These modest results can be explained by several
factors, one being that the human body responds to weight
ISSN Print 0021-972X ISSN Online 1945-7197
Printed in U.S.A.
Copyright © 2010 by The Endocrine Society
doi: 10.1210/jc.2009-0983 Received May 8, 2009. Accepted December 3, 2009.
First Published Online January 22, 2010
Abbreviations: AUC, Area under the curve; BMI, body mass index; GEE, generalized estimating equation; MED, medical treatment; PYY, peptide YY; RYGB, Roux-en-Y gastric
bypass; SG, sleeve gastrectomy; STM, standard test meal; VAS, visual analog scale.
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PYY in Medical and Surgical Obesity Treatments
loss via compensatory changes in energy intake and expenditure, changes that may be triggered mainly from adipose tissue signaling (3). On the other hand, surgery for
obesity has been shown to produce significant and sustained weight loss and is associated with a persistent reduction of caloric intake and changes in appetite (4). The
current hypotheses regarding the underlying mechanisms
that lead to the differing successes of surgical compared
with medical treatments for obesity are: 1) a restriction of
gastric volume; 2) nutrient malabsorption; and 3) modification of the gut hormones that modulate perceptions of
hunger and satiety (5). One of these hormones is peptide
YY (PYY), a member of the PP-fold peptide family that is
produced by L-type endocrine cells of the intestinal mucosa. PYY tissue concentrations vary remarkably in different portions of the gut, and PYY content increases from
the proximal to the distal gut. PYY levels increase postprandially, and its main effects include a reduction of food
intake, a delay in gastric emptying, and a decrease in gastric secretion. The peptide has two circulating forms,
PYY1-36 and PYY3-36, and current evidence suggests that
only the 3-36 form has an anorectic effect in humans (6).
Recent studies found that PYY secretion increases after
some types of bariatric surgeries (7–23), and some of these
studies associate this increase with favorable changes in
appetite (10 –13, 19). Nevertheless, it has not been clearly
established whether these changes can explain the differing results among patients who undergo surgical vs. medical treatments for obesity because the groups of obese
subjects differ in terms of their degrees of obesity and
weight loss.
Our aim was to study the effects of medical treatment
for obesity and two types of bariatric surgeries on PYY
levels as well as hunger and satiety perceptions in subjects
with similar magnitudes of obesity and weight reduction
achieved after the interventions.
Subjects and Methods
The study was approved by the School of Medicine Ethics Committee of the Pontificia Universidad Católica de Chile, and all
subjects provided informed consent. We designed a nonrandomized prospective study with three groups of obese patients
matched by body mass index (BMI). They were invited from the
Program of Treatment for Obesity at the Faculty of Medicine.
The inclusion criteria were age 18 – 60 yr and BMI between 30
and 50 kg/m2. Exclusion criteria included severe medical conditions or psychiatric illness; substance abuse; previous gastrointestinal surgery; and use of medications known to affect hunger, satiety, or intestinal function. The subjects were evaluated
before any intervention and 2 months after medical or surgical
treatment for obesity. In addition, we evaluated eight healthy,
lean volunteers (lean group) 20 –50 yr of age with BMIs between
18.5 and 24.5 kg/m2 as a control group.
J Clin Endocrinol Metab, March 2010, 95(3):1069 –1075
Roux en-Y gastric bypass (RYGB) and Sleeve
Gastrectomy (SG) protocols
At our institution, the bariatric procedures are standardized
and performed laparoscopically by a group of five surgeons.
RYGB includes a complete section of the stomach, leaving
only a 15- to 30-cc gastric pouch. A hand-sewn gastrojejunal
anastomosis is constructed with a 150-cm Roux-en-Y limb and
a 30-cm biliopancreatic limb (24).
SG is performed over a 60 French bougie using 60-mm linear
staplers. The staplers are used to remove the greater curvature of
the stomach, including the complete fundus up to the angle of His
as well as the majority of the corpus and antrum. Patients are not
vagotomized in either surgery.
The postsurgical dietary recommendations were similar for
both procedures. During the first month, the diet included a daily
intake of 600 – 800 kcal with 70 g of protein plus vitamin supplements. During the second month, the daily intake recommendations were 1000 kcal and 80 –100 g of protein. This was
achieved with multiple small meals and snacks and, in some
cases, with commercial protein supplements. The food consistencies that patients were allowed to ingest progressed over 8 wk
in the following four successive stages according to individual
tolerance: liquid, semiliquid, semisolid, and solid.
Medical treatment protocol
Medical treatment (MED) included a low-calorie diet of
1300 –1800 kcal/d (20 –25 kcal/kg of ideal weight), behavioral
modification, and a routine of 180 min/wk of aerobic and resistance exercise. Subjects participated in a daily care program in the
Center for Obesity Treatment of our institution and ate all of their
meals at the center. Body weight was measured weekly. All subjects
were seen by a physician and a registered dietitian every 15 d.
Study protocol
Patients were scheduled to be seen in clinic at 0800 h after a
12-h overnight fast. Weight and height were recorded for all
patients. Excess weight was calculated as the difference between
their current body weight and a body weight corresponding to a
BMI of 25 kg/m2. In a sitting position, a topical anesthetic
(EMLA cream; AstraZeneca, Wilmington, DE) was applied to
the forearm 15 min before an iv catheter was placed. Blood samples were drawn before and at 30, 60, 90, 120, and 180 min after
the intake of 237 ml of a standard test meal (STM; Ensure Plus,
355 kcal, 13 g protein, 50 g carbohydrate, 11 g fat; Abbott
Laboratories, Columbus, OH). Caloric intake was estimated by
a 24-h dietary recall for 3 d of the previous week. Dietary surveys
were analyzed using a computer program (Food Processor II;
ESHA Research, Salem, OR) that was previously validated for
Chilean food (25).
PYY assessment
Blood samples were drawn and placed in tubes containing
EDTA and a protease inhibitor (Trasylol, 500 kIU/ml; Bayer,
Leverkusen, Germany), centrifuged immediately at 4 C during
the collection period, and stored at ⫺70 C until analyzed. Total
plasma PYY levels were measured with a commercially available
RIA kit (Linco Research, Inc., St. Charles, MO). This assay uses
125
I-labeled PYY and a PYY antiserum to determine the levels of
both the 1-36 and 3-36 forms of human PYY in serum or plasma.
The lower limit of detection for the PYY assay is 10 pg/ml. The
J Clin Endocrinol Metab, March 2010, 95(3):1069 –1075
intra- and interassay coefficients of variation were both less than
10%.
Hunger and satiety ratings
All subjects completed two visual analog scales (VASs) for
hunger and satiety at the same time blood samples for PYY measurements were drawn. The VAS was composed of 100-mm
lines, with a phrase at each end describing the extremes. Subjects
were told to make a mark across the line corresponding to their
perceptions of hunger and satiety. Quantification was done by
measuring the distance from the left end of the scale to the mark.
This VAS was previously validated by Flint et al. (27) and has
been used in similar studies (10 –13, 19).
Statistical analysis
Data are expressed as mean ⫾ SEM. The Kolgomorov-Smirnov
test was used to assess the normality of the residuals. Values for
the area under the curve (AUC) for PYY, hunger, and satiety after
a standard mixed-liquid meal were calculated using the trapezoidal method and were compared using ANOVA or a pairedsamples t test. A generalized estimating equation (GEE) model
was constructed to analyze the effects of the treatments and time
on PYY, hunger, and satiety before and after interventions. Relationships between the AUCs for PYY, hunger, and satiety were
analyzed using the two-tailed Pearson’s correlation. A regression
model was performed to adjust the changes in the AUC for PYY
levels by changes in body weight. Statistical analysis was performed using SPSS 15.0 (SPSS, Inc., Chicago, IL) and R software
version 2.8.1. (R Foundation for Statistical Computing, Vienna,
Austria) P ⬍ 0.05 was considered statistically significant.
Results
Weight loss and PYY levels
Eight subjects were recruited in four groups; the RYGB,
SG, MED, and lean control groups. The lean control subjects (n ⫽ 8, female ⫽ 4) were 36.4 ⫾ 3.1 yr old, weighed
67.0 ⫾ 3.0 kg, and had a mean BMI of 21.7 ⫾ 0.7 kg/m2.
The characteristics of the obese patients in the RYGB, SG,
and MED groups are shown in Table 1. At baseline evaluation, four patients in the surgical group had a BMI less
than 35 kg/m2 because they had lost weight since the initial
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operative consultation, but that weight loss was less than
5% in all cases. Only one surgical procedure (RYGB) required conversion to open surgery. Two patients in the
RYGB group and two patients in the SG group were diagnosed with type 2 diabetes mellitus at the preoperative evaluation, but they did not receive oral hypoglycemic agents.
There were no intraoperative or postoperative complications. The three groups of patients did not differ significantly
by age or BMI, but the patients in the MED group weighed
more at baseline than the surgical patients (Table 1).
Two months after the initial evaluation, all patients
exhibited a reduction in body weight and BMI, regardless of
the type of treatment they received, without significant differences noted between groups in terms of percentage of
weight loss or excess weight loss, although all of them were
still obese (Table 1). Additionally, there were no significant
differences noted between groups in terms of caloric intake during the week before the second evaluation (data not shown).
Before treatment, the fasting PYY levels of patients in the
three obese groups were lower than those of subjects in the
lean control group, and in the MED and the SG groups these
differences were statistically significant from those of the lean
controls. PYY response to a STM, which was measured as
AUC0-180, was higher in the lean controls compared with the
obese patients, but this difference was significant only among
patients in the MED group (Table 2).
Two months after treatment, fasting PYY levels did not
change in the RYGB or SG group, but they decreased in the
MED group (Fig. 1 and Table 2). In the RYGB and SG
groups, the AUC0-180 for total PYY levels significantly
increased compared with presurgical values and were
higher in the RGYB group than the SG group (P ⫽ 0.02).
The PYY response after RYGB was higher compared with
the lean control group (P ⫽ 0.03), although the SG group
reached a similar PYY value (Table 2 and Fig. 1). In the
MED group, no significant change in the PYY AUC0-180
was observed after the medical intervention (Table 2). In
addition, this group had a PYY AUC0-180 value lower than
TABLE 1. Clinical characteristics of the three obese groups before and after intervention
n (females)
Baseline
Age (yr)
Weight (kg)
BMI (kg/m2)
Two months after intervention
BMI (kg/m2)
Weight loss, %
EWL, %
Caloric intake
MED
8 (4)
RYGB
8 (8)
SG
8 (8)
P value
32.1 ⫾ 3.3
117.4 ⫾ 10.6
39.1 ⫾ 1.7
38.7 ⫾ 4.5
96.5 ⫾ 1.5
37.8 ⫾ 0.8
40.2 ⫾ 2.0
92.2 ⫾ 3.3
35.3 ⫾ 0.7
NS
0.03a
NS
32.5 ⫾ 1.3
16.6 ⫾ 1.4
47.4 ⫾ 3.7
1367 ⫾ 210
30.9 ⫾ 0.8
17.7 ⫾ 1.1
52.8 ⫾ 3.2
1084 ⫾ 122
30.1 ⫾ 0.5
14.9 ⫾ 0.8
50.9 ⫾ 2.7
1090 ⫾ 619
NS
NS
NS
NS
Values are presented as mean ⫾ SEM. EWL, Excess weight loss; NS, not significant.
a
MED vs. RYGB and SG (ANOVA).
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J Clin Endocrinol Metab, March 2010, 95(3):1069 –1075
TABLE 2. PYY, hunger, and satiety scores in lean control subjects and the three obese groups at baseline and
2 months after intervention
Fasting PYY (pg/ml)
Baseline
Two months after intervention
PYY AUC0-180 (pg/ml⫺1 䡠 min)
Baseline
Two months after intervention
Hunger AUC0-180 (VAS score per minute)
Baseline
Two months after intervention
Satiety AUC0-180 (VAS score per minute)
Baseline
Two months after intervention
Lean
MED
RYGB
SG
P value
149.2 ⫾ 15.6
84.8 ⫾ 8.6
58.1 ⫾ 8.6b
115.6 ⫾ 14.8
122.8 ⫾ 16.4
89.2 ⫾ 12.7
114.6 ⫾ 18.6
0.02a
31,812 ⫾ 3,180
17,373 ⫾ 2,885
14,095 ⫾ 1,913
25,305 ⫾ 2,426
42,247 ⫾ 3,158d
23,383 ⫾ 2,765
32,805 ⫾ 2,022e
0.01c
8,666 ⫾ 1,529
3,804 ⫾ 841
4,586 ⫾ 1,221
7,357 ⫾ 1,312
2,981 ⫾ 939f
6,815 ⫾ 1,429
3,729 ⫾ 1127
NS
7,901 ⫾ 871
7,616 ⫾ 1,681
7,072 ⫾ 1,414
8,596 ⫾ 613
12,992 ⫾ 1,437f
10,254 ⫾ 1,128
13,459 ⫾ 921g
NS
Values are presented as mean ⫾ SEM.
a
Lean vs. MED and SG groups; b P ⫽ 0.03, values for the comparison between baseline values and values observed 2 months after intervention
(paired t test, unadjusted)3; c Lean vs. MED (ANOVA); d P ⫽ 0.001, values for the comparison between baseline values and values observed 2
months after intervention (paired t test, unadjusted); e P ⫽ 0.01, values for the comparison between baseline values and values observed 2 months
after intervention (paired t test, unadjusted); f P ⫽ 0.003, values for the comparison between baseline values and values observed 2 months after
intervention (paired t test, unadjusted); g P ⫽ 0.04, values for the comparison between baseline values and values observed 2 months after
intervention (paired t test, unadjusted).
both of the surgical groups (P ⬍ 0.001). A GEE model
detected a significant PYY increase in the RYGB group at
30, 60, 90, and 120 min after consumption of a STM
compared with their presurgical values. A significant increase was also observed in the SG group’s response to a
STM at 30 and 60 min after food consumption. In contrast, in the MED group, PYY levels were observed to have
significantly decreased compared with their baseline levels
at 30 and 180 min after STM consumption (Fig. 1C).
Hunger and satiety
Two months after treatment, rates of hunger and satiety in the fasting state showed did not differ compared
with the initial evaluation. After standard meal ingestion,
FIG. 1. Total PYY levels observed in response to a standard liquid meal in lean control volunteers and obese patients before (A) and 2 months
after (B) RYGB, SG, and MED initiation. Changes (picograms per milliliter) in total PYY levels 2 months after intervention in comparison with
baseline conditions observed after fasting and 30, 60, 90, 120, and180 min after the intake of a standard meal in the MED, RYGB, and SG groups
(C). Data are expressed as mean ⫾ SEM. *, P ⬍ 0.05 (GEE model for multiple comparisons at different time points).
J Clin Endocrinol Metab, March 2010, 95(3):1069 –1075
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FIG. 2. AUC of hunger (A) and satiety (B) VAS scores (millimeters) in response to a standard liquid meal in lean control subjects and obese patients
before and after RYGB, SG, and MED. Values are expressed as mean ⫾ SEM. The P values listed reflect the comparison between the two study time
points (paired t test, unadjusted).
hunger and satiety scores changed significantly in the
RYGB and SG groups compared with baseline. The hunger AUC0-180 decreased in both surgical groups but was
statistically significant only in the RYGB group (Fig. 2A).
The satiety AUC0-180 was found to be significantly augmented in the RYGB and SG groups (Fig. 2B). In contrast,
patients in the MED group showed no significant changes
in terms of hunger and satiety AUC0-180 at 2 months after
the initial evaluation compared with their baseline values
(Fig. 2). A GGE model detected a significant decrease in
hunger in the RYGB group at 30 min after STM consumption (P ⫽ 0.02) and also observed a decrease in hunger at
120 min after STM consumption in SG group (P ⫽ 0.04)
compared with their baseline values. A significant increase
in satiety was observed at 30 and 60 min after eating (P ⫽
0.02) in both surgical groups. In the MED group, a decrease in satiety was detected 180 min after eating (P ⫽
0.007) compared with the baseline value.
Relationship between appetite score, PYY levels,
and weight loss
There were no correlations observed between percentage of weight loss and change in PYY AUC0-180 in the
whole sample (r ⫽ 0.06, P ⫽ 0.8) or within each surgical
group (RYGB: r ⫽ ⫺0.28, P ⫽ 0.5; SG: r ⫽ 0.27, P ⫽ 0.5).
We observed a significant positive correlation between
PYY level AUC0-180 and the satiety AUC0-180 (r ⫽ 0.35,
P ⫽ 0.01) in the three obese groups before and after interventions. There was no correlation observed between the
PYY level AUC0-180 and the hunger AUC0-180 (r ⫽ ⫺0.18,
P ⫽ 0.2). We observed a significant positive correlation between the AUC changes in PYY levels and satiety in all
obese groups (r ⫽ 0.47, P ⫽ 0.02). The significant increase
in satiety observed 2 months after both surgical interventions at 30 and 60 min after STM consumption was correlated with a significant augmentation in PYY levels at
the same time points (30 min: r ⫽ 0.41, P ⫽ 0.046; 60 min:
r ⫽ 0.42, P ⫽ 0.039). The regression model performed to
adjust the PYY AUC0-180 changes was not significant
with regard to percentage of weight loss (P ⫽ 0.7), ini-
tial BMI (P ⫽ 0.6), or intervention group (P ⫽ 0.1).
Additionally, the regression analysis performed in each
group to adjust the PYY AUC0-180 changes by weight
loss achieved was not significant (RYGB, P ⫽ 0.5; SG,
P ⫽ 0.5; MED, P ⫽ 0.8).
Discussion
In this prospective study, we observed that, as a treatment
for obesity, RYGB and SG produced a significant increase
in PYY levels in response to a standard meal 2 months after
the procedures. Remarkably, medical intervention does
not have the same effect, despite a similar amount of
weight loss among subjects with comparable BMIs. Since
1997 several cross-sectional and prospective studies have
been performed to evaluate the effects of different surgical
procedures on PYY levels during the fasting state and after
meal intake. The effects of RYGB, gastric banding, and
biliopancreatic diversion on fasting PYY levels that have
been observed are diverse and inconclusive. However,
PYY response after a meal has been found to increase in all
derivative surgeries studied, such as RYGB (9, 13, 16, 18,
19, 21), ileal transposition with SG (20), jejunoileal bypass
(7), and digestive adaptation with intestinal reversal, a
procedure described by Santoro et al. (14). This increase in
postprandial PYY response is not observed in purely restrictive surgeries, such as gastric banding (11, 12) and vertical
banded gastroplasty (8). The exception to this rule could be
SG. Recently Karamanakos et al. (19) reported an increase of
PYY levels during fasting and 2 h after meal consumption in
six patients at 3, 6, and 12 months after SG.
Our results clearly agree with theirs. Our study suggests
that the transit derivation of nutrients along the duodenum is not necessary to improve the postprandial secretion
of the satiety hormone PYY. Two theories could explain
this finding. First, it is probable that the SG procedure
changes neuronal or humoral signaling that regulates PYY
secretion after meals. To date, only ghrelin levels have
been studied in SG surgery patients (19, 27). After gastric
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PYY in Medical and Surgical Obesity Treatments
fundus removal, ghrelin levels decrease in both the fasting
and postprandial states, but it is not known whether these
changes explain the augmentation in PYY levels that are
observed. A second explanation could be that SG produces
a decrease in gastric acid secretion and a faster gastric
emptying rate (28), an effect not observed in other restrictive surgeries like gastric banding (29). Both of these
changes would lead to a faster arrival of undigested nutrients to the duodenum and would therefore increase the
PYY response to the meal. The augmentation in postprandial PYY secretion observed after fundoplication in patients with gastroesophageal reflux supports the second
explanation (30).
Interestingly, weight loss achieved by medical treatment, despite being similar in magnitude to that achieved
by RYGB and SG, was not associated with positive
changes in the PYY AUC response to a meal. Additionally,
we observed a significant decrease in PYY secretion after
meal test ingestion (Fig. 1B). Few studies have evaluated
the impact of weight loss after medical treatment for obesity on PYY secretion. Moran et al. (31) did not observe
changes in PYY secretion after a weight loss of 5 kg in 28
obese women, and Pfluger et al. (32) in a study of 17 obese
patients observed that a 5.4% weight loss was associated
with a 30% decrease in fasting PYY. The subjects in our
medical treatment group received a caloric restriction diet
and followed an exercise routine. The effect of exercise on
PYY secretion has been recently investigated, and a slight
increase in postprandial PYY levels has been reported (33–
35). However, these studies measured the effects of exercise on PYY levels in an acute manner in lean subjects. The
decrease in PYY secretion observed after weight loss by
medical treatment could mean that this hormone has a role
in the long-term regulation of body weight, similar to leptin, insulin, and ghrelin. We can conclude that the increase
in PYY response to meal consumption after RYGB and SG
surgeries is not related to changes in body weight or caloric
restriction and that medical treatments for obesity could
negatively affect the secretion of this satiety hormone.
The changes in PYY response observed after 2 months
of intervention were associated with a diminution in hunger and an increase in satiety for both surgeries. We found
that PYY levels can explain a third of satiety perception
and that the increase in satiety observed after both surgical
interventions was associated with an augmentation of
PYY levels. On the other hand, the decrease of satiety
observed after medical treatment was associated with a
decrease in PYY levels.
We observed lower PYY levels in obese patients compared with lean subjects at baseline. A similar finding was
described previously, and it has been suggested that this
J Clin Endocrinol Metab, March 2010, 95(3):1069 –1075
alteration could have a role in the initiation or maintenance of obesity (36, 37).
This study was designed with a short-term follow-up
because our aim was to create a medical group with a
similar degree of weight loss as surgical groups. This objective would be unlikely to be successful in a study with
longer-term follow-up. Also, the caloric state in which the
patients were studied may have altered the PYY results
because surgical patients continue to lose weight for up to
9 months after surgery and lose more weight than diettreated patients, who tend to plateau after 3– 4 months
and achieve a lesser degree of total weight loss. This was
a nonrandomized study because the risks involved in the
alternative treatment were considered too different to allow randomization.
Finally, we conclude that RYGB and SG produce an
increase in PYY response associated with a decrease in
appetite perception. It is notable that SG produced this
change without duodenal exclusion. Medical treatment
fails to augment PYY secretion and does not modify hunger or satiety in subjects with a comparable degree of obesity who achieved similar magnitudes of weight loss. On
the other hand, the weight loss observed after medical and
surgical interventions in our study were not related to the
changes in the PYY response. This suggests that the augmentation in PYY secretion observed after these surgeries explains the change in appetite perception among
the medically and surgically treated groups but may not
be responsible for the changes in body weight we observed. Whether these observations persist in the long
term remains to be determined.
Acknowledgments
Address all correspondence and requests for reprints to: Juan P.
Valderas, Department of Nutrition, Diabetes, and Metabolism,
Pontificia Universidad Católica de Chile, Marcoleta 367,
6510260 Santiago, Chile. E-mail: [email protected].
This work was supported by grants from the Department of
Nutrition, Diabetes, and Metabolism, School of Medicine, Pontificia Universidad Católica de Chile.
Disclosure Summary: The authors have nothing to disclose.
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