Ghrelin and peptide YY increase with weight loss during a 12-month intervention to reduce dietary energy density in obese women

doi:10.1016/j.peptides.2013.09.009

Peptides

Volume 49, November 2013, Pages 138-144

https://doi.org/10.1016/j.peptides.2013.09.009 Get rights and content

Highlights

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Ghrelin and PYY increased in response to reduced ED and consequent weight loss.
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Low-ED diets were associated with lesser increases ghrelin across the intervention.
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Low-ED diets tended to be associated with increases in PYY.
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Reductions in ED may promote weight loss by blunting orexigenic hormone responses.

Abstract

Reducing dietary energy density (ED) promotes weight loss; however, underlying mechanisms are not well understood. The purpose of this study was to determine if low-ED diets facilitate weight loss through actions on ghrelin and peptide YY (PYY), independent of influences of psychosocial measures. Seventy-one obese women (BMI 30–40 kg/m²) ages 22–60 years received counseling to reduce ED. Fasting blood samples were analyzed for total ghrelin and total PYY by radioimmunoassay at months 0, 3, 6, and 12. Restraint, disinhibition, and hunger were assessed by the Eating Inventory. Body weight (−7.8 ± 0.5 kg), BMI (−2.9 ± 0.2 kg/m²), body fat (−3.0 ± 0.3%), and ED (−0.47 ± 0.05 kcal/g or −1.97 ± 0.21 kJ/g) decreased from months 0 to 6 (p < 0.05) after which no change occurred from months 6 to 12. Ghrelin increased in a curvilinear fashion (month 0: 973 ± 39, month 3: 1024 ± 37, month 6: 1109 ± 44, and month 12: 1063 ± 45 pg/ml, p < 0.001) and PYY increased linearly (month 0: 74.2 ± 3.1, month 3: 76.4 ± 3.2, month 6: 77.2 ± 3.0, month 12: 82.8 ± 3.2 pg/ml, p < 0.001). ED, body weight, and hunger predicted ghrelin, with ED being the strongest predictor (ghrelin = 2674.8 + 291.6 × ED − 19.2 × BW − 15 × H; p < 0.05). There was a trend toward a significant association between ED and PYY (PYY = 115.0 − 43.1 × ED; p = 0.05). Reductions in ED may promote weight loss and weight loss maintenance by opposing increases in ghrelin and promoting increases in PYY.

Introduction

Dietary energy density (ED; kcal/g or kJ/g) can be reduced by decreasing the proportion of fat or by increasing the water content of foods [22], [47]. Several studies [5], [6], [48] have demonstrated that humans tend to consume a consistent weight or volume of food from day to day. Thus, consuming a low-ED diet can reduce energy intake while maintaining the volume of food eaten. Decreasing dietary ED has been shown to be useful in long-term weight loss [8], [19], [24], [36], [45]; however, the underlying physiological mechanisms remain to be elucidated.

Ghrelin is an orexigenic hormone secreted into the blood from the X/A-like cells in the stomach and duodenum [16], [30]. Circulating ghrelin increases with weight loss in normal weight women [37], [38], whereas concentrations are suppressed and normalized (increased) with weight loss in obese individuals [25]. PYY is a satiety hormone secreted from L-cells in the distal gut where it slows digestion to increase absorption of nutrients [56]. PYY concentrations are suppressed and increased energy intake is needed to stimulate equivalent PYY secretion in obese individuals in comparison to normal weight counterparts [34]. With weight loss, circulating PYY does not necessarily return to concentrations observed in normal weight counterparts. Some studies have demonstrated increases [28], [33] whereas others have observed decreases [21], [46], [55] or no change [51] in PYY in response to weight loss. The current study adds to the literature on the role of PYY in weight loss.

Ghrelin and PYY may be related to psychosocial measures of eating behaviors such as dietary restraint (tendency to consciously restrict food intake to control body weight) [50], [52], disinhibition (loss of control over eating in response to emotional or social cues) [10], [41], and tendency toward hunger [32]. For example, higher circulating ghrelin has been associated with high dietary restraint in obese individuals [52] and higher scores for hunger independent of BMI in a large population of normal weight individuals [32]. These studies have begun to relate behavioral to physiological measures; however, interactions between these factors have not been determined. It is attractive to posit that altered physiological states, such as suppressed concentrations of PYY, may be modulating behavioral changes, such as increases in dietary restraint, to offset biological abnormalities that may influence meal-related hunger and satiety.

Specifically, only one study has examined the association between dietary ED and key gut hormones involved in food intake regulation such as ghrelin and PYY [29]. As well, other studies have been designed to assess the impact of variables such as meal volume [44] and gastric distention [59] on these same gastrointestinal hormones and have thus, altered the ED of test meals; however, these studies were not designed to focus on the impact of chronic alterations in ED on hormonal outcomes and consequently, assessment of ED as a physiological variable that could impact hormonal outcomes was not quantified or analyzed to determine if ED impacted hormonal outcomes independently.

The current study is an extension of a previous year-long clinical trial in which obese women received instruction in reducing dietary ED to promote weight loss [19]. Dietary ED was a significant predictor of body weight during the weight loss phase of the trial. Blood samples collected during the trial provided an opportunity to investigate how physiological mechanisms such as changes in gut hormones in response to modifications in dietary ED may promote weight loss and weight maintenance. Additionally, we sought to determine if the impact of ED on gut hormone concentrations remains significant when accounting for changes in psychosocial variables. Thus, the purpose of this study was to determine whether low-ED diets might facilitate weight loss through actions on circulating concentrations of ghrelin and PYY, independent of the influence of psychosocial measures. We hypothesized that: (1) ghrelin would increase in accordance with weight loss, but that low-ED diets would be associated with lower circulating concentrations of ghrelin, (2) PYY would decrease in response to weight loss as a compensatory mechanism to regain weight, and (3) associations between ghrelin and ED would be independent of the influence of psychosocial variables.

Section snippets

Study protocol and participants

This study is secondary analysis of data from a randomized clinical trial that assessed the effect of reducing dietary ED as a weight loss strategy in obese women [19] (NCT ID: 00108784). Inclusion in the study was based upon the following criteria: (1) women ages 20–60 years and (2) body mass index (BMI) between 30 and 40 kg/m². Exclusion was based upon the following criteria: (1) blood pressure > 140/90 mmHg, (2) serum triacylglycerols > 400 mg/dL, (3) total cholesterol > 90th percentile for age, (4)

Participants

Participant characteristics at month 0 of the intervention are presented in Table 1. Participants were obese women ranging in age from 22 to 60 years. Seventy-one participants completed the original trial and were included in the current analysis.

Energy density and energy intake

Dietary ED decreased significantly across the intervention, as did each of its components: energy intake and food weight (Table 2). The random coefficients analysis found that ED followed a curvilinear relationship over time (ED = 1.76 − 0.15 × month + 0.01 ×

Discussion

Results of this study suggest that low-ED diets are associated with a hormonal milieu that likely facilitates long-term weight loss and weight loss maintenance. Specifically, low-ED diets were associated with lower circulating concentrations of ghrelin as well as a trend toward higher circulating concentrations of PYY. The association between ED, ghrelin, and PYY persisted when accounting for psychosocial measures of eating behavior. To our knowledge, this is the first study to examine the

Disclosure

The authors have nothing to disclose. All authors have approved the final submitted manuscript.

Acknowledgements

We thank Julie Ello-Martin, the staff in the Laboratory for the Study of Human Ingestive Behavior at The Pennsylvania State University and the participants for their contributions. Brenna R. Hill is supported by Pennsylvania State University's Intercollegiate Graduate Degree Program in Physiology. The clinical trial was funded by NIH grants R37DK039177 and M01RR10732. The current study was also supported by NIH grants M01 RR 10732 and US DoD PR054531.

References (59)

T.E. Adrian et al.
Human distribution and release of a putative new gut hormone, peptide YY
Gastroenterology
(1985)
R.L. Batterham et al.
Critical role for peptide YY in protein-mediated satiation and body-weight regulation
Cell Metab
(2006)
E.A. Bell et al.
Energy density of foods affects energy intake in normal-weight women
Am J Clin Nutr
(1998)
E.A. Bell et al.
Energy density of foods affects energy intake across multiple levels of fat content in lean and obese women
Am J Clin Nutr
(2001)
M. Bes-Rastrollo et al.
Prospective study of dietary energy density and weight gain in women
Am J Clin Nutr
(2008)
B. Caan et al.
Low energy reporting may increase in intervention participants enrolled in dietary intervention trials
J Am Diet Assoc
(2004)
D.E. Cummings
Ghrelin and the short- and long-term regulation of appetite and body weight
Physiol Behav
(2006)
J.A. Ello-Martin et al.
Dietary energy density in the treatment of obesity: a year-long trial comparing 2 weight-loss diets
Am J Clin Nutr
(2007)
J.E. Flood et al.
Soup preloads in a variety of forms reduce meal energy intake
Appetite
(2007)
A.R. Kristal et al.
Dietary assessment instruments are susceptible to intervention-associated response set bias
J Am Diet Assoc
(1998)

F. Langlois et al.

Ghrelin levels are associated with hunger as measured by the Three-Factor Eating Questionnaire in healthy young adults

Physiol Behav

(2011)

J.H. Ledikwe et al.

Dietary energy density determined by eight calculation methods in a nationally representative United States population

J Nutr

(2005)

J.H. Ledikwe et al.

Reductions in dietary energy density are associated with weight loss in overweight and obese participants in the PREMIER trial

Am J Clin Nutr

(2007)

C.G. MacIntosh et al.

Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility

Am J Clin Nutr

(1999)

C. Martins et al.

Impact of restraint and disinhibition on PYY plasma levels and subjective feelings of appetite

Appetite

(2010)

R. Perez-Escamilla et al.

Dietary energy density and body weight in adults and children: a systematic review

J Acad Nutr Diet

(2012)

B.J. Rolls

The relationship between dietary energy density and energy intake

Physiol Behav

(2009)

B.J. Rolls et al.

Volume of food consumed affects satiety in men

Am J Clin Nutr

(1998)

E.A. Schur et al.

Association of cognitive restraint with ghrelin, leptin, and insulin levels in subjects who are not weight-reduced

Physiol Behav

(2008)

A.J. Stunkard et al.

The three-factor eating questionnaire to measure dietary restraint, disinhibition and hunger

J Psychosom Res

(1985)

I.L. Taylor

Role of peptide YY in the endocrine control of digestion

J Dairy Sci

(1993)

G.H. Ballantyne

Peptide YY(1–36) and peptide YY(3–36): Part I. Distribution, release and actions

Obes Surg

(2006)

A. Bandura

Health promotion by social cognitive means

Health Educ Behav

(2004)

J.F. Bergmann et al.

Correlation between echographic gastric emptying and appetite: influence of psyllium

Gut

(1992)

H. Brown et al.

Applied mixed models in medicine

(2006)

B.M. Burton-Freeman et al.

Glycemic index, cholecystokinin, satiety and disinhibition: is there an unappreciated paradox for overweight women?

Int J Obes (Lond)

(2008)

P.K. Chelikani et al.

Comparison of the inhibitory effects of PYY(3–36) and PYY(1–36) on gastric emptying in rats

Am J Physiol Regul Integr Comp Physiol

(2004)

D.E. Cummings et al.

A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans

Diabetes

(2001)

D.E. Cummings et al.

Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery

N Engl J Med

(2002)

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Specifically, 3 studies reported that fasting total ghrelin did not differ between individuals with subclinical binge-eating (Adamo et al., 2014), BED (Monteleone et al., 2005a), or food addiction (Pedram & Sun, 2014) and unaffected controls. Next, 5 studies did not find significant cross-sectional or longitudinal associations between fasting total ghrelin and disinhibition (Aldhoon Hainerová et al., 2013; Hill, Rolls, Roe, De Souza, & Williams, 2013; Schindler et al., 2004) or uncontrolled eating (Abu Dayyeh et al., 2017; Bryant et al., 2013) among patients who sought or had undergone surgical or behavioral weight loss treatment. Finally, 1 longitudinal study (Munsch et al., 2009) assessed fasting total ghrelin and BED before and after a cognitive-behavioral therapy (CBT).
Loss of control (LOC) eating is the defining feature of binge-eating disorder, and it has particular relevance for bariatric patients. The biomarkers of LOC eating are unclear; however, gut hormones (i.e., ghrelin, cholecystokinin [CCK], peptide YY [PYY], glucagon-like peptide 1 [GLP-1], and pancreatic polypeptide [PP]), adipokines (i.e., leptin, adiponectin), and pro- and anti-inflammatory cytokines/markers (e.g., high-sensitivity C-reactive protein [hsCRP]) are candidates due to their involvement in the psychophysiological mechanisms of LOC eating. This review aimed to synthesize research that has investigated these biomarkers with LOC eating. Because LOC eating is commonly examined within the context of binge-eating disorder, is sometimes used interchangeably with subclinical binge-eating, and is the latent construct underlying disinhibition, uncontrolled eating, and food addiction, these eating behaviors were included in the search. Only studies among individuals with overweight or obesity were included. Among the identified 31 studies, 2 studies directly examined LOC eating and 4 studies were conducted among bariatric patients. Most studies were case-control in design (n = 16) and comprised female-dominant (n = 13) or female-only (n = 13) samples. Studies generally excluded fasting total ghrelin, fasting CCK, fasting PYY, and fasting PP as correlates of the examined eating behaviors. However, there was evidence that the examined eating behaviors were associated with lower levels of fasting acyl ghrelin (the active form of ghrelin) and adiponectin, higher levels of leptin and hsCRP, and altered responses of postprandial ghrelin, CCK, and PYY. The use of GLP-1 analog was able to decrease binge-eating. In conclusion, this review identified potential biomarkers of LOC eating. Future studies would benefit from a direct focus on LOC eating (especially in the bariatric population), using longitudinal designs, exploring potential mediators and moderators, and increased inclusion of the male population.
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Clearly, weight loss and maintenance for 4 weeks is a very different physiological state. However, decreased leptin levels and, in many but not all cases, increased ghrelin levels persist during weight loss maintenance in humans (Hill et al., 2013; Hinkle et al., 2013; Iepsen et al., 2016; Sumithran et al., 2011). Thus, these hormonal changes could contribute to long lasting changes in the glucose sensitivity of LH orexin-GI neurons and glutamate signaling onto VTA DA neurons which, in turn, drive intake of palatable food and promote weight regain.
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The effects of ghrelin on sleep, appetite, and memory, and its possible role in depression: A review of the literature
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A loss of weight (as the result of a diet) could be accompanied by an increase in ghrelin levels. Indeed, Hill et al. found a significant increase in ghrelin levels (P < 0.001) in 71 obese women following a 12-month diet [29]. The increase in ghrelin plasma levels leads to an increase in hunger sensations and therefore in food intake [30].
Ghrelin is an orexigenic digestive hormone that plays a role in sleep and memory. Our work aims is to synthesize the effects of ghrelin on appetite, sleep and memory, and also to evidence its role in depressive disorders.
A systematic search was carried out on PubMed with no time boundaries. The following MeSH terms were used: ghrelin AND (appetite regulation OR obesity), (sleep wake disorders OR sleep) (memory OR cognition disorders) (depression OR depressive disorder OR mood disorder).
Ghrelin triggers appetite and alters meal patterns by making them longer and richer. This can lead to pathologies, obesity and insulin-resistance. Ghrelin seems to have a favourable effect on sleep in human beings. It tends to make sleep more efficacious and better quality. Finally, it seems to have an effect on synaptic plasticity in the zones involved in memory and it has been shown to improve memory capacity in rodents. Regarding depression, the administration of ghrelin leads to an anti-depressive effect in animals and in humans. Conversely, post anti-depressant ghrelin titrations have generally shown a decrease in ghrelin levels. Resistant patients seem to retain high levels. Finally, the seriousness of depression could be related to ghrelin levels.
Ghrelin plays a probable part in depression, especially for particular endophenotypes. A better understanding of ghrelin in depression could potentially help to optimize future therapeutic treatments.
La ghréline est une hormone digestive oréxigène, possédant un rôle dans le sommeil et la mémoire. Notre travail cherche à synthétiser l’effet de la ghréline sur l’appétit, le sommeil et la mémoire mais aussi à mettre en évidence son rôle dans le trouble dépressif.
Une recherche systématique sur la base de données PubMed a été réalisée sans borne de durée. Les termes MeSH suivants ont été utilisés : ghrelin AND (appetite regulation OR obesity), (sleep wake disorders OR sleep) (memory OR cognition disorders) (depression OR depressive disorder OR mood disorder).
La ghréline initie l’appétit et modifie les repas : plus longs et plus riches, Cecipouvant s’avérer pathologiques et pourvoyeurs d’obésité et d’insulino-résistance. La ghréline semble avoir un effet promoteur du sommeil chez l’homme. Elle tend à rendre le sommeil plus efficace et de meilleure qualité. Enfin, elle paraît agir sur la plasticité synaptique dans les zones impliquées dans la mémoire et améliore les capacités mnésiques des rongeurs. Sur la dépression, l’administration de ghréline entraîne un effet antidépresseur chez l’animal ou chez l’homme. De manière opposée, les dosages de ghréline après traitement antidépresseur ont globalement montré une diminution des taux. Les patients résistants garderaient des taux élevés. Enfin, la gravité pourrait être positivement corrélée aux taux de ghréline.
La ghréline a un rôle probable dans la dépression, notamment en fonction d’endophénotypes particuliers. Une meilleure compréhension de la ghréline dans la dépression pourrait potentiellement permettre d’optimiser nos prises en charge thérapeutiques futures.
A low energy-dense diet in the context of a weight-management program affects appetite control in overweight and obese women
2018, Journal of Nutrition
Low energy–dense (LED) foods reduce energy intake (EI); whether this effect is sustained over time and during weight loss is unknown.
This trial examined the effects of LED compared with high energy–dense (HED) meals on appetite, EI, and control over eating in the laboratory and during a weight-management program that encourages unrestricted intake of LED foods [Slimming World, UK (SW)] compared with a self-led Standard Care program [NHS weight-loss plan (SC)].
Overweight and obese women [n = 96; mean ± SD age: 41.03 ± 12.61 y; mean ± SD body mass index (in kg/m²): 34.00 ± 3.61] were recruited from the SW or SC programs. Primary outcomes included appetite, food preferences (liking and wanting for LED and HED foods), cravings, and evening meal EI (LED, HED) in response to calorie-matched LED (≤0.8 kcal/g) and HED (≥2.5 kcal/g) breakfast and lunch meals. Probe-day tests were conducted at weeks 3 and 4 and repeated at weeks 12 and 13 in a within-day crossover design. Secondary outcomes, including body weight and program experience, were measured from weeks 1 to 14 in a parallel-group design. Dietary compliance was monitored with the use of weighed food diaries at weeks 3 and 12.
Intention-to-treat (ITT) and completers analyses showed that the SW group lost more weight than the SC group [ITT: −5.9% (95% CI: −4.7%, –7.2%) compared with −3.5% (−2.3%, −4.8%), P < 0.05; completers: −6.2% (−4.8%, −7.6%) compared with 3.9% (−2.5%, −5.2%), P < 0.05]. The SW group reported greater control over eating and more motivation to continue the program compared with the SC group. LED meals increased sensations of fullness and reduced hunger on probe days (P < 0.001). Total-day EI was 1057 ± 73 kcal less (95% CI: 912, 1203 kcal; 36%) under LED compared with HED conditions (P < .001). Liking for LED and HED foods and wanting for HED foods were lower before lunch under LED compared with HED conditions, and liking decreased to a greater extent after the LED lunch. The SW group reported fewer cravings under LED compared with HED conditions (P < 0.05). On probe days, appetite and EI outcomes did not differ between weeks 3 and 12 or between the SW and SC groups.
LED meals improve appetite control in women attempting weight loss and the effect is sustainable. Consumption of LED meals likely contributed to weight loss in the SW program. This study was registered at clinicaltrials.gov as NCT02012426.
Weight regaining: From statistics and behaviors to physiology and metabolism
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Citation Excerpt :
A dietary manipulation that could be used to facilitate weight loss maintenance is lowering energy density of the diet [22]. Part of the effectiveness of this technique could be attributed to its hormonal effects: Lower energy density during a weight loss dietary intervention was associated with amelioration in the ghrelin increase and PYY decrease occurring during weight loss, leading to a more satiating hormonal profile [109]. Meal timing could be another factor influencing weight loss and maintenance.
Achieving maintenance of weight loss is crucial to combat obesity. However, most individuals tend to regain weight. Data from successful maintainers show that they remain vigilant and constantly apply techniques to oppose the course of regaining. On the other hand, current advances in obesity research show that the reduced obese state is a state of altered physiology in terms of energy balance. This review describes the physiological adaptations occurring after weight loss that predispose to regaining. Specifically, changes regarding body composition, hormonal background, energy expenditure and control of food intake are discussed. Moreover, metabolites that can act as regain predictors and dietary techniques to oppose regaining are presented.
The Impact of Eating Frequency and Time of Intake on Nutrient Quality and Body Mass Index: The INTERMAP Study, a Population-Based Study
2015, Journal of the Academy of Nutrition and Dietetics
Citation Excerpt :
Having fewer meals per 24 hours with large amounts of energy-dense food consumed at each meal has been shown to promote overeating and is associated with high total energy intake, especially in overweight individuals.40 Although the mechanism behind this relationship is not clear, a recent randomized clinical trial suggests that lower dietary energy density is related to a decrease in the hunger-stimulating hormone ghrelin, and an increase in peptide YY, a satiety hormone.14 The observed positive association between evening intake and BMI may be linked to a possible decline in insulin sensitivity during the evening, caused by elevation in nonessential fatty acids.41
Epidemiologic evidence is sparse on the effect of dietary behaviors and diet quality on body mass index (BMI; calculated as kg/m²), which can be important drivers of the obesity epidemic.
This study investigated the relationships of frequency of eating and time of intake to energy density, nutrient quality, and BMI using data from the International Study on Macro/Micronutrients and Blood Pressure including 2,696 men and women aged 40 to 59 years from the United States and the United Kingdom.
The International Study on Macro/Micronutrients and Blood Pressure is a cross-sectional investigation with four 24-hour dietary recalls and BMI measurements conducted between 1996 and 1999. Consumption of solid foods was aggregated into eating occasion. Nutrient density is expressed using the Nutrient Rich Food Index 9.3. The ratio of evening/morning energy intake was calculated; mean values of four visits were used.
Characteristics across eating occasion categories are presented as adjusted mean with corresponding 95% CI. Multiple linear regression models were used to examine associations of eating occasions, ratio of evening/morning energy intake, dietary energy density, and Nutrient Rich Food Index 9.3 with BMI.
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Ghrelin and peptide YY increase with weight loss during a 12-month intervention to reduce dietary energy density in obese women

Highlights

Abstract

Introduction

Section snippets

Study protocol and participants

Participants

Energy density and energy intake

Discussion

Disclosure

Acknowledgements

Gastroenterology

Cell Metab

Am J Clin Nutr

Am J Clin Nutr

Am J Clin Nutr

J Am Diet Assoc

Physiol Behav

Am J Clin Nutr

Appetite

J Am Diet Assoc

Physiol Behav

J Nutr

Am J Clin Nutr

Am J Clin Nutr

Appetite

J Acad Nutr Diet

Physiol Behav

Am J Clin Nutr

Physiol Behav

J Psychosom Res

J Dairy Sci

Peptide YY(1–36) and peptide YY(3–36): Part I. Distribution, release and actions

Obes Surg

Health promotion by social cognitive means

Health Educ Behav

Correlation between echographic gastric emptying and appetite: influence of psyllium

Gut

Applied mixed models in medicine

Glycemic index, cholecystokinin, satiety and disinhibition: is there an unappreciated paradox for overweight women?

Int J Obes (Lond)

Comparison of the inhibitory effects of PYY(3–36) and PYY(1–36) on gastric emptying in rats

Am J Physiol Regul Integr Comp Physiol

A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans

Diabetes

Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery

N Engl J Med