Dissociable hormonal responses to symptoms and stress in anorexia and bulimia nervosa

2019 ◽  
Author(s):  
Margaret L Westwater ◽  
Flavia Mancini ◽  
Jane Shapleske ◽  
Jaco Serfontein ◽  
Monique Ernst ◽  
...  
Keyword(s):  
Bulimia Nervosa ◽  
Acute Stress ◽  
Gut Hormones ◽  
Metabolic Dysfunction ◽  
Cortisol Reactivity ◽  
Psychological States ◽  
Study Session ◽  
Gut Hormone ◽  
Ad Libitum ◽  
Acyl Ghrelin

Background: Anorexia nervosa (AN) and bulimia nervosa (BN) are complex psychiatric conditions, in which both psychological and metabolic factors have been implicated. Critically, the experience of stress can precipitate loss-of-control eating in both conditions, suggesting an interplay between mental state and metabolic signaling. However, associations between psychological states, symptoms and metabolic processes in AN and BN have not been examined. Methods: Eighty-five women (n=22 AN binge/purge subtype, n=33 BN, n=30 controls) underwent remote salivary cortisol sampling and a two-day, inpatient study session to examine the effect of stress on cortisol, gut hormones (acyl-ghrelin, PYY, GLP-1) and food consumption. Participants were randomized to either an acute stress induction or control task on each day, and plasma hormones were serially measured before a naturalistic, ad libitum meal.Results: Cortisol awakening response (CAR) was augmented in AN but not BN relative to controls, with body mass index explaining the most variance in CAR (36%). Acute stress increased acyl-ghrelin and PYY in AN compared to controls; however, stress did not alter gut hormone profiles in BN. Instead, a group-by-stress interaction showed nominally reduced cortisol reactivity in BN, but not AN, compared to controls. Ad libitum consumption was lower in both patient groups and unaffected by stress.Conclusions: Findings extend previous reports of metabolic dysfunction in binge-eating disorders, identifying unique associations across disorders and under stress. Moreover, we observed disrupted homeostatic signaling in AN following psychological stress, which may explain, in part, the maintenance of dysregulated eating in this serious illness.

scholarly journals Dissociable hormonal profiles for psychopathology and stress in anorexia and bulimia nervosa

2020 ◽  
pp. 1-11 ◽  
Author(s):  
Margaret L. Westwater ◽  
Flavia Mancini ◽  
Jane Shapleske ◽  
Jaco Serfontein ◽  
Monique Ernst ◽  
...  
Keyword(s):  
Bulimia Nervosa ◽  
Acute Stress ◽  
Gut Hormones ◽  
Metabolic Dysfunction ◽  
Cortisol Reactivity ◽  
Psychological States ◽  
Gut Hormone ◽  
Ad Libitum ◽  
Glucagon Like Peptide 1 ◽  
Acyl Ghrelin

Abstract Background Anorexia nervosa (AN) and bulimia nervosa (BN) are complex psychiatric conditions, in which both psychological and metabolic factors have been implicated. Critically, the experience of stress can precipitate loss-of-control eating in both conditions, suggesting an interplay between mental state and metabolic signaling. However, associations between psychological states, symptoms and metabolic processes in AN and BN have not been examined. Methods Eighty-five women (n = 22 AN binge/purge subtype, n = 33 BN, n = 30 controls) underwent remote salivary cortisol sampling and a 2-day, inpatient study session to examine the effect of stress on cortisol, gut hormones [acyl-ghrelin, peptide tyrosine tyrosine (PYY) and glucagon-like peptide-1] and food consumption. Participants were randomized to either an acute stress induction or control task on each day, and plasma hormones were serially measured before a naturalistic, ad libitum meal. Results Cortisol-awakening response was augmented in AN but not in BN relative to controls, with body mass index explaining the most variance in post-awakening cortisol (36%). Acute stress increased acyl-ghrelin and PYY in AN compared to controls; however, stress did not alter gut hormone profiles in BN. Instead, a group-by-stress interaction showed nominally reduced cortisol reactivity in BN, but not in AN, compared to controls. Ad libitum consumption was lower in both patient groups and unaffected by stress. Conclusions Findings extend previous reports of metabolic dysfunction in binge-eating disorders, identifying unique associations across disorders and under stress. Moreover, we observed disrupted homeostatic signaling in AN following psychological stress, which may explain, in part, the maintenance of dysregulated eating in this serious illness.

scholarly journals Caloric Restriction Prevents Metabolic Dysfunction and the Changes in Hypothalamic Neuropeptides Associated with Obesity Independently of Dietary Fat Content in Rats

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2128
Author(s):  
Marina Martín ◽  
Amaia Rodríguez ◽  
Javier Gómez-Ambrosi ◽  
Beatriz Ramírez ◽  
Sara Becerril ◽  
...  
Keyword(s):  
Weight Loss ◽  
Caloric Restriction ◽  
Normal Diet ◽  
Energy Restriction ◽  
Metabolic Dysfunction ◽  
Gut Hormone ◽  
Male Wistar Rats ◽  
Food Efficiency Ratio ◽  
Hypothalamic Neuropeptides ◽  
Ad Libitum

Energy restriction is a first therapy in the treatment of obesity, but the underlying biological mechanisms have not been completely clarified. We analyzed the effects of restriction of high-fat diet (HFD) on weight loss, circulating gut hormone levels and expression of hypothalamic neuropeptides. Ten-week-old male Wistar rats (n = 40) were randomly distributed into four groups: two fed ad libitum a normal diet (ND) (N group) or a HFD (H group) and two subjected to a 25% caloric restriction of ND (NR group) or HFD (HR group) for 9 weeks. A 25% restriction of HFD over 9 weeks leads to a 36% weight loss with regard to the group fed HFD ad libitum accompanied by normal values in adiposity index and food efficiency ratio (FER). This restriction also carried the normalization of NPY, AgRP and POMC hypothalamic mRNA expression, without changes in CART. Caloric restriction did not succeed in improving glucose homeostasis but reduced HFD-induced hyperinsulinemia. In conclusion, 25% restriction of HFD reduced adiposity and improved metabolism in experimental obesity, without changes in glycemia. Restriction of the HFD triggered the normalization of hypothalamic NPY, AgRP and POMC expression, as well as ghrelin and leptin levels.

scholarly journals Acute exposure to a hot ambient temperature reduces energy intake but does not affect gut hormones in men during rest

2020 ◽  
pp. 1-9
Author(s):  
Julia K. Zakrzewski-Fruer ◽  
Rachel N. Horsfall ◽  
Diane Cottrill ◽  
John Hough
Keyword(s):  
Ambient Temperature ◽  
Energy Intake ◽  
Gut Hormones ◽  
Sensitivity Analyses ◽  
Acylated Ghrelin ◽  
Ambient Temperatures ◽  
Gut Hormone ◽  
Hormone Responses ◽  
Ad Libitum ◽  
Glucagon Like Peptide 1

Abstract This study examined the effect of ambient temperature on energy intake, perceived appetite and gut hormone responses during rest in men. Thirteen men (age 21·5 (sd 1·4) years; BMI 24·7 (sd 2·2) kg/m2) completed three, 5·5 h conditions in different ambient temperatures: (i) cold (10°C), (ii) thermoneutral (20°C) and (iii) hot (30°C). A standardised breakfast was consumed after fasting measures, and an ad libitum lunch provided at 4–4·5 h. Blood samples (analysed for plasma acylated ghrelin, total peptide tyrosine-tyrosine (PYY) and total glucagon-like peptide 1 (GLP-1) concentrations), perceived appetite and thermoregulatory responses were collected throughout. Linear mixed models were used for statistical analyses. Ad libitum energy intake was 1243 (sd 1342) kJ higher in 10°C and 1189 (sd 1219) kJ higher in 20 v. 30°C (P = 0·002). Plasma acylated ghrelin, total PYY and GLP-1 concentrations did not differ significantly between the conditions (P ≥ 0·303). Sensitivity analyses for the 4 h pre-lunch period showed that perceived overall appetite was lower in both 30 and 10°C when compared with 20°C (P ≤ 0·019). In conclusion, acutely resting in a hot compared with a thermoneutral and cold ambient temperature reduced lunchtime ad libitum energy intake in healthy men. Suppressed perceived appetite may have contributed to the reduced energy intake in the hot compared with thermoneutral ambient temperature, whereas gut hormones did not appear to play an important role.

The impact of acute stress on the neural processing of food cues in bulimia nervosa: Replication in two samples.

2017 ◽  
Vol 126 (5) ◽  
pp. 540-551 ◽  
Author(s):  
Brittany Collins ◽  
Lauren Breithaupt ◽  
Jennifer E. McDowell ◽  
L. Stephen Miller ◽  
James Thompson ◽  
...  
Keyword(s):  
Bulimia Nervosa ◽  
Acute Stress ◽  
Neural Processing ◽  
Food Cues ◽  
Two Samples ◽  
The Impact

scholarly journals Effect of the Natural Sweetener Xylitol on Gut Hormone Secretion and Gastric Emptying in Humans: A Pilot Dose-Ranging Study

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 174
Author(s):  
Anne Christin Meyer-Gerspach ◽  
Jürgen Drewe ◽  
Wout Verbeure ◽  
Carel W. le Roux ◽  
Ludmilla Dellatorre-Teixeira ◽  
...  
Keyword(s):  
Uric Acid ◽  
Gastric Emptying ◽  
Blood Lipids ◽  
Tap Water ◽  
Hormone Secretion ◽  
Gastrointestinal Symptoms ◽  
Gut Hormones ◽  
Double Blind ◽  
Gut Hormone ◽  
Dose Dependent

Sugar consumption is associated with a whole range of negative health effects and should be reduced and the natural sweetener xylitol might be helpful in achieving this goal. The present study was conducted as a randomized, placebo-controlled, double-blind, cross-over trial. Twelve healthy, lean volunteers received intragastric solutions with 7, 17 or 35 g xylitol or tap water on four separate days. We examined effects on: gut hormones, glucose, insulin, glucagon, uric acid, lipid profile, as well as gastric emptying rates, appetite-related sensations and gastrointestinal symptoms. We found: (i) a dose-dependent stimulation of cholecystokinin (CCK), active glucagon-like peptide-1 (aGLP-1), peptide tyrosine tyrosine (PYY)-release, and decelerated gastric emptying rates, (ii) a dose-dependent increase in blood glucose and insulin, (iii) no effect on motilin, glucagon, or glucose-dependent insulinotropic peptide (GIP)-release, (iv) no effect on blood lipids, but a rise in uric acid, and (v) increased bowel sounds as only side effects. In conclusion, low doses of xylitol stimulate the secretion of gut hormones and induce a deceleration in gastric emptying rates. There is no effect on blood lipids and only little effect on plasma glucose and insulin. This combination of properties (low-glycemic sweetener which stimulates satiation hormone release) makes xylitol an attractive candidate for sugar replacement.

scholarly journals Energy intake, gastrointestinal transit, and gut hormone release in response to oral triglycerides and fatty acids in men with and without severe obesity

2019 ◽  
Vol 316 (3) ◽  
pp. G332-G337 ◽  
Author(s):  
Carsten Dirksen ◽  
Jesper Graff ◽  
Stefan Fuglsang ◽  
Jens F. Rehfeld ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Olive Oil ◽  
Energy Intake ◽  
Severe Obesity ◽  
Gastrointestinal Transit ◽  
Calorie Intake ◽  
Double Blind ◽  
Gut Hormone ◽  
Ad Libitum

Dietary fat, and particularly fatty acids (FAs) from hydrolyzed triglycerides (TGs), reduces appetite, whereas paradoxically, a high-fat diet leads to excess calorie intake. We therefore hypothesized that the appetite-regulating effects of FAs are perturbed in obesity. Ten men with severe obesity [median body mass index (BMI) of 51.0 kg/m2(range of 47.9–69.0)] and 10 men without obesity [BMI of 24.6 kg/m2(range of 21.7–26.8)] were recruited for a double-blind randomized crossover study. On two occasions, participants were given isocaloric (2,660 kJ) and isovolemic (80 ml) loads of either oleic acid (long-chain FA) or olive oil (TG) containing radiolabeled lipid and water markers. Postload scintigraphy, blood sampling, and assessment of appetite were performed for 10 h, after which an ad libitum meal was served. Compared with olive oil, oleic acid slowed gastric mean emptying time (GMET) for lipids ( P < 0.001), accelerated orocoecal transit time (OCTT; P = 0.005), increased postload cholecystokinin section ( P < 0.001), and suppressed ad libitum energy intake ( P = 0.028) in men with severe obesity, and similar effects were seen in the nonobese group (no group × lipid interactions). However, independent of lipid loads, GMET and OCTT were slower (GMETlipidP = 0.046; GMETwaterP = 0.003; OCTT P = 0.001), and basal and postload secretion of glucagon-like peptide-1 (GLP-1) was attenuated ( P = 0.045 and P = 0.048, respectively) in men with severe obesity compared with men without obesity. We conclude that the more potent appetite-regulating effects of oleic acid versus olive oil are unimpaired in men with severe obesity. However, regardless of lipid formulations, severe obesity is associated with slowed gastrointestinal transit and attenuated GLP-1 secretion.NEW & NOTEWORTHY Orally ingested fatty acids more efficiently reduce appetite and energy intake than triglycerides also in men with severe obesity. Men with severe obesity have delayed gastrointestinal transit and attenuated early gut hormone responses after an oral lipid load compared with men without obesity.

scholarly journals Neurotensin Is Coexpressed, Coreleased, and Acts Together With GLP-1 and PYY in Enteroendocrine Control of Metabolism

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 176-194 ◽  
Author(s):  
Kaare V. Grunddal ◽  
Cecilia F. Ratner ◽  
Berit Svendsen ◽  
Felix Sommer ◽  
Maja S. Engelstoft ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Secretory Granules ◽  
Gut Hormones ◽  
Distal Small Intestine ◽  
Cell Ablation ◽  
Target Organs ◽  
Gut Hormone ◽  
Toxin Receptor ◽  
Functional Consequences ◽  
Glucagon Like Peptide 1

Abstract The 2 gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are well known to be coexpressed, costored, and released together to coact in the control of key metabolic target organs. However, recently, it became clear that several other gut hormones can be coexpressed in the intestinal-specific lineage of enteroendocrine cells. Here, we focus on the anatomical and functional consequences of the coexpression of neurotensin with GLP-1 and PYY in the distal small intestine. Fluorescence-activated cell sorting analysis, laser capture, and triple staining demonstrated that GLP-1 cells in the crypts become increasingly multihormonal, ie, coexpressing PYY and neurotensin as they move up the villus. Proglucagon promoter and pertussis toxin receptor-driven cell ablation and reappearance studies indicated that although all the cells die, the GLP-1 cells reappear more quickly than PYY- and neurotensin-positive cells. High-resolution confocal fluorescence microscopy demonstrated that neurotensin is stored in secretory granules distinct from GLP-1 and PYY storing granules. Nevertheless, the 3 peptides were cosecreted from both perfused small intestines and colonic crypt cultures in response to a series of metabolite, neuropeptide, and hormonal stimuli. Importantly, neurotensin acts synergistically, ie, more than additively together with GLP-1 and PYY to decrease palatable food intake and inhibit gastric emptying, but affects glucose homeostasis in a more complex manner. Thus, neurotensin is a major gut hormone deeply integrated with GLP-1 and PYY, which should be taken into account when exploiting the enteroendocrine regulation of metabolism pharmacologically.

Hyperglycemia abolishes meal-induced satiety by a dysregulation of ghrelin and peptide YY3–36 in healthy overweight/obese humans

2014 ◽  
Vol 306 (2) ◽  
pp. E225-E231 ◽  
Author(s):  
Sine H. Knudsen ◽  
Kristian Karstoft ◽  
Thomas P. J. Solomon
Keyword(s):  
Visual Analog Scale ◽  
Plasma Glucose ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Polynomial Functions ◽  
Analog Scale ◽  
Healthy Humans ◽  
Gut Hormone ◽  
Obese Subjects ◽  
Circulating Levels

Satiety and satiety-regulating gut hormone levels are abnormal in hyperglycemic individuals. We aimed to determine whether these abnormalities are secondary to hyperglycemia. Ten healthy overweight/obese subjects (age: 56 ± 3 yr; BMI: 30.3 ± 1.2 kg/m2) received three equicaloric meals at t = 0, 4, and 8 h in the absence (control trial) and presence of experimental hyperglycemia (hyperglycemia trial; 5.4 mM above basal). Circulating levels of glucose, insulin, ghrelin, and peptide YY (PYY)3–36 and visual analog scale ratings of satiety were measured throughout each trial. In the control trial, glucose, insulin, PYY3–36, and the feeling of fullness were increased in the postprandial periods, whereas ghrelin was decreased. In the hyperglycemia trial, in which plasma glucose was increased to 11.2 ± 0.1 mmol/l, postprandial meal responses (AUC: 0–2, 4–6, and 8–10 h) of PYY3–36 were lower ( meal 1, P < 0.0001; meal 2, P < 0.001; meal 3, P < 0.05), whereas insulin ( meal 1, P < 0.01; meal 2, P < 0.001; meal 3, P < 0.05) and ghrelin ( meal 1, P < 0.05; meal 2, P > 0.05; meal 3, P > 0.05) were higher compared with the control trial. Furthermore, the incremental (Δ0–0.5, 4–4.5, and 8–8.5 h) ghrelin response to the first and third meals was higher in the hyperglycemia trial in contrast to control (Δ: 2.3 ± 8.0, P = 0.05; Δ: 14.4 ± 2.5, P < 0.05). Also, meal-induced fullness was prevented ( meal 1, P = 0.06; meal 2, P = 0.01; meal 3, P = 0.08) by experimental hyperglycemia. Furthermore, trends in ghrelin, PYY3–36, and fullness were described by different polynomial functions between the trials. In conclusion, hyperglycemia abolishes meal-induced satiety and dysregulates postprandial responses of the gut hormones PYY3–36 and ghrelin in overweight/obese healthy humans.

DIFFERENTIAL EFFECTS OF BILE ACIDS ON THE POST-PRANDIAL SECRETION OF GUT HORMONES: a randomised crossover study

2021 ◽  
Author(s):  
Emma Rose McGlone ◽  
Khalefah Malallah ◽  
Joyceline Cuenco ◽  
Nicolai J. Wewer Albrechtsen ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Bile Acids ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Mixed Meal ◽  
Gut Hormone ◽  
Mixed Meal Test ◽  
Hormone Responses ◽  
Glucagon Like Peptide 1 ◽  
Fibroblast Growth Factor 19 ◽  
Insulinotropic Peptide

AIMS Bile acids (BA) regulate post-prandial metabolism directly and indirectly by affecting the secretion of gut hormones like glucagon-like peptide-1 (GLP-1). The post-prandial effects of BA on the secretion of other metabolically active hormones are not well understood. The objective of this study was to investigate the effect of oral ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) on post-prandial secretion of GLP-1, oxyntomodulin (OXM), peptide YY (PYY), glucose-dependent insulinotropic peptide (GIP), glucagon and ghrelin. METHODS Twelve healthy volunteers underwent a mixed meal test 60 minutes after ingestion of UDCA (12-16 mg/kg), CDCA (13-16 mg/kg) or no BA in a randomised cross-over study. Glucose, insulin, GLP-1, OXM, PYY, GIP, glucagon, ghrelin and fibroblast growth factor 19 were measured prior to BA administration at -60, 0 (just prior to mixed meal) and 15, 30, 60, 120, 180 and 240 minutes after the meal. RESULTS UDCA and CDCA provoked differential gut hormone responses: UDCA did not have any significant effects, but CDCA provoked significant increases in GLP-1 and OXM and a profound reduction in GIP. CDCA increased fasting GLP-1 and OXM secretion in parallel with an increase in insulin. On the other hand, CDCA reduced post-prandial secretion of GIP, with an associated reduction in post-prandial insulin secretion. CONCLUSIONS Exogenous CDCA can exert multiple salutary effects on the secretion of gut hormones; if these effects are confirmedin obesity and type 2 diabetes, CDCA may be a potential therapy for these conditions.

scholarly journals A Pilot Study of Gut-Brain Signaling After Octreotide Therapy for Unintentional Weight Loss After Esophagectomy

2020 ◽  
Vol 106 (1) ◽  
pp. e204-e216
Author(s):  
Conor F Murphy ◽  
Nicholas Stratford ◽  
Neil G Docherty ◽  
Brendan Moran ◽  
Jessie A Elliott ◽  
...  
Keyword(s):  
Weight Loss ◽  
Pilot Study ◽  
Food Intake ◽  
Eating Behavior ◽  
Hormone Secretion ◽  
Symptom Burden ◽  
Octreotide Lar ◽  
Gut Hormone ◽  
Ad Libitum ◽  
Brain Reward

Abstract Background Recurrence-free patients after esophageal cancer surgery face long-term nutritional consequences, occurring in the context of an exaggerated postprandial gut hormone response. Acute gut hormone suppression influences brain reward signaling and eating behavior. This study aimed to suppress gut hormone secretion and characterize reward responses and eating behavior among postesophagectomy patients with unintentional weight loss. Methods This pilot study prospectively studied postoperative patients with 10% or greater body weight loss (BWL) beyond 1 year who were candidates for clinical treatment with long-acting octreotide (LAR). Before and after 4 weeks of treatment, gut hormone secretion, food cue reactivity (functional magnetic resonance imaging), eating motivation (progressive ratio task), ad libitum food intake, body composition, and symptom burden were assessed. Results Eight patients (7 male, age: mean ± SD 62.8 ± 9.4 years, postoperative BWL: 15.5 ± 5.8%) participated. Octreotide LAR did not significantly suppress total postprandial plasma glucagon-like peptide-1 response at 4 weeks (P = .08). Postprandial symptom burden improved after treatment (Sigstad score median [range]: 12 [2-28] vs 8 [3-18], P = .04) but weight remained stable (pre: 68.6 ± 12.8 kg vs post: 69.2 ± 13.4 kg, P = .13). There was no significant change in brain reward system responses, during evaluation of high-energy or low-energy food pictures, nor their appeal rating. Moreover, treatment did not alter motivation to eat (P = .41) nor ad libitum food intake(P = .46). Conclusion The protocol used made it feasible to characterize the gut-brain axis and eating behavior in this cohort. Inadequate suppression of gut hormone responses 4 weeks after octreotide LAR administration may explain the lack of gut-brain pathway alterations. A higher dose or shorter interdose interval may be required to optimize the intervention.

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