scholarly journals Oral preload of calcium reduces food intake via enhanced PYY secretion in rats

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Tohru Hira ◽  
Shono Ogasawara ◽  
Hiroshi Hara
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Taste Aversion ◽  
Calcium Chloride ◽  
Lithium Chloride ◽  
Hormone Secretion ◽  
Gut Hormones ◽  
Standard Diet ◽  
Saccharin Preference ◽  
Gut Hormone

AbstractIntroductionDietary calcium has been proposed to reduce appetite (or to enhance satiety) in human studies. However, underlying mechanisms are still unclear. In animal and cell studies, it has been demonstrated that activation of the calcium-sensing receptor induced secretion of anorexic gut hormones such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) from enteroendocrine cells. In the present study, we tested the hypothesis that calcium suppresses appetite thorough enhanced gut hormone secretion, by using rats.Materials and MethodsMale Sprague Dawley rats were maintained by feeding a standard diet (AIN-93G, n = 6–8 per group). As calcium sources, calcium chloride, calcium carbonate, and calcium lactate were tested. These calcium salts were orally preloaded in fasted rats by using a feeding tube, and subsequent food intake was monitored until 24 hours. To assess conditioned taste aversion, saccharin preference test was conducted after conditioning with calcium or lithium chloride. To investigate involvements of gut hormones such as CCK, GLP-1, and peptide-YY (PYY), specific receptor antagonists for respective gut hormones were intraperitoneally injected just after oral preload of calcium, and then food intake was monitored. Portal blood samples were collected 15 or 30 min after oral preload of calcium for measurement of gut hormones by ELISA.Results and discussionAt the same dose of calcium (150 mg/kg), preload of calcium chloride reduced food intake for 4 hours compared to preload of the control solution (P < 0.05), while other compounds had minor effects on food intake. Saccharin preference ratio was only reduced by conditioning with lithium chloride (P < 0.01), but not by that with calcium compounds, indicating no conditional taste aversion was occurred by calcium. Suppressive effect of calcium chloride on food intake was partially reversed by pretreatment with a PYY receptor antagonist (BIIE0246) but not by that with a CCK- or a GLP-1 receptor antagonist. Portal PYY concentrations were higher in calcium chloride-treated rats than in the control rats (P < 0.05), 15 min after the preload and re-feeding. Changes in serum calcium concentrations were not observed by preload of calcium.These results suggest that oral preload of calcium chloride reduces subsequent food intake via enhanced PYY secretion in rats.

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 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.

scholarly journals Peripheral Pathways in the Food-Intake Control towards the Adipose-Intestinal Missing Link

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Hugo Mendieta Zerón ◽  
Ma. Victoria Domínguez García ◽  
María del Socorro Camarillo Romero ◽  
Miriam V. Flores-Merino
Keyword(s):  
Diabetes Mellitus ◽  
Genetic Basis ◽  
Physiological State ◽  
Hormone Secretion ◽  
Gut Hormones ◽  
Diabetic Patients ◽  
Early Presentation ◽  
Gut Hormone ◽  
Unknown Factor

In the physiological state a multitude of gut hormones are released into the circulation at the same time depending on the quality and quantity of the diet. These hormones interact with receptors at various points in the “gut-brain axis” to affect short-term and intermediate-term feelings of hunger and satiety. The combined effects of macronutrients on the predominant gut hormone secretion are still poorly understood. Besides, adipokines form an important part of an “adipoinsular axis” dysregulation which may contribute toβ-cell failure and hence to type 2 diabetes mellitus (T2DM). Even more, gestational diabetes mellitus (GDM) and T2DM seem to share a genetic basis. In susceptible individuals, chronic exaggerated stimulation of the proximal gut with fat and carbohydrates may induce overproduction of an unknown factor that causes impairment of incretin production and/or action, leading to insufficient or untimely production of insulin, so that glucose intolerance develops. The bypass of the duodenum and jejunum might avoid a putative hormone overproduction in the proximal foregut in diabetic patients that might counteract the action of insulin, while the early presentation of undigested or incompletely digested food to the ileum may anticipate the production of hormones such as GLP1, further improving insulin action.

scholarly journals The gut hormone Allatostatin C regulates food intake and metabolic homeostasis under nutrient stress

2020 ◽  
Author(s):  
Olga Kubrak ◽  
Line Jensen ◽  
Nadja Ahrentløv ◽  
Takashi Koyama ◽  
Alina Malita ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Somatostatin Receptors ◽  
Gut Hormones ◽  
Peptide Hormone ◽  
Nutrient Stress ◽  
Metabolic Homeostasis ◽  
Adipokinetic Hormone ◽  
Energy Mobilization ◽  
Gut Hormone

AbstractThe intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the specific gut hormones that communicate energy availability to target organs to induce appropriate metabolic and behavioral responses are poorly defined. Here we show that the enteroendocrine cells (EECs) of the Drosophila gut sense nutrient stress via the intracellular TOR pathway, and in response secrete the peptide hormone allatostatin C (AstC). Gut-derived AstC induces secretion of glucagon-like adipokinetic hormone (AKH) via its receptor AstC-R2, a homolog of mammalian somatostatin receptors, to coordinate food intake and energy mobilization. Loss of gut AstC or its receptor in the AKH-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders.

scholarly journals Short-term treatment with olanzapine does not modulate gut hormone secretion: olanzapine disintegrating versus standard tablets

2010 ◽  
Vol 162 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Solrun Vidarsdottir ◽  
Ferdinand Roelfsema ◽  
Trea Streefland ◽  
Jens J Holst ◽  
Jens F Rehfeld ◽  
...  
Keyword(s):  
Weight Gain ◽  
Peptide Yy ◽  
Hormone Secretion ◽  
Gut Hormones ◽  
Term Treatment ◽  
Short Term ◽  
Short Term Treatment ◽  
Healthy Men ◽  
Gut Hormone ◽  
Glucagon Like Peptide 1

BackgroundTreatment with olanzapine (atypical antipsychotic drug) is frequently associated with various metabolic anomalies, including obesity, dyslipidemia, and diabetes mellitus. Recent data suggest that olanzapine orally disintegrating tablets (ODT), which dissolve instantaneously in the mouth, might cause less weight gain than olanzapine standard oral tablets (OST).Design and methodsTen healthy men received olanzapine ODT (10 mg o.d., 8 days), olanzapine OST (10 mg o.d., 8 days), or no intervention in a randomized crossover design. At breakfast and dinner, blood samples were taken for measurement of pancreatic polypeptide, peptide YY, glucagon-like peptide-1, total glucagon, total ghrelin, and cholecystokinin (CCK) concentrations.ResultsWith the exception of pre- and postprandial concentration of ghrelin at dinner and preprandial CCK concentrations at breakfast, which were all slightly increased (respectivelyP=0.048,P=0.034 andP=0.042), olanzapine did not affect gut hormone concentrations. Thus, olanzapine ODT and OST had similar effects on gut hormone secretion.ConclusionShort-term treatment with olanzapine does not have major impact on the plasma concentration of gut hormones we measured in healthy men. Moreover, despite pharmacological difference, gut hormone concentrations are similar during treatment with olanzapine ODT and OST. The capacity of olanzapine to induce weight gain and diabetes is unlikely to be caused by modulation of the secretion of gut hormones measured here. We cannot exclude the possibility that olanzapine's impact on other gut hormones, to impair insulin sensitivity and stimulate weight gain, exists.

scholarly journals Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans

2014 ◽  
Vol 306 (7) ◽  
pp. G622-G630 ◽  
Author(s):  
Rune E. Kuhre ◽  
Fiona M. Gribble ◽  
Bolette Hartmann ◽  
Frank Reimann ◽  
Johanne A. Windeløv ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Hormone Secretion ◽  
Gut Hormones ◽  
Glucagon Secretion ◽  
Healthy Humans ◽  
Murine Cell Line ◽  
Gut Hormone ◽  
Glucagon Like Peptide 1 ◽  
Cell Depolarization ◽  
Gip Release

Nutrients often stimulate gut hormone secretion, but the effects of fructose are incompletely understood. We studied the effects of fructose on a number of gut hormones with particular focus on glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). In healthy humans, fructose intake caused a rise in blood glucose and plasma insulin and GLP-1, albeit to a lower degree than isocaloric glucose. Cholecystokinin secretion was stimulated similarly by both carbohydrates, but neither peptide YY3–36nor glucagon secretion was affected by either treatment. Remarkably, while glucose potently stimulated GIP release, fructose was without effect. Similar patterns were found in the mouse and rat, with both fructose and glucose stimulating GLP-1 secretion, whereas only glucose caused GIP secretion. In GLUTag cells, a murine cell line used as model for L cells, fructose was metabolized and stimulated GLP-1 secretion dose-dependently (EC50= 0.155 mM) by ATP-sensitive potassium channel closure and cell depolarization. Because fructose elicits GLP-1 secretion without simultaneous release of glucagonotropic GIP, the pathways underlying fructose-stimulated GLP-1 release might be useful targets for type 2 diabetes mellitus and obesity drug development.

Feeding motivation of sows fed a sugarbeet pulp diet

1992 ◽  
Vol 1992 ◽  
pp. 146-146
Author(s):  
F Brouns ◽  
S A Edwards ◽  
P R English
Keyword(s):  
Food Intake ◽  
Taste Aversion ◽  
Metabolic Effects ◽  
Standard Diet ◽  
Measured Rate ◽  
Feeding Motivation ◽  
High Fibre ◽  
Ad Libitum ◽  
Voluntary Food Intake

Voluntary food intake of dry sows fed ad libitum diets containing high levels of unmolassed sugarbeet pulp (SBP) was low in comparison to those fed other high fibre diets (Brouns et al., 1991). It is not known whether this is caused by a taste aversion, or whether physical/metabolic effects during digestion restrict intake. In this experiment the feeding motivation of sows fed SBP diets was determined by measuring their rate of feeding.Twelve multiparous pregnant sows housed in straw bedded pens, but individually fed in feeding stalls, were used for this experiment. The sows were allocated between two treatments according to their measured rate of eating when given a standard diet on 2 pretrial days. Treatments were 2.3 kg of a diet containing 500g/kg SBP or 2.0 kg of a barley-based diet (C) (Table 1) providing the same total DE. Both diets were fed once a day in pelleted form. Any refusals were recorded to calculate intake.

scholarly journals Translating biased signaling in the ghrelin receptor system into differential in vivo functions

2018 ◽  
Vol 115 (43) ◽  
pp. E10255-E10264 ◽  
Author(s):  
Franziska Mende ◽  
Cecilie Hundahl ◽  
Bianca Plouffe ◽  
Louise Julie Skov ◽  
Bjørn Sivertsen ◽  
...  
Keyword(s):  
Food Intake ◽  
G Protein ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Receptor System ◽  
Physiological Functions ◽  
Ghrelin Receptor ◽  
Gut Hormone ◽  
Biased Signaling

Biased signaling has been suggested as a means of selectively modulating a limited fraction of the signaling pathways for G-protein–coupled receptor family members. Hence, biased ligands may allow modulation of only the desired physiological functions and not elicit undesired effects associated with pharmacological treatments. The ghrelin receptor is a highly sought antiobesity target, since the gut hormone ghrelin in humans has been shown to increase both food intake and fat accumulation. However, it also modulates mood, behavior, growth hormone secretion, and gastric motility. Thus, blocking all pathways of this receptor may give rise to potential side effects. In the present study, we describe a highly promiscuous signaling capacity for the ghrelin receptor. We tested selected ligands for their ability to regulate the various pathways engaged by the receptor. Among those, a biased ligand, YIL781, was found to activate the Gαq/11 and Gα12 pathways selectively without affecting the engagement of β-arrestin or other G proteins. YIL781 was further characterized for its in vivo physiological functions. In combination with the use of mice in which Gαq/11 was selectively deleted in the appetite-regulating AgRP neurons, this biased ligand allowed us to demonstrate that selective blockade of Gαq/11, without antagonism at β-arrestin or other G-protein coupling is sufficient to decrease food intake.

A functional role for central glucagon-like peptide-1 receptors in lithium chloride-induced anorexia

1999 ◽  
Vol 277 (5) ◽  
pp. R1537-R1540 ◽  
Author(s):  
Linda Rinaman
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Lithium Chloride ◽  
Neural Pathways ◽  
Sprague Dawley ◽  
Receptor Signalling ◽  
Sprague Dawley Rats ◽  
Licl Treatment ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The present study sought to determine whether central glucagon-like peptide-1 (GLP-1)-receptor signalling contributes to the anorexigenic effects of systemically administered lithium chloride (LiCl). Male Sprague-Dawley rats with chronic intracerebroventricular (ICV) cannulas were acclimated to a feeding schedule that included daily 30-min access to palatable mash. In the first experiment, ICV infusion of a GLP-1-receptor antagonist [exendin-4-(3—39)] significantly attenuated (10 μg dose) or completely blocked (20 μg dose) the inhibition of food intake produced by subsequent ICV infusion of GLP-1-(7—36) amide (5 μg). In the second experiment, rats were infused with 0, 10, or 20 μg of the GLP-1-receptor antagonist ICV, followed by injection of 0.15 M LiCl (50 mg/kg ip) or the same volume of 0.15 M NaCl. The ability of LiCl treatment to suppress food intake was significantly attenuated in rats that were pretreated with the GLP-1-receptor antagonist. These results support the view that central mechanisms underlying LiCl-induced anorexia include a prominent role for endogenous GLP-1 neural pathways.

scholarly journals The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress

2021 ◽  
Author(s):  
Olga Kubrak ◽  
Line Jensen ◽  
Nadja Ahrentloev ◽  
Takashi Koyama ◽  
Alina Malita ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Somatostatin Receptors ◽  
Gut Hormones ◽  
Peptide Hormone ◽  
Nutrient Stress ◽  
Metabolic Homeostasis ◽  
Adipokinetic Hormone ◽  
Energy Mobilization ◽  
Gut Hormone

Abstract The intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the specific gut hormones that communicate energy availability to target organs to induce appropriate metabolic and behavioral responses are poorly defined. Here we show that the enteroendocrine cells (EECs) of the Drosophila gut sense nutrient stress via the intracellular TOR pathway, and in response secrete the peptide hormone allatostatin C (AstC), a Drosophila Somatostatin homolog. Gut-derived AstC induces secretion of glucagon-like adipokinetic hormone (AKH) via its receptor AstC-R2, a homolog of mammalian somatostatin receptors, to coordinate food intake and energy mobilization. Loss of gut AstC or its receptor in the AKH-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders.

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