Ghrelin Responses Research Articles

Gastric Emptying Impacts the Timing of Meal Glucose Peak in Subjects With Uncomplicated Type 1 Diabetes.

Diabetes mellitus is associated with gastrointestinal (GI) motility dysfunction, ranging from delayed to accelerated gastric emptying (GE). To evaluate GE in patients with type 1 diabetes mellitus (T1DM) without chronic complications and to investigate its relation with postprandial glucose and GI hormone responses. Cross-sectional study. Forty-two patients with T1DM free of chronic complications referred to Federico II University and 31 healthy controls similar for age, sex, and body mass index. GE was assessed by using the 13C-octanoate breath test with a standardized solid meal. During the meal, plasma glucose, ghrelin, and glucagon-like peptide 1 (GLP-1) responses were assessed, and GI symptoms were evaluated by a specific questionnaire. Patients with T1DM showed a significantly slower GE half-emptying time (GE t1/2) (113 ± 34 minutes) than did controls (89 ± 17 minutes; P < 0.001). Thirty-six percent of T1DM showed a delayed GE (t1/2 > 120 minutes), whereas all controls showed a normal GE. When patients with T1DM were stratified according to GE t1/2, postmeal glucose response was significantly different between those with delayed and those with normal GE (P = 0.013). In particular, patients with T1DM and delayed GE showed a significantly longer mean time to peak glucose than did patients with normal GE (P = 0.004). In addition, GE t1/2 was an independent predictor of the time to peak glucose (β = 0.329; P = 0.025). GLP-1 and ghrelin responses to the test meal, as well as the prevalence of GI symptoms, were similar between patients with T1DM and controls and between patients with T1DM with normal GE and those with delayed GE. Delayed GE time is associated with a longer time to peak glucose. GE evaluation could be useful for individualizing the timing of preprandial insulin bolus in patients with T1DM.

Effects of Two Doses of Curry Prepared with Mixed Spices on Postprandial Ghrelin and Subjective Appetite Responses-A Randomized Controlled Crossover Trial.

Spices are known to provide orosensory stimulation that can potentially influence palatability, appetite, and energy balance. Previous studies with individual spices have shown divergent effects on appetite and energy intake measures. In a real-life context, however, several spices are consumed in combinations, as in various forms of curries. Therefore, we investigated changes in postprandial appetite and plasma ghrelin in response to the intake of two doses of curry prepared with mixed spices. The study was undertaken in healthy Chinese men, between 21 and 40 years of age and body mass index ≤27.5 kg/m2. Appetite was measured using visual analogue scales (VAS) and plasma ghrelin was measured using multiplex assay. Compared with the control meal (Dose 0 Control (D0C), 0 g mixed spices), we found significantly greater suppression in ‘hunger’ (both p < 0.05, after Bonferroni adjustments) as well in ‘desire to eat’ (both p < 0.01) during the Dose 1 Curry (D1C, 6 g mixed spices) and Dose 2 Curry (D2C, 12 g mixed spices) intake. There were no differences, however, in plasma ghrelin or in other appetite measures such as in ‘fullness’ or in ‘prospective eating’ scores. Overall, the results of our study indicate greater inter-meal satiety due to mixed spices consumption, independent of any changes in plasma ghrelin response.

A high carbohydrate, but not fat or protein meal attenuates postprandial ghrelin, PYY and GLP-1 responses in Chinese men.

It is known that the macronutrient content of a meal has different impacts on the postprandial satiety and appetite hormonal responses. Whether obesity interacts with such nutrient-dependent responses is not well characterized. We examined the postprandial appetite and satiety hormonal responses after a high-protein (HP), high-carbohydrate (HC), or high-fat (HF) mixed meal. This was a randomized cross-over study of 9 lean insulin-sensitive (mean±SEM HOMA-IR 0.83±0.10) and 9 obese insulin-resistant (HOMA-IR 4.34±0.41) young (age 21–40 years), normoglycaemic Chinese men. We measured fasting and postprandial plasma concentration of glucose, insulin, active glucagon-like peptide-1 (GLP-1), total peptide-YY (PYY), and acyl-ghrelin in response to HP, HF, or HC meals. Overall postprandial plasma insulin response was more robust in the lean compared to obese subjects. The postprandial GLP-1 response after HF or HP meal was higher than HC meal in both lean and obese subjects. In obese subjects, HF meal induced higher response in postprandial PYY compared to HC meal. HP and HF meals also suppressed ghrelin greater compared to HC meal in the obese than lean subjects. In conclusion, a high-protein or high-fat meal induces a more favorable postprandial satiety and appetite hormonal response than a high-carbohydrate meal in obese insulin-resistant subjects.

Ozone modifies the metabolic and endocrine response to glucose: Reproduction of effects with the stress hormone corticosterone

Air pollution is associated with increased incidence of metabolic disease (e.g. metabolic syndrome, obesity, diabetes); however, underlying mechanisms are poorly understood. Air pollutants increase the release of stress hormones (human cortisol, rodent corticosterone), which could contribute to metabolic dysregulation. We assessed acute effects of ozone, and stress axis involvement, on glucose tolerance and on the metabolic (triglyceride), endocrine/energy regulation (insulin, glucagon, GLP-1, leptin, ghrelin, corticosterone), and inflammatory/endothelial (TNF, IL-6, VEGF, PAI-1) response to exogenous glucose. Male Fischer-344 rats were exposed to clean air or 0.8 ppm ozone for 4 h in whole body chambers. Hypothalamic-pituitary-adrenal (HPA) axis involvement in ozone effects was tested through subcutaneous administration of the glucocorticoid synthesis inhibitor metyrapone (50 mg/kg body weight), corticosterone (10 mg/kg body weight), or vehicle (40% propylene glycol) prior to exposure. A glucose tolerance test (2 g/kg body weight glucose) was conducted immediately after exposure, with blood samples collected at 0, 30, 60, 90, and 120 min. Ozone exposure impaired glucose tolerance, an effect accompanied by increased plasma triglycerides but no impairment of insulin release. Ozone diminished glucagon, GLP-1, and ghrelin responses to glucose, but did not significantly impact inflammatory/endothelial analytes. Metyrapone reduced corticosterone but increased glucose and triglycerides, complicating evaluation of the impact of glucocorticoid inhibition. However, administration of corticosterone reproduced the profile of ozone effects, supporting a role for the HPA axis. The results show that ozone-dependent changes in glucose tolerance are accompanied by altered metabolic and endocrine responses to glucose challenge that are reproduced by exogenous stress hormone.

Dose-Dependent Effects of Randomized Intraduodenal Whey-Protein Loads on Glucose, Gut Hormone, and Amino Acid Concentrations in Healthy Older and Younger Men.

Protein-rich supplements are used widely for the prevention and management of malnutrition in older people. We have reported that healthy older, compared to younger, adults have less suppression of energy intake by whey-protein—effects on appetite-related hormones are unknown. The objective was to determine the effects of intraduodenally administered whey-protein on glucose, gut hormone, and amino acid concentrations, and their relation to subsequent ad libitum energy intake at a buffet meal, in healthy older and younger men. Hydrolyzed whey-protein (30 kcal, 90 kcal, and 180 kcal) and a saline control (~0 kcal) were infused intraduodenally for 60 min in 10 younger (19–29 years, 73 ± 2 kg, 22 ± 1 kg/m2) and 10 older (68–81 years, 79 ± 2 kg, 26 ± 1 kg/m2) healthy men in a randomized, double-blind fashion. Plasma insulin, glucagon, gastric inhibitory peptide (GIP), glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY), and amino acid concentrations, but not blood glucose, increased, while ghrelin decreased during the whey-protein infusions. Plasma GIP concentrations were greater in older than younger men. Energy intake correlated positively with plasma ghrelin and negatively with insulin, glucagon, GIP, GLP-1, PYY, and amino acids concentrations (p < 0.05). In conclusion, intraduodenal whey-protein infusions resulted in increased GIP and comparable ghrelin, insulin, glucagon, GIP, GLP-1, PYY, and amino acid responses in healthy older and younger men, which correlated to subsequent energy intake.

Restoration of metabolic inflammation-related ghrelin resistance by weight loss.

High-fat diet (HFD)-induced metabolic inflammation in the central and peripheral organs contributes to the pathogenesis of obesity. Long-term HFD blunts signaling by ghrelin, a gastric-derived orexigenic peptide, in the vagal afferent nerve via a mechanism involving in situ activation of inflammation. This study was undertaken to investigate whether ghrelin resistance is associated with progressive development of metabolic inflammation. In mice, ghrelin’s orexigenic activity was abolished 2–4 weeks after the commencement of HFD (60% of energy from fat), consistent with the timing of accumulation and activation of macrophages and microglia in the nodose ganglion and hypothalamus. Calorie-restricted weight loss after 12-week HFD feeding restored ghrelin responsiveness and alleviated the upregulation of macrophage/microglia activation markers and inflammatory cytokines. HSP72, a chaperone protein, was upregulated in the hypothalamus of HFD-fed mice, potentially contributing to prevention of irreversible neuron damage. These results demonstrate that ghrelin resistance is reversible following reversal of the HFD-induced inflammation and obesity phenotypes.

Inhibition of hormonal and behavioral effects of stress by tryptophan in rats

Objectives: Stress in known to alter hormonal systems. Pharmacological doses of tryptophan, the essential amino acid precursor of serotonin, increase circulating leptin and decrease ghrelin in normal healthy adults. Because systemically injected leptin inhibits stress-induced behavioral deficits and systemically injected serotonin modulates leptin release from the adipocytes, we used tryptophan as a pharmacological tool to modulate hormonal and behavioral responses in unstressed and stressed rats.Methods: Leptin, ghrelin, serotonin, tryptophan, and behavior were studied in unstressed and stressed rats following oral administration of 0, 100, 200, and 300 mg/kg of tryptophan.Results: Following oral administration of tryptophan at a dose of 300 mg/kg, circulating levels of serotonin and leptin increased and those of ghrelin decreased in unstressed animals. No effect occurred on 24-hours cumulative food intake and elevated plus maze performance. Exposure to 2 hours immobilization stress decreased 24 hours cumulative food intake and impaired performance in elevated plus maze monitored next day. Serum serotonin decreased, leptin increased, and no effect occurred on ghrelin. Stress effects on serotonin, leptin, food intake, and elevated plus maze performance did not occur in tryptophan-pretreated animals. Tryptophan-induced decreases of ghrelin also did not occur in stressed animals.Conclusion: The findings show an important role of serum serotonin, leptin, and ghrelin in responses to stress and suggest that the essential amino acid tryptophan can improve therapeutics in stress-induced hormonal and behavioral disorders.

Ghrelin stimulation by hypothalamic-pituitary-adrenal axis activation depends on increasing cortisol levels.

Ghrelin plasma concentration increases in parallel to cortisol after a standardized psychological stress in humans, but the physiological basis of this interaction is unknown. We aimed to elucidate this question by studying the ghrelin response to pharmacological manipulation of the hypothalamic–pituitary–adrenal (HPA) axis. Six lean, healthy male volunteers were examined under four experimental conditions. Blood samples were collected every 30 min for two sequential periods of two hours. Initially, a baseline period was followed by intravenous injection of a synthetic analog of ACTH (250 μg). Subsequently, a single dose of metyrapone was administered at midnight and in the following morning, blood samples were collected for 2 h, followed by an intravenous injection of hydrocortisone (100 mg) with continued sampling. We show that increased cortisol serum levels secondary to ACTH stimulation or hydrocortisone administration are positively associated with plasma ghrelin levels, whereas central stimulation of the HPA axis by blocking cortisol synthesis with metyrapone is associated with decreased plasma ghrelin levels. Collectively, this suggests that HPA-axis-mediated elevations in ghrelin plasma concentration require increased peripheral cortisol levels, independent of central elevation of ACTH and possibly CRH levels.

Study of termination of postprandial gastric contractions in humans, dogs and Suncus murinus: role of motilin- and ghrelin-induced strong contraction.

Stomach contractions show two types of specific patterns in many species, that is migrating motor contraction (MMC) and postprandial contractions (PPCs), in the fasting and fed states respectively. We found gastric PPCs terminated with migrating strong contractions in humans, dogs and suncus. In this study, we reveal the detailed characteristics and physiological implications of these strong contractions of PPC. Human, suncus and canine gastric contractions were recorded with a motility-monitoring ingestible capsule and a strain-gauge force transducer. The response of motilin and ghrelin and its receptor antagonist on the contractions were studied by using free-moving suncus. Strong gastric contractions were observed at the end of a PPC in human, dog and suncus models, and we tentatively designated this contraction to be a postprandial giant contraction (PPGC). In the suncus, the PPGC showed the same property as those of a phase III contraction of MMC (PIII-MMC) in the duration, motility index and response to motilin or ghrelin antagonist administration. Ghrelin antagonist administration in the latter half of the PPC (LH-PPC) attenuated gastric contraction prolonged the duration of occurrence of PPGC, as found in PII-MMC. It is thought that the first half of the PPC changed to PII-MMC and then terminated with PIII-MMC, suggesting that PPC consists of a digestive phase (the first half of the PPC) and a discharge phase (LH-PPC) and that LH-PPC is coincident with MMC. In this study, we propose a new approach for the understanding of postprandial contractions.

Assessments of plasma ghrelin levels in the early stages of parkinson's disease.

Gastrointestinal symptoms are early events in Parkinson's disease (PD). The gastrointestinal hormone ghrelin was neuroprotective in the nigrostriatal dopamine system. The objective of this study was to assess ghrelin levels in the early stages of PD. Plasma was collected in the fasting state in 291 PD patients in stages 1-3 and 303 age- and sex-matched healthy controls. Additional samples were taken in the glucose response test to assess nutrition-related ghrelin levels in 20 PD patients and 20 healthy controls. The enzyme-linked immunosorbent assay was used to measure total and active plasma ghrelin levels. We reported that total and active plasma ghrelin levels were decreased in PD, although there was no difference across progressive PD stages. Postprandial ghrelin suppression and preprandial peak responses were both attenuated in PD. Plasma ghrelin levels were decreased in PD; however, this event might be irrelevant to PD progression. Ghrelin responses to meals were also impaired in PD. © 2017 International Parkinson and Movement Disorder Society.

Individual Variation in Hunger, Energy Intake, and Ghrelin Responses to Acute Exercise.

This study aimed to characterize the immediate and extended effect of acute exercise on hunger, energy intake, and circulating acylated ghrelin concentrations using a large data set of homogenous experimental trials and to describe the variation in responses between individuals. Data from 17 of our group's experimental crossover trials were aggregated yielding a total sample of 192 young, healthy males. In these studies, single bouts of moderate to high-intensity aerobic exercise (69% ± 5% V˙O2 peak; mean ± SD) were completed with detailed participant assessments occurring during and for several hours postexercise. Mean hunger ratings were determined during (n = 178) and after (n = 118) exercise from visual analog scales completed at 30-min intervals, whereas ad libitum energy intake was measured within the first hour after exercise (n = 60) and at multiple meals (n = 128) during the remainder of trials. Venous concentrations of acylated ghrelin were determined at strategic time points during (n = 118) and after (n = 89) exercise. At group level, exercise transiently suppressed hunger (P < 0.010, Cohen's d = 0.77) but did not affect energy intake. Acylated ghrelin was suppressed during exercise (P < 0.001, Cohen's d = 0.10) and remained significantly lower than control (no exercise) afterward (P < 0.024, Cohen's d = 0.61). Between participants, there were notable differences in responses; however, a large proportion of this spread lay within the boundaries of normal variation associated with biological and technical assessment error. In young men, acute exercise suppresses hunger and circulating acylated ghrelin concentrations with notable diversity between individuals. Care must be taken to distinguish true interindividual variation from random differences within normal limits.

Leptin, Adiponectin, And Ghrelin Responses To Different Temperature Conditions With Endurance Exercise

Obesity can result from a lack of energy expenditure or excessive energy intake. The appetite-regulating hormones leptin, adiponectin, and ghrelin may help decrease energy intake by affecting appetite. Exercise and exposure to extreme temperatures can independently affect these hormones. However, less is known on how exercise and temperature interact to affect appetite. PURPOSE: To determine the effect of exercise in different temperatures on the circulating concentrations of leptin, adiponectin, ghrelin, and acylated ghrelin. METHODS: Eleven recreationally-trained male participants completed three separate 1 h cycling bouts at 60% Wmax in different environmental temperatures (Hot 33 °C, Cold 7 °C, Room Temperature 20 °C), followed by 3 h recovery at room temperature. Blood was drawn pre-exercise, post-exercise, and 3 h post-exercise from the antecubital vein. Hematocrit and hemoglobin were measured to account for changes in plasma volume. RESULTS: Leptin concentrations were lower at post and 3 h post-exercise compared to pre-exercise, with and without correcting for plasma volume shifts, regardless of temperature (p < 0.05). Adiponectin was higher post-exercise than pre-exercise (p = 0.021) and then returned to pre-exercise levels by 3 h post-exercise (p = 0.084) without correction for plasma volume shifts. However, adiponectin concentrations were not different at any time point when plasma volume shifts were accounted for (p > 0.05). Ghrelin and acylated ghrelin concentrations were not affected at post and 3 h post-exercise compared to pre-exercise, with and without correcting for plasma volume shifts, regardless of temperature (p > 0.05). No differences in leptin, adiponectin, ghrelin or acylated ghrelin were found between trials (p > 0.05). CONCLUSION: Temperature does not effect the circulating concentrations of leptin, adiponectin, or ghrelin during an acute bout of endurance exercise. Supported by the University of Nebraska-Omaha University Committee on Research and Creative Activity and the National Institute for General Medical Science (5P20GM103427).

Ghrelin response to hedonic eating in underweight and short-term weight restored patients with anorexia nervosa

IntroductionRecently, anorexia nervosa (AN) has been conceptualized as a reward-related disorder, and brain imaging studies have shown functional and structural abnormalities in areas of the brain involved in reward processes in both acute and recovered AN patients. However, the role of endogenous biochemical mediators, such as Ghrelin, in the modulation of reward processes has been poorly investigated in this eating disorder.ObjectivesHedonic eating, that is the consumption of food exclusively for pleasure and not to maintain energy homeostasis, is a useful paradigm to investigate the physiology of food-related reward.AimsWe assessed the Ghrelin response to food-related reward in symptomatic AN women in order to further explore the modulation of reward processes in this severe and debilitating disorder.MethodsPlasma levels of Ghrelin were measured in 7 underweight and 7 recently weight-restored satiated AN patients before and after the ingestion of a favorite (hedonic eating) and non-favorite (non-hedonic eating) food. Ghrelin responses were compared it that of previously studied healthy controls.ResultsWe found that in satiated underweight patients with AN plasma Ghrelin levels progressively decreased after the exposure and the consumption of both the favorite and non-favorite food whereas in satiated weight-restored AN patients and satiated healthy controls plasma Ghrelin concentrations significantly increased after the exposure to the favorite food and after eating it, but decreased after the non-favorite food.ConclusionsThese results suggest a derangement in the Ghrelin modulation of food-related pleasurable and rewarding feelings, which might sustain the reduced motivation toward food intake of acute AN patients.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Short-term, high-fat overfeeding impairs glycaemic control but does not alter gut hormone responses to a mixed meal tolerance test in healthy, normal-weight individuals - ERRATUM.

Obesity is undoubtedly caused by a chronic positive energy balance. However, the early metabolic and hormonal responses to overeating are poorly described. This study determined glycaemic control and selected gut hormone responses to nutrient intake before and after 7 d of high-fat overfeeding. Nine healthy individuals (five males, four females) performed a mixed meal tolerance test (MTT) before and after consuming a high-fat (65 %), high-energy (+50 %) diet for 7 d. Measurements of plasma glucose, NEFA, acylated ghrelin, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and serum insulin were taken before (fasting) and at 30-min intervals throughout the 180-min MTT (postprandial). Body mass increased by 0·79 (sem 0·14) kg after high-fat overfeeding (P<0·0001), and BMI increased by 0·27 (sem 0·05) kg/m2 (P=0·002). High-fat overfeeding also resulted in an 11·6 % increase in postprandial glucose AUC (P=0·007) and a 25·9 % increase in postprandial insulin AUC (P=0·005). Acylated ghrelin, GLP-1 and GIP responses to the MTT were all unaffected by the high-fat, high-energy diet. These findings demonstrate that even brief periods of overeating are sufficient to disrupt glycaemic control. However, as the postprandial orexigenic (ghrelin) and anorexigenic/insulintropic (GLP-1 and GIP) hormone responses were unaffected by the diet intervention, it appears that these hormones are resistant to short-term changes in energy balance, and that they do not play a role in the rapid reduction in glycaemic control.

Leptin, adiponectin, and ghrelin responses to endurance exercise in different ambient conditions

ABSTRACTExcessive positive energy balance is a major factor leading to obesity. The ability to alter the appetite-regulating hormones leptin, adiponectin, and ghrelin may help decrease excessive energy intake. Exercise and exposure to extreme temperatures can independently affect these appetite-regulating hormones. PURPOSE: To determine the effect of exercising in different environmental conditions on the circulating concentrations of leptin, adiponectin, and ghrelin. METHODS: Eleven recreationally-trained male participants completed 3 separate 1 h cycling bouts at 60% Wmax in hot, cold, and room temperature conditions (33°C, 7°C, 20°C), followed by a 3 h recovery at room temperature. Blood was drawn pre-exercise, post-exercise, and 3 h post-exercise. Hematocrit and hemoglobin were measured to account for change in plasma volume. RESULTS: Leptin concentrations were lower at post and 3 h post-exercise compared with pre-exercise, with and without correction for plasma volume shifts, regardless of temperature (p < 0.05). Adiponectin was higher post-exercise compared with pre-exercise (p = 0.021) but not 3 h post-exercise (p = 0.084) without correction for plasma volume shifts. However, adiponectin concentrations were not different at any time point when plasma volume shifts were accounted for (p > 0.05). Total ghrelin and acylated ghrelin concentrations were not affected at post and 3 h post-exercise compared with pre-exercise, with and without correcting for plasma volume shifts, regardless of ambient temperature (p > 0.05). No differences in leptin, adiponectin, or ghrelin were found between trials (p > 0.05). CONCLUSION: Temperature does not affect the circulating concentrations of appetite-regulating hormones during an acute bout of endurance exercise.

Short-term, high-fat overfeeding impairs glycaemic control but does not alter gut hormone responses to a mixed meal tolerance test in healthy, normal-weight individuals.

Obesity is undoubtedly caused by a chronic positive energy balance. However, the early metabolic and hormonal responses to overeating are poorly described. This study determined glycaemic control and selected gut hormone responses to nutrient intake before and after 7 d of high-fat overfeeding. Nine healthy individuals (five males, four females) performed a mixed meal tolerance test (MTT) before and after consuming a high-fat (65 %), high-energy (+50 %) diet for 7 d. Measurements of plasma glucose, NEFA, acylated ghrelin, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and serum insulin were taken before (fasting) and at 30-min intervals throughout the 180-min MTT (postprandial). Body mass increased by 0·79 (sem 0·14) kg after high-fat overfeeding (P<0·0001), and BMI increased by 0·27 (sem 0·05) kg/m2 (P=0·002). High-fat overfeeding also resulted in an 11·6 % increase in postprandial glucose AUC (P=0·007) and a 25·9 % increase in postprandial insulin AUC (P=0·005). Acylated ghrelin, GLP-1 and GIP responses to the MTT were all unaffected by the high-fat, high-energy diet. These findings demonstrate that even brief periods of overeating are sufficient to disrupt glycaemic control. However, as the postprandial orexigenic (ghrelin) and anorexigenic/insulintropic (GLP-1 and GIP) hormone responses were unaffected by the diet intervention, it appears that these hormones are resistant to short-term changes in energy balance, and that they do not play a role in the rapid reduction in glycaemic control.

Acute effect of exercise intensity and duration on acylated ghrelin and hunger in men.

Acute exercise transiently suppresses the orexigenic gut hormone acylated ghrelin, but the extent to which exercise intensity and duration determine this response is not fully understood. The effects of manipulating exercise intensity and duration on acylated ghrelin concentrations and hunger were examined in two experiments. In experiment one, nine healthy males completed three, 4-h conditions (control, moderate-intensity running (MOD) and vigorous-intensity running (VIG)), with an energy expenditure of ~2.5 MJ induced in both MOD (55-min running at 52% peak oxygen uptake (V.O2peak)) and VIG (36-min running at 75% V.O2peak). In experiment two, nine healthy males completed three, 9-h conditions (control, 45-min running (EX45) and 90-min running (EX90)). Exercise was performed at 70% V.O2peak In both experiments, participants consumed standardised meals, and acylated ghrelin concentrations and hunger were quantified at predetermined intervals. In experiment one, delta acylated ghrelin concentrations were lower than control in MOD (ES = 0.44, P = 0.01) and VIG (ES = 0.98, P < 0.001); VIG was lower than MOD (ES = 0.54, P = 0.003). Hunger ratings were similar across the conditions (P = 0.35). In experiment two, delta acylated ghrelin concentrations were lower than control in EX45 (ES = 0.77, P < 0.001) and EX90 (ES = 0.68, P < 0.001); EX45 and EX90 were similar (ES = 0.09, P = 0.55). Hunger ratings were lower than control in EX45 (ES = 0.20, P = 0.01) and EX90 (ES = 0.27, P = 0.001); EX45 and EX90 were similar (ES = 0.07, P = 0.34). Hunger and delta acylated ghrelin concentrations remained suppressed at 1.5 h in EX90 but not EX45. In conclusion, exercise intensity, and to a lesser extent duration, are determinants of the acylated ghrelin response to acute exercise.

The Effect of a 20 km Run on Appetite Regulation in Long Distance Runners.

The purpose of the present study was to investigate appetite-related hormonal responses and energy intake after a 20 km run in trained long distance runners. Twenty-three male long-distance runners completed two trials: either an exercise trial consisting of a 20 km outdoor run (EX) or a control trial with an identical period of rest (CON). Blood samples were collected to determine plasma acylated ghrelin, peptide YY3-36 (PYY3-36) and other hormonal and metabolite concentrations. Energy intake during a buffet test meal was also measured 30 min after the exercise or rest periods. Although plasma acylated ghrelin concentrations were significantly decreased after the 20 km run (p < 0.05), plasma PYY3-36 did not change significantly following exercise. Absolute energy intake during the buffet test meal in EX (1325 ± 55 kcal) was significantly lower than that in CON (1529 ± 55 kcal), and there was a relatively large degree of individual variability for exercise-induced changes in energy intake (−40.2% to 12.8%). However, exercise-induced changes in energy intake were not associated with plasma acylated ghrelin or PYY3-36 responses. The results demonstrated that a 20 km run significantly decreased plasma acylated ghrelin concentrations and absolute energy intake among well-trained long distance runners.

Green tea extract and catechol-O-methyltransferase genotype modify the post-prandial serum insulin response in a randomised trial of overweight and obese post-menopausal women.

Green tea extract (GTE) may be involved in a favourable post-prandial response to high-carbohydrate meals. The catechol-O-methyltransferase (COMT) genotype may modify these effects. We examined the acute effects of GTE supplementation on the post-prandial response to a high-carbohydrate meal by assessing appetite-associated hormones and glucose homeostasis marker concentrations in women who consumed 843mg of (-)-epigallocatechin-3-gallate (EGCG) or placebo capsules for 11-12months. Sixty Caucasian post-menopausal women (body mass index≥25.0kgm-2 ) were included in a randomised, double-blind feeding study. GTE was consumed with a breakfast meal [2784.0kJ (665.4kcal); 67.2% carbohydrate]. Blood samples were drawn pre-meal, post-meal, and every 30min for 4h. Participants completed six satiety questionnaires. Plasma leptin, ghrelin and adiponectin did not differ between GTE and placebo at any time point; COMT genotype did not modify these results. Participants randomised to GTE with the high-activity form of COMT (GTE-high COMT) had higher insulin concentrations at time 0, 0.5 and 1.0h post-meal compared to all COMT groups randomised to placebo. Insulin remained higher in the GTE-high COMT group at 1.5, 2.0 and 2.5h compared to Placebo-low COMT (P<0.02). GTE-high COMT had higher insulin concentrations at times 0, 0.5, 1.0, 1.5 and 2.0h compared to the GTE-low COMT (P≤0.04). Area under the curve measurements of satiety did not differ between GTE and placebo. GTE supplementation and COMT genotype did not alter acute post-prandial responses of leptin, ghrelin, adiponectin or satiety, although it may be involved in post-meal insulinaemic response of overweight and obese post-menopausal women.

Different systemic and peripheral ghrelin responses in metabolic disorders

Different systemic and peripheral ghrelin responses in metabolic disorders