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Background: Colonic fermentation of dietary fibre to short-chain fatty acids (SCFA) influences appetite hormone secretion in animals, but SCFA production is excessive in obese animals. This suggests there may be resistance to the effect of SCFA on appetite hormones in obesity. Objectives: To determine the effects of inulin (IN) and resistant starch (RS) on postprandial SCFA, and gut hormone (glucagon-like peptide (GLP-1), peptide–tyrosine–tyrosine (PYY) and ghrelin) responses in healthy overweight/obese (OWO) vs lean (LN) humans. Subjects/Methods: Overnight-fasted participants (13 OWO and 12 LN) consumed 300 ml water containing 75 g glucose (GLU) as control or 75 g GLU plus 24 g IN, or 28.2 g RS using a randomised, single-blind, cross-over design. Blood for appetite hormones and SCFA was collected at intervals over 6 h. A standard lunch was served 4 h after the test drink. Results: Relative to GLU, IN, but not RS, significantly increased SCFA areas under the curve (AUC) from 4–6 h (AUC 4–6 ). Neither IN nor RS affected GLP-1 or PYY-AUC 4–6 . Although neither IN nor RS reduced ghrelin-AUC 4–6 compared with GLU, ghrelin at 6 h after IN was significantly lower than that after GLU ( P <0.05). After IN, relative to GLU, the changes in SCFA-AUC 4–6 were negatively related to the changes in ghrelin-AUC 4–6 ( P =0.017). SCFA and hormone responses did not differ significantly between LN and OWO. Conclusions: Acute increases in colonic SCFA do not affect GLP-1 or PYY responses in LN or OWO subjects, but may reduce ghrelin. The results do not support the hypothesis that SCFA acutely stimulate PYY and GLP-1 secretion; however, a longer adaptation to increased colonic fermentation or a larger sample size may yield different results.

Background The mechanisms of amelioration of glycemic control early after laparoscopic Roux-en-Y gastric bypass (LRYGB) or laparoscopic sleeve gastrectomy (LSG) are not fully understood. Methods In this prospective, randomized 1-year trial, outcomes of LRYGB and LSG patients were compared, focusing on possibly responsible mechanisms. Twelve patients were randomized to LRYGB and 11 to LSG. These non-diabetic patients were investigated before and 1 week, 3 months, and 12 months after surgery. A standard test meal was given after an overnight fast, and blood samples were collected before, during, and after food intake for hormone profiles (cholecystokinin (CCK), ghrelin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY)). Results In both groups, body weight and BMI decreased markedly and comparably leading to an identical improvement of abnormal glycemic control (HOMA index). Post-surgery, patients had markedly increased postprandial plasma GLP-1 and PYY levels ( p  < 0.05) with ensuing improvement in glucose homeostasis. At 12 months, LRYGB ghrelin levels approached preoperative values. The postprandial, physiologic fluctuation returned, however, while LSG ghrelin levels were still markedly attenuated. One year postoperatively, CCK concentrations after test meals increased less in the LRYGB group than they did in the LSG group, with the latter showing significantly higher maximal CCK concentrations ( p  < 0.012 vs. LRYGB). Conclusions Bypassing the foregut is not the only mechanism responsible for improved glucose homeostasis. The balance between foregut (ghrelin, CCK) and hindgut (GLP-1, PYY) hormones is a key to understanding the underlying mechanisms.

OBJECTIVES: A difference in cortical treatment of taste information could alter food intake promoting the development of obesity. The main purpose was to compare, in subjects living with obesity (OB) and normal-weight subjects (NW), the characteristics of gustatory evoked potentials (GEP) for sucrose solution (10 g.100 mL(-1)) before and after a standard lunch. The secondary objective was to evaluate the correlations between GEP and the plasmatic levels of acylated ghrelin, leptin, insulin and serotonin. METHODS: Each subject had 2 randomized sessions spaced by an interval of 2 days. During one session, subjects were fasting and during the other, subjects took a lunch low in sugar. In each session, subjects had a blood test before a first GEP recording followed by a second GEP recording either after a lunch (feeding session) or no lunch (fasting session). RESULTS: Twenty-eight OB (BMI: 38.6 ± 9.0 kg.m(-2)) were matched to 22 NW (BMI: 22.3 ± 2.2 kg.m(-2)). GEP latencies were prolonged in OB regardless the sessions and the time before and after lunch, compared with NW (in Cz at the morning: 170 ± 33 ms vs 138 ± 25 ms respectively; p < 0.001). The increase in latency observed in NW after lunch was not observed in OB. Negative or positive correlations were noted in all participants between GEP latencies and ghrelin, leptin, insulin plasmatic levels (P1Cz, r = -0.38, r = 0.33, r = 0.37 respectively, p < 0.0001). CONCLUSIONS: This study highlights a slower activation in the taste cortex in OB compared with NW.

The human circadian system regulates hunger independently of behavioral factors, resulting in a trough in the biological morning and a peak in the biological evening. However, the role of the only known orexigenic hormone, ghrelin, in this circadian rhythm is unknown. Furthermore, although shift work is an obesity risk factor, the separate effects of the endogenous circadian system, the behavioral cycle, and circadian misalignment on ghrelin has not been systematically studied. Here we show—by using two 8-day laboratory protocols—that circulating active (acylated) ghrelin levels are significantly impacted by endogenous circadian phase in healthy adults. Active ghrelin levels were higher in the biological evening than the biological morning (fasting +15.1%, P = 0.0001; postprandial +10.4%, P = 0.0002), consistent with the circadian variation in hunger (P = 0.028). Moreover, circadian misalignment itself (12-h behavioral cycle inversion) increased postprandial active ghrelin levels (+5.4%; P = 0.04). While not significantly influencing hunger (P > 0.08), circadian misalignment increased appetite for energy-dense foods (all P < 0.05). Our results provide possible mechanisms for the endogenous circadian rhythm in hunger, as well as for the increased risk of obesity among shift workers.

Background: Studies associate sleeping and eating late in the day with poor dietary quality and higher obesity risk but differences in sleep duration confound this association. We aimed to determine whether sleep and meal timing, independent of sleep duration, influenced food intake in healthy adults. Methods: This was a controlled, 2 × 2 inpatient crossover study with normal (0000-0800 h) or late (0330-1130 h) sleep and normal (1, 5, 11, and 12.5 h after awakening) or late (4.5, 8.5, 14.5, and 16 h after awakening) meals. Food intake was controlled while blood samples were obtained for determination of appetite-regulating hormones on days 3-4. Self-selected food intake was assessed on day 5. Data were analyzed using linear mixed model analysis with sleep, meal, and sleep x meal interaction as dependent variables. Results: Five participants completed all phases (mean age 25.1 ± [SD] 3.9 y, body mass index 29.2 ± 2.7 kg/m 2 ). There was a significant sleep x meal interaction on energy intake (P = 0.035) and trends on fat and sodium intakes (P < 0.10). Overnight ghrelin concentrations were higher under normal sleep and meal conditions relative to late (P < 0.005) but lower when both were combined (P < 0.001). Overnight leptin concentrations were higher under normal meal conditions (P = 0.012). There was a significant sleep x meal interaction on ghrelin (P = 0.032) and glucagon-like peptide 1 (P = 0.041) concentrations, but not leptin (P = 0.83), in response to a test meal. Conclusions: Our results suggest that alignment of sleep and meals may influence food choice and energy balance. Additional research is necessary to expand and confirm our findings.

How pre-exercise meal composition influences metabolic and health responses to exercise later in the day is currently unclear. Examine the effects of substituting carbohydrate for protein at lunch on subsequent exercise metabolism, appetite, and energy intake. Twelve healthy males completed 3 trials in randomized, counterbalanced order. Following a standardized breakfast (779 ± 66 kcal; ∼08:15), participants consumed a lunch (1186 ± 140 kcal; ∼13:15) containing either 0.2 g·kg-1 carbohydrate and ∼2 g·kg-1 protein (LO-CARB), or 2 g·kg-1 carbohydrate and ∼0.4 g·kg-1 protein (HI-CARB), or they fasted (FAST). Participants later cycled at ∼60% V̇O2peak for 1 hour (∼16:15) and post-exercise ad libitum energy intake was measured (∼18:30). Substrate oxidation, subjective appetite, and plasma concentrations of glucose, insulin, nonesterified fatty acids (NEFA), peptide YY (PYY), glucagon-like peptide 1 (GLP-1), and acylated ghrelin were measured for 5 hours post-lunch. Fat oxidation was greater during FAST (+11.66 ± 6.63 g) and LO-CARB (+8.00 ± 3.83 g) than HI-CARB (P < .001), with FAST greater than LO-CARB (+3.67 ± 5.07 g; P < .05). NEFA were lowest in HI-CARB and highest in FAST, with insulin demonstrating the inverse response (all P < .01). PYY and GLP-1 demonstrated a stepwise pattern, with LO-CARB greatest and FAST lowest (all P < .01). Acylated ghrelin was lower during HI-CARB and LO-CARB vs FAST (P < .01). Energy intake in LO-CARB was lower than FAST (-383 ± 233 kcal; P < .001) and HI-CARB (-313 ± 284 kcal; P < .001). Substituting carbohydrate for protein in a pre-exercise lunch increased fat oxidation, suppressed subjective and hormonal appetite, and reduced post-exercise energy intake.

Abstract Context Altered satiety hormones in women with polycystic ovarian syndrome (PCOS) may contribute to obesity. Diets with a low glycemic load (GL) may influence appetite-regulating hormones including glucagon and ghrelin. Objective To test the hypothesis that following a 4-week, eucaloric low vs high GL diet habituation, a low vs high GL meal will increase glucagon and decrease ghrelin to reflect greater satiety and improve self-reported fullness. Methods Secondary analysis of a randomized crossover trial. Participants Thirty women diagnosed with PCOS. Intervention Participants were provided low (41:19:40% energy from carbohydrate:protein:fat) and high (55:18:27) GL diets for 8 weeks each. At each diet midpoint, a solid meal test was administered to examine postprandial ghrelin, glucagon, glucose, insulin, and self-reported appetite scores. Results After 4 weeks, fasting glucagon was greater with the low vs high GL diet (P = .035), and higher fasting glucagon was associated with lesser feelings of hunger (P = .009). Significant diet effects indicate 4-hour glucagon was higher (P < .001) and ghrelin was lower (P = .009) after the low vs high GL meal. A trending time × diet interaction (P = .077) indicates feelings of fullness were greater in the early postprandial phase after the high GL meal, but no differences were observed the late postprandial phase. Conclusion These findings suggest after low GL diet habituation, a low GL meal reduces ghrelin and increases glucagon in women with PCOS. Further research is needed to determine the influence of diet composition on ad libitum intake in women with PCOS.

We recently indicated that four-week probiotic supplementation significantly reduced depression along with microbial and neural changes in people with depression. Here we further elucidated the biological modes of action underlying the beneficial clinical effects of probiotics by focusing on immune-inflammatory processes. The analysis included a total of N = 43 participants with depression, from which N = 19 received the probiotic supplement and N = 24 received a placebo over four weeks, in addition to treatment as usual. Blood and saliva were collected at baseline, at post-intervention (week 4) and follow-up (week 8) to assess immune-inflammatory markers (IL-1β, IL-6, CRP, MIF), gut-related hormones (ghrelin, leptin), and a stress marker (cortisol). Furthermore, transcriptomic analyses were conducted to identify differentially expressed genes. Finally, we analyzed the associations between probiotic-induced clinical and immune-inflammatory changes. We observed a significant group x time interaction for the gut hormone ghrelin, indicative of an increase in the probiotics group. Additionally, the increase in ghrelin was correlated with the decrease in depressive symptoms in the probiotics group. Transcriptomic analyses identified 51 up- and 57 down-regulated genes, which were involved in functional pathways related to enhanced immune activity. We identified a probiotic-dependent upregulation of the genes ELANE, DEFA4 and OLFM4 associated to immune activation and ghrelin concentration. These results underscore the potential of probiotic supplementation to produce biological meaningful changes in immune activation in patients with depression. Further large-scale mechanistic trials are warranted to validate and extend our understanding of immune-inflammatory measures as potential biomarkers for stratification and treatment response in depression. Trial Registration: www.clinicaltrials.gov , identifier: NCT02957591.

Pulmonary cachexia is common in advanced chronic obstructive pulmonary disease (COPD), culminating in exercise intolerance and a poor prognosis. Ghrelin is a novel growth hormone (GH)-releasing peptide with GH-independent effects. The efficacy and safety of adding ghrelin to pulmonary rehabilitation (PR) in cachectic COPD patients were investigated. In a multicenter, randomized, double-blind, placebo-controlled trial, 33 cachectic COPD patients were randomly assigned PR with intravenous ghrelin (2 µg/kg) or placebo twice daily for 3 weeks in hospital. The primary outcomes were changes in 6-min walk distance (6-MWD) and the St. George Respiratory Questionnaire (SGRQ) score. Secondary outcomes included changes in the Medical Research Council (MRC) scale, and respiratory muscle strength. At pre-treatment, serum GH levels were increased from baseline levels by a single dose of ghrelin (mean change, +46.5 ng/ml; between-group p<0.0001), the effect of which continued during the 3-week treatment. In the ghrelin group, the mean change from pre-treatment in 6-MWD was improved at Week 3 (+40 m, within-group p = 0.033) and was maintained at Week 7 (+47 m, within-group p = 0.017), although the difference between ghrelin and placebo was not significant. At Week 7, the mean changes in SGRQ symptoms (between-group p = 0.026), in MRC (between-group p = 0.030), and in maximal expiratory pressure (MEP; between-group p = 0.015) were better in the ghrelin group than in the placebo group. Additionally, repeated-measures analysis of variance (ANOVA) indicated significant time course effects of ghrelin versus placebo in SGRQ symptoms (p = 0.049) and MEP (p = 0.021). Ghrelin treatment was well tolerated. In cachectic COPD patients, with the safety profile, ghrelin administration provided improvements in symptoms and respiratory strength, despite the lack of a significant between-group difference in 6-MWD. UMIN Clinical Trial Registry C000000061.

Plant-derived proteins are often deficient in essential amino acids and have lower rates of digestibility than animal-derived proteins. Blending different plant-derived proteins could compensate for these deficiencies and may augment postprandial aminoacidemia over single-source plant proteins. This study assessed plasma amino acids and appetite hormones, appetite sensations and ad libitum energy intake following ingestion of a pea-rice protein blend (BLEND), compared with pea-only (PEA) and whey (WHEY) protein. In a randomised, double-blind, crossover design, ten healthy adults (M n 4, F n 6; mean (sd) age 22 (sd 3) years; BMI 24 (sd 3) kg·m2) ingested 0·3 g·kg·body mass–1 of BLEND, PEA or WHEY. Arterialised venous blood samples and appetite ratings were obtained in the fasted state and over 240 min postprandially. Energy intake was measured via an ad libitum buffet-style test meal. Mean plasma essential amino acid incremental AUC was higher in WHEY, compared with PEA (P < 0·01; mean diff (95 % CI): 44 218 (15 806, 72 631) μmol·240 min·l–1) and BLEND (P < 0·01; 14 358 (16 031, 101 121) μmol·240 min·l–1), with no differences between PEA and BLEND (P = 0·67). Plasma ghrelin and glucagon-like peptide-1, appetite ratings and ad libitum energy intake responses did not differ between treatments (P > 0·05 for all). Ingestion of a pea-rice protein blend did not augment postprandial aminoacidemia above pea protein, perhaps attributable to marginal differences in essential amino acid composition. No between-treatment differences in appetite or energy intake responses were apparent, suggesting that the influence of protein ingestion on perceived appetite ratings and orexigenic hormonal responses may not be solely determined by postprandial plasma aminoacidemia.