Network-targeted transcranial direct current stimulation of the hypothalamus appetite-control network: a feasibility study.

The hypothalamus is the key regulator for energy homeostasis and is functionally connected to striatal and cortical regions vital for the inhibitory control of appetite. Hence, the ability to non-invasively modulate the hypothalamus network could open new ways for the treatment of metabolic diseases. Here, we tested a novel method for network-targeted transcranial direct current stimulation (net-tDCS) to influence the excitability of brain regions involved in the control of appetite. Based on the resting-state functional connectivity map of the hypothalamus, a 12-channel net-tDCS protocol was generated (Neuroelectrics Starstim system), which included anodal, cathodal and sham stimulation. Ten participants with overweight or obesity were enrolled in a sham-controlled, crossover study. During stimulation or sham control, participants completed a stop-signal task to measure inhibitory control. Overall, stimulation was well tolerated. Anodal net-tDCS resulted in faster stop signal reaction time (SSRT) compared to sham (p = 0.039) and cathodal net-tDCS (p = 0.042). Baseline functional connectivity of the target network correlated with SSRT after anodal compared to sham stimulation (p = 0.016). These preliminary data indicate that modulating hypothalamus functional network connectivity via net-tDCS may result in improved inhibitory control. Further studies need to evaluate the effects on eating behavior and metabolism.

Body weight change during a smoking cessation intervention for individuals with overweight or obesity.

INTRODUCTION: A more comprehensive understanding of the factors regarding weight control in individuals with overweight or obesity after quitting smoking is needed. The study aimed to analyze the changes of in-treatment variables during a smoking cessation intervention and examine their impact on weight. METHODS: A total of 120 individuals who smoke with overweight or obesity (MBMI = 31.75 ± 4.31; 54.16 % female) participated in a cognitive-behavioral therapy for smoking cessation and weight control or the same treatment plus contingency management. Weight, smoking variables (cotinine and continuous abstinence), eating behaviors (appetite, grazing), exercise, and sleep were assessed weekly throughout the treatment. RESULTS: More participants gained weight over time with reduced nicotine use or abstinence. There was a tendency during treatment to increase appetite and exercise time, while grazing episodes and sleeping hours remained stable. Higher baseline weight (p < .001), greater cotinine reduction (p = .021) and time (p = .009) were associated with greater weight gain, while more hours of exercise (p = .003), no appetite changes (p = .003) and diminished appetite (p < .001) were associated with less gain over the treatment. Both treatment conditions showed similar results in all in-treatment variables. DISCUSSION: Individuals with overweight and obesity with higher baseline weight and higher baseline cotinine levels during smoking cessation interventions may require special attention to improve weight outcomes. Exercise and appetite regulation may be useful for mitigating weight gain in smoking cessation interventions for individuals with overweight or obesity.

Relationships of emerging biomarkers of cancer cachexia with quality of life, appetite, and cachexia.

PURPOSE: Quality of life (QoL), appetite, cachexia, and biomarkers [albumin, hemoglobin (Hb), neutrophils, lymphocytes, platelets, C-reactive protein (CRP), tumor necrosis factor alpha (TNFα), interleukin 6 (IL-6), interleukin 8 (IL-8), C-X-C motif chemokine ligand 5 (CXCL5) and citrullinated histoneH3 (H3Cit)] were compared for 40 cases with advanced cancer and 40 healthy controls. Baseline differences and significant relationships were explored for biomarkers with QoL, appetite, and cachexia. METHODS: In a prospective case-control, age and sex matched study, the European Organisation for the Research and Treatment of Cancer Quality of Life-C30 questionnaire (EORTC-QLQ-C30) for QoL, the Functional Assessment of Anorexia and Cachexia Therapy assessment (FAACT A/CS-12) for appetite, and a five-factor cachexia assessment tool for cachexia assessment were performed. Routine hematological measurements and blood chemistry analyses together with ELISA procedures and a Multiplex® bead array platform, were used for biomarker analysis. Descriptive statistics and regression analyses were undertaken. P < 0.05 defined statistical significance. RESULTS: Global health status (QL-G), functional scales (QL-FS), and symptom scales (QL-SS) differed for cases and controls (p < 0.01). In cases, differences were observed for QL-G (p < 0.01), QL-FS (p < 0.01), and QL-SS (p = 0.01) compared to standardized references values. FAACT A/CS-12 scores differed significantly between cases and controls (p < 0.01) and 30% of cases scored "poor" appetites. Cachexia was present in 60% of cases. Albumin, lymphocytes, platelets, Hb, platelet to lymphocyte ratio (PLR), systemic immune-inflammation index (SII), CRP, TNFα, all at p < 0.01, neutrophil to lymphocyte ratio (NLR) (p = 0.02), IL-6 (p < 0.04), and IL-8 (p = 0.02) differed significantly between cases and controls. No difference was found for CXCL5 or H3Cit. Albumin NLR, Hb, PLR, SII, TNFα, IL-8, and CRP showed significant relationships with all aspects of QoL. QL-FS was significantly related to CXCL5 (p = 0.04), significant relationships with FAACT A/CS-12 included: NLR (p = 0.002), Hb (p < 0.001), and PLR (p < 0.01). NLR, PLR, SII, TNFα, IL-6, IL-8, and CRP correlated positively to cachexia and albumin while Hb and lymphocyte count correlated negatively to cachexia. CONCLUSION: CXCL5 and H3Cit were not reliable biomarkers for cancer cachexia, nor significantly related to QoL, appetite or cachexia. Albumin, NLR, Hb, PLR, SII, TNFα, IL-8, and CRP were reliable indicators of QoL, appetite, and cachexia. Future research should include other novel biomarkers namely growth differentiation factor-15 (GDF-15), fibroblast growth factor 21 (FGF-21), fractakline, interferon gamma (IFN-y), IL-16, macrophage colony stimulating factor (M-CSF), and macrophage procoagulant-inducing factor (MPIF).

Ovulatory cycle shifts in human motivational prioritisation of sex and food.

Previous research on the endogenous effects of ovarian hormones on motivational states in women has focused on sexual motivation. The Motivational Priority Shifts Hypothesis has a broader scope. It predicts a shift from somatic to reproductive motivation when fertile. In a highly powered preregistered online diary study across 40 days, we tested whether 390 women report such an ovulatory shift in sexual and eating motivation and behaviour. We compared 209 naturally cycling women to 181 women taking hormonal contraceptives (HC) to rule out non-ovulatory changes across the cycle as confounders. We found robust ovulatory decreases in food intake and increases in general sexual desire, in-pair sexual desire and initiation of dyadic sexual behaviour. Extra-pair sexual desire increased mid-cycle, but the effect did not differ significantly in HC women, questioning an ovulatory effect. Descriptively, solitary sexual desire and behaviour, dyadic sexual behaviour, appetite, and satiety showed expected mid-cycle changes that were diminished in HC women, but these failed to reach our strict preregistered significance level. Our results provide insight into current theoretical debates about ovulatory cycle shifts while calling for future research to determine motivational mechanisms behind ovulatory changes in food intake and considering romantic partners' motivational states to explain the occurrence of dyadic sexual behaviour.

The associations between attentional bias to food cues, parent-report appetitive traits, and concurrent adiposity among adolescents.

OBJECTIVE: To assess whether attentional bias to food cues and appetitive traits are independently and interactively associated with adiposity in adolescents. METHOD: Eighty-five adolescents, 14-17-years had their attentional bias to food images measured in a sated state by computing eye tracking measures of attention (first fixation duration, cumulative fixation duration) to food and control distractor images that bordered a computer game. Parents reported adolescent appetitive traits including the food approach domains of enjoyment of food, food responsiveness, emotional overeating, and the food avoidance domains of satiety responsiveness and emotional overeating through the Children's Eating Behavior Questionnaire. RESULTS: First fixation bias to food cues was positively associated with enjoyment of food, and negatively associated with satiety responsiveness. In a series of regression models adjusted for relevant covariates, first fixation bias to food cues (ß = 0.83, p = 0.007), higher food responsiveness (ß = 0.74, p < 0.001), higher emotional overeating (ß = 0.51, p = 0.002), and a composite appetite score (ß = 1.42, p < 0.001) were each significantly associated with greater BMI z-scores. In models assessing the interactive effects between attentional bias and appetitive traits, higher first fixation bias to food cues interacted synergistically with food responsiveness and emotional overeating in relation to BMI z-score. A synergistic interaction between first fixation bias to food cues and the composite appetite score in relation to BMI z-score was also observed. CONCLUSION: Individuals with high attentional bias to food cues and obesogenic appetitive traits may be particularly susceptible to weight gain.

Medium-chain triglyceride-specific appetite is regulated by the ß-oxidation of medium-chain fatty acids in the liver.

Most studies on fat appetite have focused on long-chain triglycerides (LCTs) due to their obesogenic properties. Medium-chain triglycerides (MCTs), conversely, exhibit antiobesogenic effects; however, the regulation of MCT intake remains elusive. Here, we demonstrate that mice can distinguish between MCTs and LCTs, and the specific appetite for MCTs is governed by hepatic ß-oxidation. We generated liver-specific medium-chain acyl-CoA dehydrogenase (MCAD)-deficient (MCADL-/-) mice and analyzed their preference for MCT and LCT solutions using glyceryl trioctanoate (C8-TG), glyceryl tridecanoate (C10-TG), corn oil, and lard oil in two-bottle choice tests conducted over 8 days. In addition, we used lick microstructure analyses to evaluate the palatability and appetite for MCT and LCT solutions. Finally, we measured the expression levels of genes associated with fat ingestion (Galanin, Qrfp, and Nmu) in the hypothalamus 2 h after oral gavage of fat. Compared with control mice, MCADL-/- mice exhibited a significantly reduced preference for MCT solutions, with no alteration in the preference for LCTs. Lick analysis revealed that MCADL-/- mice displayed a significantly decreased appetite for MCT solutions only while the palatability of both MCT and LCT solutions remained unaffected. Hypothalamic Galanin expression in control mice was elevated by oral gavage of C8-TG but not by LCTs, and this response was abrogated in MCADL-/- mice. In summary, our data suggest that hepatic ß-oxidation is required for MCT-specific appetite but not for LCT-specific appetite. The induction of hypothalamic galanin upon MCT ingestion, dependent on hepatic ß-oxidation, could be involved in the regulation of MCT-specific appetite.NEW & NOTEWORTHY Whether and how medium-chain triglyceride (MCT) intake is regulated remains unknown. Here, we showed that mice can discriminate between MCTs and LCTs. Hepatic ß-oxidation participates in MCT-specific appetite, and hypothalamic galanin may be one of the factors that regulate MCT intake. Because of the antiobesity effects of MCTs, studying MCT-specific appetite may help combat obesity by promoting the intake of MCTs instead of LCTs.

Downloading appetite? Investigating the role of parasocial relationship with favorite social media food influencer in followers' disordered eating behaviors.

PURPOSE: Although a number of investigations have been carried out on the marketing outcomes of parasocial relationships (PSR) with food influencers on social media, little attention has been paid to the potential contribution of these one-sided emotional bonds to followers' eating attitudes and habits. Drawing on the Parasocial Theory, the role of parasocial attachment with food influencers was investigated in predicting eating disorders, food addiction, and grazing. To increase the accuracy of PSR measurement, a brief self-report scale was developed to gauge social media users' feelings of mutual awareness, attention, and adjustment with their favorite food influencer at a distance through social media. METHODS: Participants were a convenience sample of 405 Iranian social media users (231women; Mage = 28.16, SDage = 9.40), who followed a favorite food influencer on social media. RESULTS: The 8-item Parasocial Relationship with Favorite Food Influencer Scale (PSRFFIS) revealed a unidimensional structure with excellent content and construct validity and internal consistency. Regarding gender differences, men showed stronger parasocial attachment to their favorite food influencers. Adjusting age, gender, and subjective social status as control variables, PSR with favorite food influencers partially contributed to the explanation of eating disorder symptom severity, food addiction, and grazing. CONCLUSION: These findings show that PSR with favorite food influencers appears to be associated with followers' craving for food, which, in turn, may contribute to maladaptive eating habits. This highlights media-related factors, such as PSR with food influencers, as potential drivers of dysfunctional eating habits in the digital age, particularly in countries like Iran where disordered eating is prevalent. LEVEL OF EVIDENCE: Level V-based on cross-sectional data (correlational study; scale development).

Physiology of the weight-loss plateau in response to diet restriction, GLP-1 receptor agonism, and bariatric surgery.

OBJECTIVE: The objective of this study was to investigate why different weight-loss interventions result in varying durations of weight loss prior to approaching plateaus. METHODS: A validated mathematical model of energy metabolism and body composition dynamics was used to simulate mean weight- and fat-loss trajectories in response to diet restriction, semaglutide 2.4 mg, tirzepatide 10 mg, and Roux-en-Y gastric bypass (RYGB) surgery interventions. Each intervention was simulated by adjusting two model parameters affecting energy intake to fit the mean weight-loss data. One parameter represented the persistent shift of the system from baseline equilibrium, and the other parameter represented the strength of the feedback control circuit relating weight loss to increased appetite. RESULTS: RYGB surgery resulted in a persistent intervention magnitude more than threefold greater than diet restriction and about double that of tirzepatide and semaglutide. All interventions except diet restriction substantially weakened the appetite feedback control circuit, resulting in an extended period of weight loss prior to the plateau. CONCLUSIONS: These preliminary mathematical modeling results suggest that both glucagon-like peptide 1 (GLP-1) receptor agonism and RYGB surgery interventions act to weaken the appetite feedback control circuit that regulates body weight and induce greater persistent effects to shift the body weight equilibrium compared with diet restriction.

Adaptive thermogenesis, at the level of resting energy expenditure, after diet alone or diet plus bariatric surgery.

OBJECTIVE: The objective of this study was to compare the magnitude of adaptive thermogenesis (AT), at the level of resting energy expenditure (REE), after a very low-energy diet alone or combined with Roux-en-Y gastric bypass or sleeve gastrectomy, as well as to investigate the association between AT and changes in appetite. METHODS: A total of 44 participants with severe obesity underwent 10 weeks of a very low-energy diet alone or combined with Roux-en-Y gastric bypass or sleeve gastrectomy. Body weight and composition, REE, subjective appetite feelings, and plasma concentrations of gastrointestinal hormones were measured at baseline and week 11. AT, at the level of REE, was defined as a significantly lower measured versus predicted (using a regression model with baseline data) REE. RESULTS: Participants lost 18.4 ± 3.9 kg of body weight and experienced AT, at the level of REE (-121 ± 188 kcal/day; p < 0.001), with no differences among groups. The larger the AT, at the level of REE, the greater the reduction in fasting ghrelin concentrations and the smaller the reduction in feelings of hunger and desire to eat in the postprandial state. CONCLUSIONS: Weight-loss modality does not seem to modulate the magnitude of AT, at the level of REE. The greater the AT, at the level of REE, the greater the drive to eat following weight loss.

Sensing stretch to suppress appetite.

Food intake activates a mechanosensitive ion channel that inhibits ghrelin production and reduces appetite.

Brain sodium sensing for regulation of thirst, salt appetite, and blood pressure.

The brain possesses intricate mechanisms for monitoring sodium (Na) levels in body fluids. During prolonged dehydration, the brain detects variations in body fluids and produces sensations of thirst and aversions to salty tastes. At the core of these processes Nax , the brain's Na sensor, exists. Specialized neural nuclei, namely the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT), which lack the blood-brain barrier, play pivotal roles. Within the glia enveloping the neurons in these regions, Nax collaborates with Na+ /K+ -ATPase and glycolytic enzymes to drive glycolysis in response to elevated Na levels. Lactate released from these glia cells activates nearby inhibitory neurons. The SFO hosts distinct types of angiotensin II-sensitive neurons encoding thirst and salt appetite, respectively. During dehydration, Nax -activated inhibitory neurons suppress salt-appetite neuron's activity, whereas salt deficiency reduces thirst neuron's activity through cholecystokinin. Prolonged dehydration increases the Na sensitivity of Nax via increased endothelin expression in the SFO. So far, patients with essential hypernatremia have been reported to lose thirst and antidiuretic hormone release due to Nax -targeting autoantibodies. Inflammation in the SFO underlies the symptoms. Furthermore, Nax activation in the OVLT, driven by Na retention, stimulates the sympathetic nervous system via acid-sensing ion channels, contributing to a blood pressure elevation.

Gastric mechanosensitive channel Piezo1 regulates ghrelin production and food intake.

Ghrelin, produced mainly by gastric X/A-like cells, triggers a hunger signal to the central nervous system to stimulate appetite. It remains unclear whether X/A-like cells sense gastric distention and thus regulate ghrelin production. Here we show that PIEZO1 expression in X/A-like cells decreases in patients with obesity when compared to controls, whereas it increases after sleeve gastrectomy. Male and female mice with specific loss of Piezo1 in X/A-like cells exhibit hyperghrelinaemia and hyperphagia and are more susceptible to overweight. These phenotypes are associated with impairment of the gastric CaMKKII/CaMKIV-mTOR signalling pathway. Activation of PIEZO1 by Yoda1 or gastric bead implantation inhibits ghrelin production, decreases energy intake and induces weight loss in mice. Inhibition of ghrelin production by Piezo1 through the CaMKKII/CaMKIV-mTOR pathway can be recapitulated in a ghrelin-producing cell line mHypoE-42. Our study reveals a mechanical regulation of ghrelin production and appetite by PIEZO1 of X/A-like cells, which suggests a promising target for anti-obesity therapy.

Influence of the gut microbiome on appetite-regulating neuropeptides in the hypothalamus: Insight from conventional, antibiotic-treated, and germ-free mouse models of anorexia nervosa.

Recent research highlights the profound impact of the gut microbiome on neuropsychiatric disorders, shedding light on its potential role in shaping human behavior. In this study, we investigate the role of the gut microbiome in appetite regulation using activity-based anorexia (ABA) mouse model of anorexia nervosa (AN) - a severe eating disorder with significant health consequences. ABA was induced in conventional, antibiotic-treated, and germ-free mice. Our results show the clear influence of the gut microbiome on the expression of four orexigenic (neuropeptide Y, agouti-related peptide, melanin-concentrating hormone, and orexin) and four anorexigenic peptides (cocaine- and amphetamine-regulated transcript, corticotropin-releasing hormone, thyrotropin-releasing hormone, and pro-opiomelanocortin) in the hypothalamus. Additionally, we assessed alterations in gut barrier permeability. While variations were noted in germ-free mice based on feeding and activity, they were not directly attributable to the gut microbiome. This research emphasizes that the gut microbiome is a pivotal factor in AN's appetite regulation beyond just dietary habits or physical activity.

Gut hormones and appetite regulation.

PURPOSE OF REVIEW: Various gut hormones interact with the brain through delicate communication, thereby influencing appetite and subsequent changes in body weight. This review summarizes the effects of gut hormones on appetite, with a focus on recent research. RECENT FINDINGS: Ghrelin is known as an orexigenic hormone, whereas glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), postprandial peptide YY (PYY), and oxyntomodulin (OXM) are known as anorexigenic hormones. Recent human studies have revealed that gut hormones act differently in various systems, including adipose tissue, beyond appetite and energy intake, and even involve in high-order thinking. Environmental factors including meal schedule, food contents and quality, type of exercise, and sleep deprivation also play a role in the influence of gut hormone on appetite, weight change, and obesity. Recently published studies have shown that retatrutide, a triple-agonist of GLP-1, GIP, and glucagon receptor, and orforglipron, a GLP-1 receptor partial agonist, are effective in weight loss and improving various metabolic parameters associated with obesity. SUMMARY: Various gut hormones influence appetite, and several drugs targeting these receptors have been reported to exert positive effects on weight loss in humans. Given that diverse dietary and environmental factors affect the actions of gut hormones and appetite, there is a need for integrated and largescale long-term studies in this field.

Exploring relationships among appetitive traits, negative affect, and binge eating in adults with overweight or obesity.

Binge eating (BE) is a significant public health concern due to its prevalence and impact on mental and physical health. While research has suggested both negative affect and appetitive traits are associated with BE, few studies have investigated these constructs concurrently. Structural equation modeling (SEM) evaluated relationships between negative affect, reward-related appetitive traits, and BE among 293 adults with overweight or obesity (OW/OB) seeking treatment for BE, overeating, and weight management (m age = 46.6; m body mass index[BMI] = 34.5; 81.2 % female; 20.1 % Latinx, 60.8 % White non-Latinx). BE was related to negative affect (ß = 0.53; p < 0.01) and appetitive traits (ß = 1.53; p < 0.001). Negative affect and appetitive traits were related to one another (r = 0.42; p < 0.001), and the full model accounted for 77 % of the variance in BE. In an exploratory follow-up analysis, multigroup SEM evaluated the above relationships in models stratified by sex. Exploratory findings demonstrated both negative affect and appetitive traits were related to BE across sex, particularly when examining BE cognitions and behaviors. However, relationships in men depended upon BE assessment tool. These findings highlight that both negative affect and appetitive traits are related to BE, and jointly may represent significant risk and maintenance factors, particularly in adults with OW/OB. Our findings also highlight the importance of future investigation of sex differences in BE and the potential impact of assessment method.

The effects of environmental changes on the endocrine regulation of feeding in fishes.

Fishes are exposed to natural and anthropogenic changes in their environment, which can have major effects on their behaviour and their physiology, including feeding behaviour, food intake and digestive processes. These alterations are owing to the direct action of environmental physico-chemical parameters (i.e. temperature, pH, turbidity) on feeding physiology but can also be a consequence of variations in food availability. Food intake is ultimately regulated by feeding centres of the brain, which receive and process information from endocrine signals from both brain and peripheral tissues such as the gastrointestinal tract. These endocrine signals stimulate or inhibit food intake, and interact with each other to maintain energy homeostasis. Changes in environmental conditions might change feeding habits and rates, thus affecting levels of energy stores, and the expression of endocrine appetite regulators. This review provides an overview of how environmental changes and food availability could affect feeding and these endocrine networks in fishes. This article is part of the theme issue 'Endocrine responses to environmental variation: conceptual approaches and recent developments'.

Anorexia of ageing is associated with elevated fasted and lower post-prandial ghrelin, independent of ghrelin O-acyltransferase.

The role of ghrelin metabolism in anorexia of ageing is unclear. The aim of this study was to determine acyl-ghrelin, total ghrelin, and ghrelin O-acyltransferase concentrations when fasted and in responses to feeding in older adults exhibiting anorexia of ageing. Twenty-five older adults (OA; 15f, 74 ± 7 years, 24.5 kg·m-2) and twelve younger adults (YA; 6f, 21 ± 2 years, 24.4 kg·m-2) provided a fasted measure of subjective appetite and fasted blood sample (0 min) before consuming a standardised porridge breakfast meal (450 kcal). Appetite was measured every 30 min for 240 min and blood was sampled at 30, 60, 90, 120, 180 and 240 min while participants rested. At 240 min, an ad libitum pasta-based lunch meal was consumed. Older adults were identified as those with healthy appetite (HA-OA) or low appetite (LA-OA), based on habitual energy intake, self-report appetite, BMI, and ad libitum lunch intake. YA ate more at lunch (1108 ± 235 kcal) than HA-OA (653 ± 133 kcal, p = 0.007) and LA-OA (369 ± 168 kcal; p < 0.001). LA-OA, but not HA-OA, had higher fasted concentrations of acyl- and total ghrelin than YA (acyl-ghrelin: 621 ± 307 pg·mL-1 vs. 353 ± 166 pg·mL-1, p = 0.047; total ghrelin: 1333 ± 702 pg·mL-1 vs. 636 ± 251 pg·mL-1, p = 0.006). Acyl-ghrelin (60 min and 90 min) and total ghrelin (90 min) were suppressed to a greater extent for LA-OA than for YA (p < 0.05). No differences were observed in subjective appetite, acyl-to-total ghrelin ratio, or plasma GOAT content (p > 0.1). Higher fasting ghrelin and an augmented ghrelin response to feeding in LA-OA, but not HA-OA, suggests that alterations to ghrelin metabolism are not functions of ageing per se and may be independent causal mechanisms of anorexia of ageing.

Low- and high-load resistance training exercise to volitional fatigue generate exercise-induced appetite suppression.

Research on exercise-induced appetite suppression often does not include resistance training (RT) exercise and only compared matched volumes. PURPOSE: To compare the effects of low-load and high-load RT exercise completed to volitional fatigue on appetite-regulation. METHODS: 11 resistance-trained males (24 ± 2 y) completed 3 sessions in a crossover experimental design: 1) control (CTRL); 2) RT exercise at 30% 1-repetition maximum (RM); and 3) RT exercise at 90% 1-RM. RT sessions consisted of 3 sets of 5 exercises completed to volitional fatigue. Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), active peptide tyrosine (PYY), lactate, and subjective appetite perceptions were measured pre-exercise, 0-, 60-, and 120-min post-exercise. Energy intake was recorded the day before, of, and after each session. RESULTS: Lactate was elevated following both 30% (0-, 60-, 120-min post-exercise) and 90% (0-, 60-min post-exercise; P < 0.001, d > 3.92) versus CTRL, with 30% greater than 90% (0-min post-exercise; P = 0.011, d = 1.14). Acylated ghrelin was suppressed by 30% (P < 0.007, d > 1.22) and 90% (P < 0.028, d > 0.096) post-exercise versus CTRL, and 30% suppressed concentrations versus 90% (60-min post-exercise; P = 0.032, d = 0.95). There was no effect on PYY (P > 0.171, ηp2 <0.149) though GLP-1 was greater at 60-min post-exercise in 90% (P = 0.052, d = 0.86) versus CTRL. Overall appetite was suppressed 0-min post-exercise following 30% and 90% versus CTRL (P < 0.013, d > 1.10) with no other differences (P > 0.279, d < 0.56). There were no differences in energy intake (P > 0.101, ηp2 <0.319). CONCLUSIONS: RT at low- and high-loads to volitional fatigue induced appetite suppression coinciding with changes in acylated ghrelin though limited effects on anorexigenic hormones or free-living energy intake were present.

Postprandial plasma amino acid and appetite responses with ingestion of a novel salmon-derived protein peptide in healthy young adults.

This study assessed postprandial plasma aminoacidemia, glycemia, insulinemia and appetite responses to ingestion of a novel salmon-derived protein peptide (Salmon PP) compared with milk protein isolate (Milk PI). In a randomised, participant-blind crossover design, eleven healthy adults (M = 5, F = 6; mean ± sd age: 22 ± 3 years; BMI: 24 ± 3 kg/m2) ingested 0·3 g/kg/body mass of Salmon PP or Milk PI. Arterialised blood samples were collected whilst fasted and over a 240-min postprandial period. Appetite sensations were measured via visual analogue scales. An ad libitum buffet-style test meal was administered after each trial. The incremental AUC (iAUC) plasma essential amino acid (EAA) response was similar between Salmon PP and Milk PI. The iAUC plasma leucine response was significantly greater following Milk PI ingestion (P < 0·001), whereas temporal and iAUC plasma total amino acid (P = 0·001), non-essential amino acid (P = 0·002), glycine (P = 0·0025) and hydroxyproline (P < 0·001) responses were greater following Salmon PP ingestion. Plasma insulin increased similarly above post-absorptive values following Salmon PP and Milk PI ingestion, whilst plasma glucose was largely unaltered. Indices of appetite were similarly altered following Salmon PP and Milk PI ingestion, and total energy and macronutrient intake during the ad libitum meal was similar between Salmon PP and Milk PI. The postprandial plasma EAA, glycine, proline and hydroxyproline response to Salmon PP ingestion suggest this novel protein source could support muscle and possibly connective tissue adaptive remodelling, which warrants further investigation, particularly as the plasma leucine response to Salmon PP ingestion was inferior to Milk PI.