The first systematic reviews of the effects of exercise on appetite-regulation and energy intake demonstrated changes in appetite-regulating hormones consistent with appetite suppression and decreases in subsequent relative energy intake over a decade ago. More recently, an intensity-dependent effect and several potential mechanisms were proposed, and this review aims to highlight advances in this field. While exercise-induced appetite suppression clearly involves acylated ghrelin, glucagon-like peptide-1 may also be involved, though recent evidence suggests peptide tyrosine tyrosine may not be relevant. Changes in subjective appetite perceptions and energy intake continue to be equivocal, though these results are likely due to small sample sizes and methodological inconsistencies. Of the proposed mechanisms responsible for exercise-induced appetite suppression, lactate has garnered the most support through in vitro and in vivo rodent studies as well as a growing amount of work in humans. Other potential modulators of exercise-induced appetite suppression may include sex hormones, growth-differentiation factor 15, Lac-Phe, brain-derived neurotrophic factor, and asprosin. Research should focus on the mechanisms responsible for the changes and consider these other modulators (i.e., myokines/exerkines) of appetite to improve our understanding of the role of exercise on appetite regulation.

Commercial culture of channel catfish (Ictalurus punctatus) occurs in earthen ponds that are characterized by diel swings in dissolved oxygen concentration that can fall to severe levels of hypoxia, which can suppress appetite and lead to suboptimal growth. Given the significance of the hypothalamus in regulating these processes in other fishes, an investigation into the hypothalamus transcriptome was conducted to identify specific genes and expression patterns responding to hypoxia. Channel catfish in normoxic water were compared with catfish subjected to 12 h of hypoxia (20% oxygen saturation; 1.8 mg O2/L; 27°C) followed by 12 h of recovery in normoxia to mimic 24 h in a catfish aquaculture pond. Fish were sampled at 0-, 6-, 12-, 18-, and 24-h timepoints, with the 6- and 12-h samplings occurring during hypoxia. A total of 190 genes were differentially expressed during the experiment, with most occurring during hypoxia and returning to baseline values within 6 h of normoxia. Differentially expressed genes were sorted by function into Gene Ontology biological processes and revealed that most were categorized as \"response to hypoxia,\" \"sprouting angiogenesis,\" and \"cellular response to xenobiotic stimulus.\" The patterns of gene expression reported here suggest that transcriptome responses to hypoxia are broad and quickly reversibly with the onset of normoxia. Although no genes commonly reported to modulate appetite were found to be differentially expressed in this experiment, several candidates were identified for future studies investigating the interplay between hypoxia and appetite in channel catfish, including adm, igfbp1a, igfbp7, and stc2b.NEW & NOTEWORTHY Channel catfish are an economically important species that experience diel episodic periods of hypoxia that can reduce appetite. This is the first study to investigate their transcriptome from the hypothalamus in a simulated 24-h span in a commercial catfish pond, with 12 h of hypoxia and 12 h of normoxia. The research revealed functional groups of genes relating to hypoxia, angiogenesis, and glycolysis as well as individual target genes possibly involved in appetite regulation.

Alzheimer\'s disease (AD) remains a significant health challenge, with an increasing prevalence globally. Recent research has aimed to deepen the understanding of the disease pathophysiology and to find potential therapeutic interventions. In this regard, G protein-coupled receptors (GPCRs) have emerged as novel potential therapeutic targets to palliate the progression of neurodegenerative diseases such as AD. Orexin and cannabinoid receptors are GPCRs capable of forming heteromeric complexes with a relevant role in the development of this disease. On the one hand, the hyperactivation of the orexins system has been associated with sleep-wake cycle disruption and Aβ peptide accumulation. On the other hand, cannabinoid receptor overexpression takes place in a neuroinflammatory environment, favoring neuroprotective effects. Considering the high number of interactions between cannabinoid and orexin systems that have been described, regulation of this interplay emerges as a new focus of research. In fact, in microglial primary cultures of APPSw/Ind mice model of AD there is an important increase in CB2R-OX1R complex expression, while OX1R antagonism potentiates the neuroprotective effects of CB2R. Specifically, pretreatment with the OX1R antagonist has been shown to strongly potentiate CB2R signaling in the cAMP pathway. Furthermore, the blockade of OX1R can also abolish the detrimental effects of OX1R overactivation in AD. In this sense, CB2R-OX1R becomes a new potential therapeutic target to combat AD.

This was a preliminary study that examined whether appetite regulation is altered during the menstrual cycle or with oral contraceptives. Ten naturally cycling females (NON-USERS) and nine tri-phasic oral contraceptive using females (USERS) completed experimental sessions during each menstrual phase (follicular phase: FP; ovulatory phase: OP; luteal phase: LP). Appetite perceptions and blood samples were obtained fasted, 30, 60, and 90 min post-prandial to measure acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and total peptide tyrosine tyrosine (PYY). Changes were considered important if p < 0.100 and the effect size was ≥medium. There appeared to be a three-way (group x phase x time) interaction for acylated ghrelin where concentrations appeared to be greater in USERS versus NON-USERS during the OP 90-min post-prandial and during the LP fasted, and 90-min post-prandial. In USERS, ghrelin appeared to be greater 90-min post-prandial in the OP versus the FP with no other apparent differences between phases. There were no apparent differences between phases in NON-USERS. There appeared to be a three-way interaction for PYY where concentrations appeared to be greater in USERS during the FP 60-min post-prandial and during the OP 30-min post-prandial. In USERS PYY appeared to be greater 60-min post-prandial during the OP versus the LP with no other apparent differences. There were no apparent differences between phases in NON-USERS. There appeared to be no effect of group or phase on GLP-1, or appetite perceptions. These data demonstrate small effects of menstrual cycle phase and oral contraceptive use on the acylated ghrelin and total PYY response to a standardized meal, with no effects on active GLP-1 or perceived appetite, though more work with a large sample size is necessary.

Exercise in young adults (18-25 yr) suppresses appetite in a dose-response relationship with exercise intensity. Although several mechanisms have been proposed to explain this response, lactate is the most well established. To date, no study has investigated this specifically in middle-aged adults where the appetite response to a meal is different. To explore the effects of submaximal, near maximal, and supramaximal intensity exercise on appetite regulation in middle-aged adults. Nine participants (age: 45 ± 10 yr) completed four experimental sessions: 1) no-exercise control (CTRL); 2) moderate-intensity continuous training [MICT; 30 min, 65% maximal oxygen consumption (V̇o2max)]; 3) high-intensity interval training (HIIT; 10 × 1 min efforts, 90% heart rate maximum, 1 min recovery); and 4) sprint interval training (SIT; 8 × 15 s \"all-out\" efforts, 2 min recovery). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), active peptide tyrosine tyrosine (PYY), lactate, and subjective appetite perceptions were measured pre-exercise, 0-, 30-, and 90-min postexercise. Energy intake was recorded the day before and day of each session. Acylated ghrelin was suppressed (P < 0.001, [Formula: see text] = 0.474) by HIIT (0-min and 30-min postexercise; P < 0.091, d > 1.84) and SIT (0-min, 30-min, and 90-min postexercise; P < 0.037, d > 1.72) compared with CTRL, and SIT suppressed concentrations compared with MICT (0-min and 30-min postexercise; P < 0.91, d > 1.19). There were no effects of exercise on active PYY, active GLP-1, appetite perceptions, or free-living energy intake (P > 0.126, [Formula: see text] < 0.200). Intense interval exercise that generates lactate accumulation suppresses acylated ghrelin with little effect on anorexigenic hormones, overall appetite, or free-living energy intake.NEW & NOTEWORTHY We explored the effects of submaximal, near maximal, and supramaximal intensity exercise on appetite regulation in middle-aged adults. Our data support the intensity-dependent effect of exercise on acylated ghrelin suppression that is closely related to lactate accumulation, though there appears to be little effect on anorexigenic hormones [active peptide tyrosine tyrosine (PYY), active glucagon-like peptide-1 (GLP-1)], overall appetite, or free-living energy intake. These data support previous results in younger adults where lactate was implicated in the exercise-induced suppression of acylated ghrelin.

Neuronal circuits regulating appetite are dominated by arcuate nucleus neurons, which include appetite-promoting and -suppressing neurons that release the orexigenic neuropeptide agouti-related protein (AgRP) and anorexigenic neuropeptide pro-opiomelanocortin, respectively, to compete for melanocortin receptors to modulate feeding behavior. In this study, we expressed novel agrp promoters, including different lengths of the 5\' flanking regions of the agrp gene (4749 bp) in the zebrafish genome. We used the agrp promoter to derive the enhanced green fluorescent protein (EGFP)-nitroreductase (NTR) fusion protein, allowing expression of the green fluorescence signal in the AgRP neurons. Then, we treated the transgenic zebrafish AgRP4.7NTR (Tg [agrp-EGFP-NTR]) with metronidazole to ablate the AgRP neurons in the larvae stage and observed a decline in their appetite and growth. The expression of most orexigenic and growth hormone/insulin-like growth factor axis genes decreased, whereas that of several anorexigenic genes increased. Our findings demonstrate that AgRP is a critical regulator of neuronal signaling for zebrafish appetite and energy intake control. Thus, AgRP4.7NTR can be used as a drug-screening platform for therapeutic targets to treat human appetite disorders, including obesity. Furthermore, the unique agrp promoter we identified can be a powerful tool for research on AgRP neurons, especially AgRP neuron-mediated pathways in the hypothalamus, and appetite.

UNASSIGNED: Frailty, is a geriatric syndrome that reduces the resistance to stress situations caused by activities of daily living and increases morbidity and mortality. We hypothesized that a decrease in orexigenic peptides or an increase in anorexigenic peptides might be associated with frailty. We aimed to investigate the relationship between frailty and six appetite-related peptides: ghrelin, neuropeptide Y (NPY), agouti-related peptide (AgRP), cocaine-amphetamine-associated peptide (CART), peptide YY, and alpha MSH (α-MSH).
UNASSIGNED: This cross-sectional study was conducted on 85 older adults who visited the outpatient clinic. All patients underwent comprehensive geriatric assessment. Frailty status was assessed using the Fried frailty index. Plasma levels of six appetite-related peptides were studied.
UNASSIGNED: The mean age was 73.7 ± 5.4 years, 27 (31.8%) of the patients were male, and 32 of the patients (37.6%) were frail. While plasma levels of ghrelin, NPY and AgRP were significantly lower in frail patients, CART and α-MSH levels were higher compared to non-frail patients (p < .05 for all). Peptide YY was found to be higher in the frail group, however, the difference did not reach statistical significance (p = .052). In multivariate logistic regression analysis, the ghrelin, AgRP, CART, and α-MSH levels were independent predictors of frailty. Moreover, a weak correlation was found between all peptides(except NPY) and handgrip strength and Lawton-Brody score.
UNASSIGNED: Ghrelin, AgRP, CART, and α-MSH levels were found to be independent predictors of frailty. Our results suggest that appetite-related peptides might be playing roles in the pathogenesis of frailty. Further larger prospective studies are needed to test this hypothesis.

Limited work examining woman\'s appetite-regulatory response to exercise has been focused on the follicular phase (FP) of the menstrual cycle. This is an important limitation as estradiol (E2) and progesterone (P4) fluctuate across phases with greater concentrations in the luteal phase (LP).
OBJECTIVE: To examine the appetite-regulatory response to vigorous-intensity continuous exercise (VICT) in the FP and LP.
METHODS: Twelve women completed 30 min of VICT at 80% V˙O2max in the FP and LP. E2, P4, acylated ghrelin, active peptide tyrosine-tyrosine (PYY), active glucagon-like peptide-1 (GLP-1), and appetite perceptions were measured pre-exercise, 0-, 30-, and 90-min post-exercise. Energy intake was recorded for a 2-day period (day before and of each session). A series of two-way repeated measure ANOVA were used to compare all dependent variables.
RESULTS: Pre-exercise E2 (P = 0.005, d = 1.00) and P4 (P < 0.001, d = 1.41) concentrations were greater in the LP than the FP and exercise increased both at 0- and 30-min post-exercise (E2: P < 0.009; P4: P < 0.001, d = 0.63). Acylated ghrelin was lower in the FP versus LP at pre-exercise as well as 0-min (P = 0.006, d = 0.97) and 90-min (P = 0.029, d = 0.72) post-exercise. There were no differences of menstrual phase on PYY (P = 0.359, ηp2 = 0.092), GLP-1 (P = 0.226, ηp2 = 0.130), or overall appetite (P = 0.514, ηp2 = 0.066). Energy intake was greater on the day of in the LP versus the FP (P = 0.003, d = 1.2).
CONCLUSIONS: Acylated ghrelin was lower in the FP compared to the LP and though there were no differences in anorexigenic hormones or subjective appetite, energy intake was greater on the day of the session in the LP suggesting important differences across the menstrual cycle where greater concentrations of ovarian hormones in the LP may blunt the exercise response.

The present study aimed to evaluate the effects of feeding or feed deprivation on the orexigenic and anorexigenic responses at the central (whole brain) and peripheral (anterior and posterior intestine, stomach, and liver) system levels in European seabass. For this purpose, a group of fish (208 g) was fed a single meal daily for 8 days (fed group) and another group was feed-deprived for 8 days (unfed group). Compared to the fed group, in the whole brain, feed deprivation did not induce changes in npy, agrp1, and cart2 expression, but increased agrp2 and pomc1 expression. In the anterior intestine, feed deprivation increased cck expression, while in the posterior intestine, the npy expression increased and pyyb decreased. In the stomach, the ghr expression decreased regardless of the feeding status. The hepatic lep expression increased in the unfed fish. The present results suggest a feed intake regulation mechanism in European seabass similar to that observed in other teleosts.

Feed is one of the most important external signals in fish that stimulates its feeding behavior and growth. The intake of feed is the main factor determining efficiency and cost, maximizing production efficiency in a fish farming firm. The physiological mechanism regulating food intake lies between an intricate connection linking central and peripheral signals that are unified in the hypothalamus consequently responding to the release of appetite-regulating genes that eventually induce or hinder appetite, such as apelin; a recently discovered peptide produced by several tissues with diverse physiological actions mediated by its receptor, such as feed regulation. Extrinsic factors have a great influence on food intake and feeding behavior in fish. Under these factors, feeding in fish is decontrolled and the appetite indicators in the brain do not function appropriately thus, in controlling conditions which result in the fluctuations in the expression of these appetite-relating genes, which in turn decrease food consumption. Here, we examine the research advancements in fish feeding behavior regarding dietary selection and preference and identify some key external influences on feed intake and feeding behavior. Also, we present summaries of the results of research findings on apelin as an appetite-regulating hormone in fish. We also identified gaps in knowledge and directions for future research to fully ascertain the functional importance of apelin in fish.