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Objective: To investigate the effects of moderate‐intensity aerobic exercise on appetite control parameters, appetite perceptions, and energy intake in sedentary males with obesity. Design: Eleven males with obesity (body fat percentage 36.5 ± 2.5%, body mass index 35.3 ± 4.2 kg/m2, V̇O2peak 29 ± 3.1 mL·kg−1·min−1) completed two experimental sessions: (1) no exercise (CTRL) and (2) 60 min of moderate‐intensity cycling exercise at 60% V̇O2peak (MICT) in a crossover design. Blood analysis included growth differentiation factor 15 (GDF‐15), total ghrelin, peptide tyrosine tyrosine3–36 (PYY3–36), total glucagon‐like peptide‐1 (GLP‐1), insulin, and glucose, as well as subjective appetite perceptions were measured in specific intervals. A standard breakfast at 0 h and an ad libitum meal postexercise was provided. Result: GDF‐15 (95% confidence interval [CI]: [2.48–27.28] ng/L, p = 0.021) increased immediately following MICT compared to CTRL. However, there were no differences for PYY3–36 (p = 0.480, ηp2=0.025 ${\eta }_{p}^{2}=0.025$), total ghrelin (p = 0.646, ηp2=0.011 ${\eta }_{p}^{2}=0.011$), and total GLP‐1 (p = 0.451, ηp2=0.029 ${\eta }_{p}^{2}=0.029$) between sessions. Appetite perceptions (95% CI: [(−20.38)–(−6.16)] mm, p = 0.001) were suppressed following MICT though energy intake was not different between the sessions (95% CI: [(−1904.9)–928.1] kJ, p = 0.480). Conclusion: Sixty minutes of MICT increased GDF‐15 while suppressing appetite perceptions in individuals with obesity. There was no energy compensation postexercise. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Nesfatin-1, deriving from a precursor protein, NUCB2, is a newly discovered molecule with anti-apoptotic, anti-inflammatory, antioxidant, and anorexigenic effects. It was initially identified in the central nervous system (CNS) and received increasing interest due to its energy-regulating properties. However, research showed that nesfatin-1 is also expressed in peripheral tissues, including the digestive system. The aim of this review is to give a résumé of the present state of knowledge regarding its structure, immunolocalization, and potential implications in diseases with inflammatory components. The main objective was to focus on its clinical importance as a diagnostic biomarker and potential therapeutic molecule in a variety of disorders, among which digestive disorders were of particular interest. Previous studies have shown that nesfatin-1 regulates the balance between pro- and antioxidant agents, which makes nesfatin-1 a promising therapeutic agent. Further in-depth research regarding the underlying mechanisms of action is needed for a better understanding of its effects. [ABSTRACT FROM AUTHOR]

The impact of heat stress (HS) on production is intricately linked with feed intake. We investigated the effects of HS on intestines and diencephalic genes in Pekin ducks. One hundred and sixty adult ducks were allocated to two treatment rooms. The control room was maintained at 22°C and the HS room at 35°C for the first 10 h of the day then reduced to 29.5°C. After 3 weeks, 10 hens and 5 drakes were euthanized from each room and jejunum and ileum collected for histology. Brains were collected for gene expression analysis using qRT‐PCR. Intestinal morphology data were analyzed with two‐way ANOVA and diencephalic gene data were analyzed with Kruskal–Wallis test. There was an increase in villi width in the ileum (p = .0136) and jejunum (p = .0019) of HS hens compared to controls. HS drakes showed a higher crypt depth (CD) in the jejunum (p = .0198) compared to controls. There was an increase in crypt goblet cells (GC) count in the ileum (p = .0169) of HS drakes compared to HS hens. There was higher villi GC count (p = .07) in the jejunum of HS drakes compared to controls. There was an increase in the crypt GC density (p = .0054) in the ileum, not jejunum, of HS drakes compared to HS hens. Further, there were no differences in the proopiomelanocortin gene expression in either sex but there was an increase in the expression of neuropeptide Y (NPY) gene in HS hens (p = .031) only and a decrease in the corticotropin releasing hormone gene in the HS drakes (p = .037) compared to controls. These data show that there are sex differences in the effect of HS on gut morphology while the upregulation in NPY gene may suggest a role in mediating response to chronic HS. [ABSTRACT FROM AUTHOR]

Abstract Objective To investigate the effects of moderate‐intensity aerobic exercise on appetite control parameters, appetite perceptions, and energy intake in sedentary males with obesity. Design Eleven males with obesity (body fat percentage 36.5 ± 2.5%, body mass index 35.3 ± 4.2 kg/m2, V̇O2peak 29 ± 3.1 mL·kg−1·min−1) completed two experimental sessions: (1) no exercise (CTRL) and (2) 60 min of moderate‐intensity cycling exercise at 60% V̇O2peak (MICT) in a crossover design. Blood analysis included growth differentiation factor 15 (GDF‐15), total ghrelin, peptide tyrosine tyrosine3–36 (PYY3–36), total glucagon‐like peptide‐1 (GLP‐1), insulin, and glucose, as well as subjective appetite perceptions were measured in specific intervals. A standard breakfast at 0 h and an ad libitum meal postexercise was provided. Result GDF‐15 (95% confidence interval [CI]: [2.48–27.28] ng/L, p = 0.021) increased immediately following MICT compared to CTRL. However, there were no differences for PYY3–36 (p = 0.480, ηp2=0.025), total ghrelin (p = 0.646, ηp2=0.011), and total GLP‐1 (p = 0.451, ηp2=0.029) between sessions. Appetite perceptions (95% CI: [(−20.38)–(−6.16)] mm, p = 0.001) were suppressed following MICT though energy intake was not different between the sessions (95% CI: [(−1904.9)–928.1] kJ, p = 0.480). Conclusion Sixty minutes of MICT increased GDF‐15 while suppressing appetite perceptions in individuals with obesity. There was no energy compensation postexercise.

Abstract 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.

Nesfatin-1, deriving from a precursor protein, NUCB2, is a newly discovered molecule with anti-apoptotic, anti-inflammatory, antioxidant, and anorexigenic effects. It was initially identified in the central nervous system (CNS) and received increasing interest due to its energy-regulating properties. However, research showed that nesfatin-1 is also expressed in peripheral tissues, including the digestive system. The aim of this review is to give a résumé of the present state of knowledge regarding its structure, immunolocalization, and potential implications in diseases with inflammatory components. The main objective was to focus on its clinical importance as a diagnostic biomarker and potential therapeutic molecule in a variety of disorders, among which digestive disorders were of particular interest. Previous studies have shown that nesfatin-1 regulates the balance between pro- and antioxidant agents, which makes nesfatin-1 a promising therapeutic agent. Further in-depth research regarding the underlying mechanisms of action is needed for a better understanding of its effects.

In living organisms, the central control of nutrition is a highly complex and vital mechanism. Central control of nutrition occurs in various regions of the brain, with the hypothalamus being the most important of which is the hypothalamus. The hypothalamus controls feeding behaviors through neural circuits, specialized nuclei, and central neurotransmitters. Different hypothalamic nuclei involved in regulating food intake include ARC, PVN, LHA, VMH, and DMH. The DMH influences feeding behavior by modulating the activity of different neurotransmitters in the brain. This nucleus receives both orexigenic and anorexic inputs through neural connections with the ARC and other regions of the brain. Due to its location in the brain, the ARC has access to nutritional inputs from the circulation. Within this nucleus, there exist two distinct neuronal populations, namely NPY and POMC. Different inputs from circulation affect two neuronal populations in the ARC. These inputs are related to second-order neurons, including DMH. The DMH integrates these inputs and sends the final output to PVN and LHA. Therefore, DMH affects the central control of feeding regulation through these neural pathways.

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). 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. 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. 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. [ABSTRACT FROM AUTHOR]

In living organisms, the central control of nutrition is a highly complex and vital mechanism. Central control of nutrition occurs in various regions of the brain, with the hypothalamus being the most important of which is the hypothalamus. The hypothalamus controls feeding behaviors through neural circuits, specialized nuclei, and central neurotransmitters. Different hypothalamic nuclei involved in regulating food intake include ARC, PVN, LHA, VMH, and DMH. The DMH influences feeding behavior by modulating the activity of different neurotransmitters in the brain. This nucleus receives both orexigenic and anorexic inputs through neural connections with the ARC and other regions of the brain. Due to its location in the brain, the ARC has access to nutritional inputs from the circulation. Within this nucleus, there exist two distinct neuronal populations, namely NPY and POMC. Different inputs from circulation affect two neuronal populations in the ARC. These inputs are related to second-order neurons, including DMH. The DMH integrates these inputs and sends the final output to PVN and LHA. Therefore, DMH affects the central control of feeding regulation through these neural pathways. [ABSTRACT FROM AUTHOR]

Simple Summary: The effect of feeding and feed deprivation on the regulation of feed intake in European seabass was evaluated. European seabass possess feed intake regulation mechanisms similar to those found in mammals and fish. Fasting and feeding conditions induce different responses in feed intake regulation mechanisms in European seabass. The present results are important to identify and understand the mechanisms of appetite regulation of European seabass, and therefore contribute to feeding optimization processes, ensuring the growth and sustainability of the aquaculture industry. 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Several mechanisms both inside and outside the central nervous system (CNS) collaborate to control feeding. The hypothalamus received food-related messages from different regions of the brain, and exports appropriate output through specific hypothalamic nuclei. One of the most important of these hypothalamic nuclei is the lateral hypothalamus area (LHA). In this review, multiple valid papers from electronic sources (including Web of Science, Scopus, PubMed, SID, Google Scholar, and ISI databases) were used; which in them the role of LHA in the central regulation of feeding investigated. The hypothalamus is responsible for the central control of food intake in the CNS. The arcuate nucleus, paraventricular nucleus, and LHA are specific regions in the hypothalamus that regulate food intake. The LHA is considered to be the center of hunger or feeding among these nuclei. With the interaction of orexigenic and anorexigenic neurons, as well as various neurotransmitters in several neuronal pathways, this nucleus produces increased food intake. The LHA eventually improved food intake via extensive brain connections. The LHA via various neurons and synaptic connections with other special hypothalamic nuclei involved in the control of nutritional behavior (graphical abstract) stimulated food intake. [ABSTRACT FROM AUTHOR]

Yayun Xu,1– 3 Feihu Chen1– 3 1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, People’s Republic of China; 2The Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, People’s Republic of China; 3The Key Laboratory of Anti-Inflammatory and Immune Medicines, Ministry of Education, Hefei, People’s Republic of ChinaCorrespondence: Feihu ChenDepartment of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, People’s Republic of ChinaEmail chenfeihu@ahmu.edu.cnAbstract: Nesfatin-1, a newly identified energy-regulating peptide, is widely expressed in the central and peripheral tissues, and has a variety of physiological activities. A large number of recent studies have shown that nesfatin-1 exhibits antioxidant, anti-inflammatory, and anti-apoptotic properties and is involved in the occurrence and progression of various diseases. This review summarizes current data focusing on the therapeutic effects of nesfatin-1 under different pathophysiological conditions and the mechanisms underlying its antioxidant, anti-inflammatory, and anti-apoptotic activities.Keywords: antioxidant, anti-inflammatory, anti-apoptotic, nesfatin-1, anorexigenic

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.

The influence of Artificial Light at Night (ALAN) is a severe interference in the biological rhythm of organisms. Feeding dysregulation might be the main factor responsible for developing metabolic diseases. The molecular basis of these physiological dysregulations is yet to be elucidated. The effect of light on appetite-regulating signal in the brain of zebrafish is still unknown. Therefore, the present study aimed to find the daily mRNA expression profile of two significant appetite and energy-balancing peptide hormone (leptin) and enzyme (goat) in the brain in various illumination conditions, LD (12Light:12Dark), LL (24L), and DD (24D). Moreover, Ga-SI, the protein level of the two appetite-regulating peptides, and brain and serum melatonin are measured after 72 h of incubation under three different photic conditions. The immunohistochemical localization of the primary mediators of appetite regulators, leptin and goat, in the brain of zebrafish, under different photic conditions, is reported for the first time in zebrafish. The study revealed that in continuous light after 72 h of incubation, feeding (Ga-SI) is found the highest and the translational level of two appetite-related genes (leptin and goat) is the lowest compared to LD. In continuous dark, this relation becomes opposite. The daily variation of mRNA expression of leptin and goat in LD shows peak expression at the light and dark phase, respectively. This pattern was abolished in continuous conditions. Thus, our study suggests that the photoperiod (zeitgeber) may influence the expression pattern (daily variation) of appetite-regulating peptide hormone and enzyme in the brain of zebrafish.

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In the mouse, the osteoblast-derived hormone Lipocalin-2 (LCN2) suppresses food intake and acts as a satiety signal. We show here that meal challenges increase serum LCN2 levels in persons with normal or overweight, but not in individuals with obesity. Postprandial LCN2 serum levels correlate inversely with hunger sensation in challenged subjects. We further show through brain PET scans of monkeys injected with radiolabeled recombinant human LCN2 (rh-LCN2) and autoradiography in baboon, macaque, and human brain sections, that LCN2 crosses the blood-brain barrier and localizes to the hypothalamus in primates. In addition, daily treatment of lean monkeys with rh-LCN2 decreases food intake by 21%, without overt side effects. These studies demonstrate the biology of LCN2 as a satiety factor and indicator and anorexigenic signal in primates. Failure to stimulate postprandial LCN2 in individuals with obesity may contribute to metabolic dysregulation, suggesting that LCN2 may be a novel target for obesity treatment.

High-intensity exercise inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY). Given lactate may mediate these effects, we used sodium bicarbonate (NaHCO3) supplementation in a double-blind, placebo-controlled, crossover design to investigate lactate’s purported role in exercise-induced appetite suppression. Eleven males completed two identical high-intensity interval training sessions (10 × 1 min cycling bouts at ~90% heart rate maximum interspersed with 1-min recovery), where they ingested either NaHCO3 (BICARB) or sodium chloride (NaCl) as a placebo (PLACEBO) preexercise. Blood lactate, acylated ghrelin, GLP-1, and PYY concentrations, as well as overall appetite were assessed preexercise and 0, 30, 60, and 90 min postexercise. Blood lactate was greater immediately (P < 0.001) and 30 min postexercise (P = 0.049) in the BICARB session with an increased (P = 0.009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 (P = 0.014) and 90 min postexercise (P = 0.016), with a decreased AUC (P = 0.039). The BICARB session had increased PYY (P = 0.034) with an increased AUC (P = 0.031). The BICARB session also tended (P = 0.060) to have increased GLP-1 at 30 (P = 0.003) and 60 min postexercise (P < 0.001), with an increased AUC (P = 0.030). The BICARB session tended (P = 0.059) to reduce overall appetite, although there was no difference in AUC (P = 0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression. NEW & NOTEWORTHY We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression, given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit. [ABSTRACT FROM AUTHOR]

Feeding is a complex behaviour comprised of satiety control, foraging, ingestion and subsequent digestion. Cichlids from the East African Great Lakes are renowned for their diverse trophic specializations, largely predicated on highly variable jaw morphologies. Thus, most research has focused on dissecting the genetic, morphological and regulatory basis of jaw and teeth development in these species. Here for the first time we explore another aspect of feeding, the regulation of appetite related genes that are expressed in the brain and control satiety in cichlid fishes. Using qPCR analysis, we first validate stably expressed reference genes in the brain of six haplochromine cichlid species at the end of larval development prior to foraging. We next evaluate the expression of 16 appetite related genes in herbivorous and carnivorous species from the parallel radiations of Lake Tanganyika, Malawi and Victoria. Interestingly, we find increased expression of two appetite-regulating genes (anorexigenic genes), cart and npy2r, in the brain of carnivorous species in all the three lakes. This supports the notion that appetite gene regulation might play a part in determining trophic niche specialization in divergent cichlid species, already prior to exposure to different diets. Our study contributes to the limited body of knowledge on the neurological circuitry that controls feeding transitions and adaptations in cichlids and other teleosts. [ABSTRACT FROM AUTHOR]

Neuropeptide Y family (NPY) is a potent orexigenic peptide and pancreatic polypeptide family comprising neuropeptide Y (Npy), peptide YYa (Pyya), and peptide YYb (Pyyb), which was previously known as peptide Y (PY), and tetrapod pancreatic polypeptide (PP), but has not been exhaustively documented in fish. Nonetheless, Npy and Pyy to date have been the key focus of countless research studies categorizing their copious characteristics in the body, which, among other things, include the mechanism of feeding behavior, cortical neural activity, heart activity, and the regulation of emotions in teleost. In this review, we focused on the role of neuropeptide Y gene (Npy) and peptide YY gene (Pyy) in teleost food intake. Feeding is essential in fish to ensure growth and perpetuation, being indispensable in the aquaculture settings where growth is prioritized. Therefore, a better understanding of the roles of these genes in food intake in teleost could help determine their feeding regime, regulation, growth, and development, which will possibly be fundamental in fish culture.

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder in the elderly population. Numerous epidemiological and experimental studies have demonstrated that patients who suffer from obesity or type 2 diabetes mellitu s have a higher risk of cognitive dysfunction and AD. Several recent studies demonstrat ed that food intakelowering (anorexigenic) peptides have the potential to improve metabolic disorders and that they may also potentially be useful in the treatment of neurodegenerative diseases. In this review, the neuroprotective effects of anorexigenic pept ides of both peripheral and central origins are discussed. Moreover, the role of leptin as a key modulator of energy homeostasis is discussed in relation to its interaction with anorexigenic peptides and their analogs in AD-like pathology. Although there is no pe rfect experimental model of human AD pathology, animal studies have already proven that anorexigenic peptides exhibit neuroprotective properties. This phenomenon is extremely important for the potential development of new drugs in view of the aging of the human population and of the significantly increasing incidence of AD. [ABSTRACT FROM AUTHOR]

NUCB2/nesfatin-1 is an anorexigenic peptide hormone first known for its effects on energy homeostasis. More recently, a growing evidence suggests a role of NUCB2/nesfatin-1 in emotion regulation, particularly in the modulation of anxiety, depression and emotional stress response. Since stress-related mood disorders are often comorbid with obesity, we investigated the effect of acute psychosocial stress on circulating NUCB2/nesfatin-1 in obese women and normal-weight controls and its association with symptoms of anxiety. Forty women, 20 obese and 20 normal-weight controls, (aged between 27 and 46 years) were exposed to the Trier Social Stress Test (TSST). We assessed changes of plasma NUCB2/nesfatin-1, salivary cortisol, heart rate and subjective emotional state. Symptoms of anxiety (GAD-7), depressiveness (PHQ-9), perceived stress (PSQ-20), disordered eating (EDE-Q, EDI-2) and health-related quality of life (SF-8) were measured psychometrically. Obese women were further subdivided in a high and low anxiety group. Women with obesity displayed higher psychopathology compared to normal-weight controls. The TSST induced a biological and psychological stress response in both groups (p < 0.001). In normal-weight controls NUCB2/nesfatin-1 increased in response to stress (p = 0.011) and decreased during recovery (p < 0.050), while in obese women only the decrease during recovery was significant (p = 0.002). Obese women with high anxiety displayed higher NUCB2/nesfatin-1 levels than those in the low anxiety group (TSST: +34 %, p = 0.008; control condition: +52 %, p = 0.013). Our data substantiate the involvement of NUCB2/nesfatin-1 in the modulation of stress and anxiety. It remains unclear whether the attenuated stress response in obese subjects is due to metabolic changes or mental comorbidity. • We compared the response of obese and normal-weight women to the TSST. • Obese women reported higher psychiatric comorbidity than healthy controls. • In healthy women circulating NUCB2/nesfatin-1 increased following a stressor. • In obese women NUCB2/nesfatin-1solely decreased during recovery. • Obese women with high anxiety showed higher NUCB2/nesfatin-1 than those with low anxiety. [ABSTRACT FROM AUTHOR]

Abstract Feeding can be inhibited by satiety, sickness, or food unpalatability. The central nucleus of the amygdala (CeA) has been considered the key region for processing multiple anorexigenic signals, although the detailed cellular and molecular mechanisms remain largely unclear. Here we identify that methyleugenol (ME), a novel agonist of A type ionotropic γ-aminobutyric acid receptors (GABA A Rs), significantly counteracts the anorexigenic effects caused by satiety or sickness in association with GABAergic inhibition in the CeA. Electrophysiologically, ME enhanced GABAergic transmission and repressed neuronal excitability of the CeA. Behaviorally, ME increased feeding but not affect locomotor activity and basal anxiety in naïve mice. Notably, both systemic and CeA-specific delivery of ME significantly rescued satiety- or sickness-induced inhibition of feeding. The effects of ME were mainly dependent on the GABA A Rs in the CeA. Indeed, viral-mediated, the CeA region-specific genetic knockdown of the γ2 subunit of GABA A Rs largely abolished the above pharmacological effects, while its re-expression in a subpopulation of GABAergic neurons in the CeA, that produce protein kinase C-δ (PKC-δ), recovered the effects of ME on anorexigenic signals. Taken together, these results reveal a novel molecular mechanism for counter-anorexigenic signals dependent on GABAergic inhibition in the CeA, suggesting the possibility of ME as a leading compound for anorexia treatment. Graphical abstract Image 1 Highlights • Methyleugenol enhances GABAergic transmission and represses neuronal excitability of the CeA. • Methyleugenol increases feeding but does not affect basal activity in mice. • Methyleugenol counteracts anorexigenic signals of satiety or sickness. • Effect of methyleugenol is associated with GABAergic inhibition in CeA. [ABSTRACT FROM AUTHOR]

The hypothalamus is a key integrator of nutrient-seeking signals in the form of hormones and metabolites originated in both the central nervous system and the periphery. The main autocrine and paracrine target of orexinergic-related hormones such as leptin, orexin/hypocretin, and ghrelin are neuropeptide Y neurons located in the arcuate nucleus of the hypothalamus. The aim of this study was to investigate the expression and the molecular and functional relationships between leptin, orexin/hypocretin and ghrelin receptors. Biophysical studies in a heterologous system showed physical interactions between them, with potential formation of heterotrimeric complexes. Functional assays showed robust allosteric interactions particularly different when the three receptors are expressed together. Further biochemical and pharmacological assays provided evidence of heterotrimer functional expression in primary cultures of hypothalamic neurons. These findings constitute evidence of close relationships in the action of the three hormones already starting at the receptor level in hypothalamic cells. [ABSTRACT FROM AUTHOR]

Alpha-melanocyte stimulating hormone (α-MSH) reduces food intake in birds and mammals. The objective of this experiment was to determine effects of α-MSH on food and water intake, and hypothalamic c-Fos immunoreactivity and appetite-associated factor mRNA in Japanese quail ( Coturnix japonica ), a species that has not undergone the same artificial selection for growth-related traits as the chicken. At 7 days post-hatch, 3-h-fasted quail were intracerebroventricularly (ICV) injected into the lateral ventricle with 0 (vehicle), 0.5, 5, or 50 pmol of α-MSH and food and water intake were recorded at 30 min intervals for 180 min. In the second and third experiment, quail were injected with 50 pmol α-MSH and hypothalami were collected at 1 h to determine c-Fos immunoreactivity and mRNA abundance, respectively. At 30 min, quail injected with 5 or 50 pmol of α-MSH ate and drank less than vehicle-injected quail. Quail injected with 50 pmol ate less for the entire duration of the experiment and drank less than vehicle-injected quail for 120 min post-injection. Hypothalamic expression of agouti-related peptide and DOPA decarboxylase were greater in vehicle- than α-MSH-injected quail, whereas melanocortin receptor 4 (MC4R) mRNA was greater in α-MSH- than vehicle-injected birds. Alpha-MSH injection was associated with more c-Fos immunoreactive cells in the ventromedial hypothalamus (VMH) and paraventricular nucleus (PVN) of the hypothalamus. Results suggest that the anorexigenic effect of α-MSH is conserved among avians and that effects in quail are associated with the VMH and PVN and involve MC4R. [ABSTRACT FROM AUTHOR]

Background Maintaining body weight homeostasis is a huge challenge for many people in developed as well as developing societies, where overweight and obesity are fast increasing. New strategies are needed to combat this trend. Scope and approach In this review we examine the effectiveness of the various approaches to modulating food intake. We analyze several pharmacological treatments that act on the brain and gut, focusing specifically on those that act on the gastrointestinal tract in order to change enteroendocrine hormones. Key findings and conclusions An initial review of the pharmacological approaches to limiting food intake in humans shows that acting on specific targets of the central nervous system (CNS) is not very effective. Instead, surgical approaches that limit the functionality of gastrointestinal fragments, which concomitantly changes the profile of secretion of several enterohormones, are the most effective. Since effectiveness seems to be mediated by multiple targeting, we review the bioactivity of various food-related compounds for different functions of the gastrointestinal tract. Treatments that limit ghrelin production within a threshold and activate anorexigenic enterohormones seem to be the most effective. We therefore suggest that an integrative approach based on the modulation of multiple targets with foods could help to limit food intake. [ABSTRACT FROM AUTHOR]

High-intensity exercise suppresses appetite partly through changes in peripheral appetite-regulating hormones. Lactate and IL-6 mediate the release of these hormones in animal/cell models and may provide a mechanistic link between exercise intensity and appetite regulation. The current study examined changes in appetite-regulating hormones, lactate, and IL-6 after different intensities of running. Eight males completed four experimental sessions: 1) moderate-intensity continuous training (MICT; 65% V̇o2max); 2) vigorous-intensity continuous training (VICT; 85% V̇o2max); 3) sprint interval training (SIT; repeated "all-out" sprints); and 4) Control (CTRL; no exercise). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), total peptide YY (PYY), lactate, IL-6, and appetite perceptions were measured pre-, immediately postexercise, 30 min postexercise, and 90 min postexercise. Energy intake was recorded over 3 days. VICT and SIT suppressed ghrelin (P < 0.001), although SIT elicited a greater (P = 0.016 vs. MICT) and more prolonged (P < 0.001 vs. all sessions) response. GLP-1 increased immediately after MICT (P < 0.001) and 30 min after VICT (P < 0.001) and SIT (P < 0.002), while VICT elicited a greater postexercise increase in PYY vs. MICT (P = 0.027). Postexercise changes in blood lactate and IL-6 correlated with the area under the curve values for ghrelin (r = -0.60, P < 0.001) and GLP-1 (r = 0.42, P = 0.017), respectively. Appetite was suppressed after exercise (P < 0.001), although more so after VICT (P < 0.027) and SIT (P < 0.001) vs. MICT, and energy intake was reduced on the day after VICT (P < 0.017 vs. MICT and CTRL) and SIT (P = 0.049 vs. MICT). These findings support an intensity-dependent paradigm for appetite regulation following exercise and highlight the potential involvement of lactate and IL-6.NEW & NOTEWORTHY This study examines the involvement of two potential mechanisms (lactate and IL-6) that may explain the intensity-dependent effects of acute exercise on appetite-related parameters. Our findings support a clear intensity-dependent paradigm for appetite regulation following exercise, as highlighted by the change in acylated ghrelin and the suppression of appetite and energy intake after vigorous exercise (continuous and intermittent). Further, our findings extend previous work in animal/cell models by providing evidence for the potential role of lactate and IL-6 in mediating changes in appetite-related parameters following exercise in humans. [ABSTRACT FROM AUTHOR]

LPLRFamide is a member of the RFamide peptide family that elicits an anorexigenic effect when centrally injected in chicks although the mechanism mediating this response is poorly understood. Therefore, the purpose of this experiment was to elucidate the hypothalamic mechanism of short-term anorexia after central administration of LPLRFamide in chicks. In Experiment 1 chicks centrally injected with LPLRFamide decreased food intake at 15 min but not 30 min following administration compared to vehicle-injected chicks. For Experiment 2, c-Fos immunoreactivity was quantified in several appetite-associated hypothalamic nuclei and in LPLRF-injected chicks, compared to vehicle-injected chicks, there was an increase in the number of reactive cells in the magnocellular division of the paraventricular nucleus. Lastly in Experiment 3, real time-PCR was performed and hypothalamic proopiomelanocortin (POMC) mRNA abundance was increased in LPRLFamide-injected chicks compared to vehicle-injected chicks. Thus, following central injection of LPLRFamide there is activation of the paraventricular nucleus of the hypothalamus and increased expression of hypothalamic POMC mRNA in chicks. [ABSTRACT FROM AUTHOR]

Background: Exercise interventions are often less effective at improving body composition for females than males, potentially due to post-exercise hormonal responses that increase energy intake in females. Recently, sprint interval training was shown to effectively reduce body fat in females despite being relatively low during exercise energy expenditure.Purpose: To determine whether any sex difference in total PYY, GLP-1 or perceived hunger exists following moderate-intensity continuous exercise (MICT) and sprint interval exercise (SIT) METHODS: Twenty-one active participants (11 females) participated in three sessions in a randomized crossover design: (1) MICT, 30-min cycling at 65% VO2max; (2) SIT, 6 × 30 s "all-out" sprints with 4-min recovery periods; (3) control (CTRL; no exercise). Blood samples were collected pre-exercise, immediately and 90 min post-exercise for the measurement of total PYY and GLP-1. Subjective perceptions of hunger were assessed using a visual analogue scale pre-breakfast and before all blood samples.Results: Concentrations of total PYY and GLP-1 were greater during MICT (P = 0.05) and SIT (P = 0.005) compared to CTRL. Total PYY increased more immediately post-exercise in males than females (P = 0.030). GLP-1 only increased in females following MICT (P = 0.034) and SIT (P = 0.024) compared to CTRL. Perceived hunger was lower immediately post-MICT (P = 0.016) and SIT (P = 0.006) compared to CTRL.Conclusions: These results suggest that total PYY and GLP-1 respond differently to exercise in males and females over 90 min following various exercise intensities. The observed post-exercise hormonal response would not be expected to create a compensatory increase in energy intake in females. [ABSTRACT FROM AUTHOR]

Exercise-induced changes in appetite-regulating hormones may be intensity-dependent, however a clear dose-response relationship has not been established. The purpose of this study was to examine changes in anorexigenic markers (total PYY and GLP-1) in response to rest or exercise at submaximal and supramaximal intensities. Ten active males completed four experimental sessions in randomized order: 1) Moderate intensity continuous training (MICT; 30 min cycling at 65% VO2max); 2) High intensity continuous training (HICT; 30 min cycling at 85% VO2max); 3) Sprint interval training (SIT; 6 × 30 s "all-out" cycling bouts with 4 min recovery periods); 4) Control (CTRL; no exercise). Blood samples were obtained immediately pre- and post-exercise, as well as 90-min post-exercise for the measurement of total PYY and GLP-1. Subjective hunger was assessed using a visual analog scale pre-breakfast and at the three blood sampling time-points. Total PYY concentrations increased immediately post-exercise following both HICT (P = 0.006) and SIT (P < 0.001) versus CTRL, while SIT was also greater (P = 0.005) compared to MICT. Total GLP-1 concentrations changed similarly across time-points (P < 0.001), with no differences between sessions (P = 0.280). Perceptions of hunger also changed similarly across time-points (P < 0.001) with no differences between trials (P = 0.085). These findings suggest that total PYY increases only after high-intensity exercise and exhibits a greater responsiveness to SIT compared to moderate-intensity exercise. Compensatory increases in hunger do not seem to occur at any exercise intensity. These findings support a dose-response relationship between exercise intensity and total PYY, though the effects on total GLP-1 and hunger perceptions seem unclear. [ABSTRACT FROM AUTHOR]

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 (E 2) and progesterone (P 4) 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 ˙ O 2 max in the FP and LP. E 2 , P 4 , 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 E 2 (P = 0.005, d = 1.00) and P 4 (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 (E 2 : P < 0.009; P 4 : 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, η p 2 = 0.092), GLP-1 (P = 0.226, η p 2 = 0.130), or overall appetite (P = 0.514, η p 2 = 0.066). Energy intake was greater on the day of in the LP versus the FP (P = 0.003, d = 1.2). Conclusion : 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. [ABSTRACT FROM AUTHOR]

In farmed animals, individualities have demonstrated links to health and welfare. However, differential modulation of orexigenic, anorexigenic neuroendocrine and endocrine factors in different individuals with different individualities remain unclear. Therefore, we investigated the contribution of the hypothalamic-pituitary-interrenal (HPI), anorexigenic and orexigenic signal molecules to the regulation of appetite in different individuals of adult olive flounder exposed to social isolation stress. We employed behavior assays to separate flounder into three behavioural types (proactive- 14%, intermediate- 30% and reactive- 56%). We found marked elevation in plasma corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol, and a stronger suppression of feeding post-stress in reactive than other groups. Reactive also had significantly higher CRH and urotensin (UI) mRNA levels in the preoptic area, hypothalamus, hind brain, spinal cord and caudal neurosecretory system (CNSS) than the rest of the groups. Similarly, brain anorexigenic cholecystokinin (CCK), serotonin (5-HT1A) and glucocorticoid receptor (GR) mRNA levels in the preoptic area, telencephalon, hypothalamus, hind brain and CNSS were all higher in reactive than other groups. Contrary, reactive had lower neuropeptide Y (NPY), ghrelin and prolactin mRNA levels in the preoptic area, telencephalon, hypothalamus and CNSS than other groups. There was no significant difference between proactive and intermediate in all measured parameters. Overall, the results demonstrate that social isolation stress is differentially modulated in different individuals and those CRH-related peptides, anorexigenic and orexigenic signalling molecules contribute to divergent stress response and regulation of appetite in P. olivaceus. [Display omitted] • The plasma stress hormones and gene expression are higher in reactive than intermediate and proactive groups. • The expression of anorexigenic factors in CNS are higher in reactive than intermediate and proactive groups. • The expression of orexigenic factors in CNS are lower in reactive than intermediate and proactive groups. • The appetite regulation is mediated by both stressor and individuality in fish. [ABSTRACT FROM AUTHOR]

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 (V̇o 2max )]; 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.

Nesfatin-1 is well established to induce an anorexigenic effect. Recently, nesfatin-1(30-59), was identified as active core of full length nesfatin-1(1-82) in mice, while its role in rats remains unclear. Therefore, we investigated the effects of nesfatin-1(30-59) injected intracerebroventricularly (icv) on the food intake microstructure in rats. To assess whether the effect was also mediated peripherally we injected nesfatin-1(30-59) intraperitoneally (ip). Since obesity affects the signaling of various food intake-regulatory peptides we investigated the effects of nesfatin-1(30-59) under conditions of diet-induced obesity (DIO). Male Sprague-Dawley rats fed ad libitum with standard diet were icv cannulated and injected with vehicle (5µl ddH2O) or nesfatin-1(30-59) at 0.37, 1.1 and 3.3 µg (0.1, 0.3, 0.9 nmol/rat) and the food intake microstructure assessed using a food intake monitoring system. Next, naïve rats were injected ip with vehicle (300 µl saline) or nesfatin-1(30-59) (8.1, 24.3, 72.9 nmol/kg). Lastly, rats were fed a high fat diet for 10 weeks and those developing DIO were icv cannulated. Nesfatin-1 (0.9 nmol/rat) or vehicle (5µl ddH2O) was injected icv and the food intake microstructure assessed. In rats fed standard diet, nesfatin-1(30-59) caused a dose-dependent reduction of dark phase food intake reaching significance at 0.9 nmol/rat in the period of 4-8 h post injection (-29%) with the strongest reduction during the 5th h (-75%), an effect detectable for 24 h (-12%, p

Type 2 diabetes is characterised by chronic hyperglycaemia and its incidence is highly increased by exaggerated food consumption. It results from a lack of insulin action/production, but growing evidence suggests that it might also involve hyperglucagonaemia and impaired control of glucose homeostasis by the brain. In recent years, the cocaine and amphetamine-regulated transcript (CART) peptides have generated a lot of interest in the battle against obesity because, via the brain, they exert anorexic effects and they increase energy expenditure. They are also localised, outside the brain, in discrete regions of the body and play a hormonal role in controlling various functions. In this issue of Diabetologia, the Wierup group (doi: ) shows that CART peptides are expressed heterogeneously in islet cells of various species, including humans, and that their expression is upregulated in diabetes. The authors also shine a spotlight on some interesting effects of CART peptides on islet function, including stimulation of insulin secretion and inhibition of glucagon release. CART peptides would thus be at the centre of a cooperation between the brain and the endocrine pancreas to control glucose homeostasis. Although the mechanisms of action of CART peptides remain enigmatic because no specific receptor for these peptides has so far been discovered, their potential therapeutic use is evident and represents a new challenge for future research. [ABSTRACT FROM AUTHOR]

Obesity is an escalating epidemic, but an effective noninvasive therapy is still scarce. For obesity treatment, anorexigenic neuropeptides are promising tools, but their delivery from the periphery to the brain is complicated because peptides have a low stability and limited ability to cross the blood-brain barrier. In this review, we summarize results of several studies with our newly designed lipidized analogs of prolactin-releasing peptide (PrRP). PrRP is involved in feeding and energy balance regulation as demonstrated by obesity phenotypes of both PrRP- and PrRP-receptor-knockout mice. Lipidized PrRP analogs showed binding affinity and signaling in PrRP receptor-expressing cells similar to natural PrRP. Moreover, these analogs showed high binding affinity also to anorexigenic neuropeptide FF (NPFF)-2 receptor. Acute peripheral administration of myristoylated and palmitoylated PrRP analogs to mice and rats induced strong and long-lasting anorexigenic effects and neuronal activation in the brain areas involved in food intake regulation. Two-week-long subcutaneous administration of palmitoylated PrRP31 and myristoylated PrRP20 lowered food intake, body weight, improved metabolic parameters and attenuated lipogenesis in mice with diet-induced obesity. A strong anorexigenic, body weight-reducing and glucose tolerance-improving effect of palmitoylated-PrRP31 was shown also in diet-induced obese rats after its repeated 2-week-long peripheral administration. Thus, the strong anorexigenic and body weight-reducing effects of palmitoylated PrRP31 and myristoylated PrRP20 make these analogs attractive candidates for antiobesity treatment. Moreover, PrRP receptor might be a new target for obesity therapy. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate changes in body mass index (BMI) and nesfatin-1 levels in patients with morbid obesity who had undergone laparoscopic sleeve gastrectomy (LSG). PATIENTS AND METHODS: Blood samples were collected from, and the BMI calculated of 30 morbidly obese patients pre-surgery and at 3 and 6 months post-surgery. Nesfatin-1 hormone levels were measured using enzyme-linked immunosorbent assay (ELISA). Descriptive statistical analysis of the data was performed using Kruskal-Wallis variance analysis, one-way ANOVA, and the Bonferroni-Dunn test. The correlations between continuous variables not displaying normal distribution and those displaying normal distributions were analyzed using the Spearman correlation test and the Pearson correlation test, respectively. RESULTS: The mean age of the 30 patients was 41.23 ± 10.37 years. The mean BMI values (kg/m2) were 49.30 ± 7.92, 39,48 ± 7.32, and 34.39 ± 7.56 presurgery, three months post-surgery, and six months post-surgery, respectively (p < 0.001). Mean nesfatin-1 levels (ng/ml) were 22.80 ± 14.16, 60.23 ± 52.92, and 96.99 ± 40.20 presurgery, three months post-surgery, and six months post-surgery, respectively (p < 0.001). The postoperative months 3 and 6 BMI values were significantly lower than the preoperative BMI value and the postoperative month 6 BMI value was significantly lower than the postoperative month 3 BMI value (p < 0.001). The postoperative months 3 and 6 nesfatin-1 levels were significantly higher than the preoperative nesfatin-1 levels. A negative correlation was found between age and preoperative nesfatin-1 values (p = 0.001, r = -0.0557). CONCLUSIONS: Observation of significant increases in nesfatin-1 hormone levels in morbidly obese patients who had undergone LSG indicate that nesfatin-1 has important anorexigenic effects post-surgery and may be an important component of future obesity treatments. [ABSTRACT FROM AUTHOR]

The physiological control of appetite regulation involves circulating hormones with orexigenic (appetite-stimulating) and anorexigenic (appetite-inhibiting) properties that induce alterations in energy intake via perceptions of hunger and satiety. As the effectiveness of exercise to induce weight loss is a controversial topic, there is considerable interest in the effect of exercise on the appetite-regulating hormones such as acylated ghrelin, peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and pancreatic polypeptide (PP). Research to date suggests short-term appetite regulation following a single exercise session is likely affected by decreases in acylated ghrelin and increases in PYY, GLP-1, and PP. Further, this exercise-induced response may be intensity-dependent. In an effort to guide future research, it is important to consider how exercise alters the circulating concentrations of these appetite-regulating hormones. Potential mechanisms include blood redistribution, sympathetic nervous system activity, gastrointestinal motility, cytokine release, free fatty acid concentrations, lactate production, and changes in plasma glucose and insulin concentrations. This review of relevant research suggests blood redistribution during exercise may be important for suppressing ghrelin, while other mechanisms involving cytokine release, changes in plasma glucose and insulin concentrations, SNS activity, and muscle metabolism likely mediate changes in the anorexigenic signals PYY and GLP-1. Overall, changes in appetite-regulating hormones following acute exercise appear to be intensity-dependent, with increasing intensity leading to a greater suppression of orexigenic signals and greater stimulation of anorexigenic signals. However, there is less research on how exercise-induced responses in appetite-regulating hormones differ between sexes or different age groups. A better understanding of how exercise intensity and workload affect appetite across the sexes and life stages will be a powerful tool in developing more successful strategies for managing weight. [ABSTRACT FROM AUTHOR]

Nutrients created by the digestion of food are proposed to active G protein coupled receptors on the luminal side of enteroendocrine cells e.g. the L-cell. This stimulates the release of gut hormones. Hormones released from the gut and adipose tissue play an important rol in the regulation of food intake and energy expenditure (1).Many circulating signals, including gut hormones, can influence the activity of the arcuate nucleus (ARC) neurons directly, after passing across the median eminence. The ARC is adjacent to the median eminence, a circumventricular organ with fenestrated capillaries and hence an incomplete blood-brain barrier (2). The ARC of the hypothalamus is believed to play a crucial role in the regulation of food intake and energy homeostasis. The ARC contains two populations of neurons with opposing effect on food intake (3). Medially located orexigenic neurons (i.e those stimulating appetite) express neuropeptide Y (NPY) and agouti-related protein (AgRP) (4-5). Anorexigenic neurons (i.e. those inhibiting appetite) in the lateral ARC express alpha-melanocyte stimulating hormone (α-MSH) derived from pro-opiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART) (6). The balance between activities of these neuronal circuits is critical to body weight regulation.In contrast, other peripheral signals influence the hypothalamus indirectly via afferent neuronal pathway and brainstem circuits. In this context gastrointestinal’s vagal afferents are activated by mechanoreceptors and chemoreceptors, and converge in the nucleus of the tractus solitaries (NTS) of the brainstem. Neuronal projections from the NTS, in turn, carry signals to the hypotalamus (1, 7). Gut hormones also alter the activity of the ascending vagal pathway from the gut to the brainstem. In the cases of ghrelin and Peptide tyrosine tyrosine (PYY), there are evidences for both to have a direct action on the arcuate nucleus and an action via the vagus nerve a

Nesfatin-1 is well-established to induce an anorexigenic effect. Recently, nesfatin-130−59, was identified as active core of full length nesfatin-11−82 in mice, while its role in rats remains unclear. Therefore, we investigated the effects of nesfatin-130−59 injected intracerebroventricularly (icv) on the food intake microstructure in rats. To assess whether the effect was also mediated peripherally we injected nesfatin-130−59 intraperitoneally (ip). Since obesity affects the signaling of various food intake-regulatory peptides we investigated the effects of nesfatin-130−59 under conditions of diet-induced obesity (DIO). Male Sprague–Dawley rats fed ad libitum with standard diet were icv cannulated and injected with vehicle (5μl ddH2O) or nesfatin-130−59 at 0.37, 1.1, and 3.3μg (0.1, 0.3, 0.9 nmol/rat) and the food intake microstructure assessed using a food intake monitoring system. Next, naïve rats were injected ip with vehicle (300 μl saline) or nesfatin-130−59 (8.1, 24.3, 72.9 nmol/kg). Lastly, rats were fed a high fat diet for 10 weeks and those developing DIO were icv cannulated. Nesfatin-1 (0.9 nmol/rat) or vehicle (5 μl ddH2O) was injected icv and the food intake microstructure assessed. In rats fed standard diet, nesfatin-130−59 caused a dose-dependent reduction of dark phase food intake reaching significance at 0.9 nmol/rat in the period of 4–8 h post injection (−29%) with the strongest reduction during the fifth hour (−75%), an effect detectable for 24 h (−12%, p < 0.05 vs. vehicle). The anorexigenic effect of nesfatin-130−59 was due to a reduction in meal size (−44%, p < 0.05), while meal frequency was not altered compared to vehicle. In contrast to icv injection, nesfatin-130−59 injected ip in up to 30-fold higher doses did not alter food intake. In DIO rats fed high fat diet, nesfatin-130−59 injected icv reduced food intake in the third hour post injection (−71%), an effect due to a reduced meal frequency (−27%, p < 0.05), while meal size was not altered. Taken together, nesfatin-130−59 is the active core of nesfatin-11−82 and acts centrally to reduce food intake in rats. The anorexigenic effect depends on the metabolic condition with increased satiation (reduction in meal size) under normal weight conditions, while in DIO rats satiety (reduction in meal frequency) is induced. [ABSTRACT FROM AUTHOR]

Obesity is a worldwide health problem that has reached epidemic proportions. To ameliorate this problem, one approach is the use of appetite suppressants. These compounds are frequently amphetamine congeners such as diethylpropion (DEP), phentermine (PHEN), and bupropion (BUP), whose effects are mediated through serotonin, norepinephrine, and dopaminergic pathways. The nucleus accumbens (NAc) shell receives dopaminergic inputs and is involved in feeding and motor activity. However, little is known about how appetite suppressants modulate its activity. Therefore, we characterized behavioral and neuronal NAc shell responses to shortterm treatments of DEP, PHEN, and BUP. These compounds caused a transient decrease in weight and food intake while increasing locomotion, stereotypy, and insomnia. They evoked a large inhibitory imbalance in NAc shell spiking activity that correlated with the onset of locomotion and stereotypy. Analysis of the local field potentials (LFPs) showed that all three drugs modulated beta, theta, and delta oscillations. These oscillations do not reflect an aversive-malaise brain state, as ascertained from taste aversion experiments, but tracked both the initial decrease in weight and food intake and the subsequent tolerance to these drugs. Importantly, the appetite suppressant-induced weight loss and locomotion were markedly reduced by intragastric (and intra-NAc shell) infusions of dopamine antagonists SCH-23390 (D1 receptor) or raclopride (D2 receptor). Furthermore, both antagonists attenuated appetite suppressant-induced LFP oscillations and partially restored the imbalance in NAc shell activity. These data reveal that appetite suppressant-induced behavioral and neuronal activity recorded in the NAc shell depend, to various extents, on dopaminergic activation and thus point to an important role for D1/D2-like receptors (in the NAc shell) in the mechanism of action for these anorexic compounds. [ABSTRACT FROM AUTHOR]