Hunger Hormone Research Articles

0265 WOMEN AND MEN ARE DIFFERENTIALLY AFFECTED BY SLEEP LOSS WITH RESPECT TO COGNITIVE PERFORMANCE AND HUNGER REGULATION

Recent studies have suggested that cognitive performance and hunger regulation in humans are differentially altered in men and women following restricted or misaligned sleep. Whether these sex differences extend to a night of total sleep loss - a typical scenario for many shift workers - has not yet been investigated. The present crossover study involved 13 women and 12 men (matched for age, body-mass index, chronotype score, and daytime sleepiness). One night of total sleep loss was compared to one night with an 8-hour sleep opportunity, with respect to morning cognitive performance (procedural and spatial memory processing, as well as working memory performance) and hunger regulation (measured by plasma concentrations of the hunger hormone ghrelin and subjective hunger scores). The results were analyzed separately for the sexes in order to evaluate if the response to acute sleep loss is different in women and men. Following one night of total sleep loss, female participants showed deficits in working memory and procedural memory processing. In contrast, sleep loss did not alter spatial memory processing or hunger regulation in women. In men, acute sleep loss impaired processing of both spatial and procedural memories, whereas working memory performance remained unaltered. Moreover, circulating concentrations of ghrelin and hunger were elevated in men following acute sleep loss. The results of the present study highlight the importance of investigating possible sex differences when studying functions of sleep and health consequences of sleep loss in humans. This study was supported by AFA Försäkring; Novo Nordisk Foundation; the Swedish Brain Foundation; and the Swedish Research Council. The funders did not have any role in study design or interpretation of the results; nor in the writing process.

Carbon dioxide in carbonated beverages induces ghrelin release and increased food consumption in male rats: Implications on the onset of obesity

The dangerous health risks associated with obesity makes it a very serious public health issue. Numerous studies verified a correlation between the increase in obesity and the parallel increase in soft drink consumption among world populations. The effects of one main component in soft drinks namely the carbon dioxide gas has not been studied thoroughly in any previous research. Male rats were subjected to different categories of drinks and evaluated for over a year. Stomach ex vivo experiments were undertaken to evaluate the amount of ghrelin upon different beverage treatments. Moreover, 20 male students were tested for their ghrelin levels after ingestion of different beverages. Here, we show that rats consuming gaseous beverages over a period of around 1 year gain weight at a faster rate than controls on regular degassed carbonated beverage or tap water. This is due to elevated levels of the hunger hormone ghrelin and thus greater food intake in rats drinking carbonated drinks compared to control rats. Moreover, an increase in liver lipid accumulation of rats treated with gaseous drinks is shown opposed to control rats treated with degassed beverage or tap water. In a parallel study, the levels of ghrelin hormone were increased in 20 healthy human males upon drinking carbonated beverages compared to controls. These results implicate a major role for carbon dioxide gas in soft drinks in inducing weight gain and the onset of obesity via ghrelin release and stimulation of the hunger response in male mammals.

Appetite responses to high-fat meals or diets of varying fatty acid composition: a comprehensive review.

Dietary fatty acids (FA) act as signaling molecules with diverse effects on physiologic function. The aim of this article is to review and summarize the clinical human studies in the literature on how dietary FA composition in meals and diets affects hunger and satiety signaling in the body. Studies examining FA saturation (monounsaturated (MUFA), saturated or polyunsaturated (PUFA) FAs) or FA chain length from high-fat meals/diets were included. Measures of appetite included visual analog scale (VAS) questionnaires, appetite hormones (Cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), gastric insulinotropic polypeptide gastric inhibitory peptide (GIP), ghrelin, leptin, insulin) and/or energy intake (EI) data. VAS measures in 9 out of 13 studies were not influenced by FA saturation. PUFAs, followed by MUFAs, tended to induce the greatest stimulatory effect on GLP-1, GIP and PYY, which was found in 6 out of 11 studies measuring appetite-related hormones. Regarding FA chain length, five of six studies show either no difference or less hunger (VAS) and greater satiety hormone levels (two of six studies) for FAs with longer chain lengths. EI does not seem to be affected by the saturation of FAs while EI was inconclusive for studies comparing FA chain length. Possibly due to the inconsistencies in study design, little agreement is observed between the studies on the impact of FA composition on hormonal and subjective measures of appetite as well as EI. Therefore, more research on the long-term impact of dietary FA composition on appetite control may provide clearer outcomes.

The Sweetener-Sensing Mechanisms of the Ghrelin Cell.

Carbohydrate administration decreases plasma levels of the ‘hunger hormone’ ghrelin. The ghrelin cell is co-localized with the sweet taste receptor subunit, TAS1R3, and the gustatory G-protein, gustducin, both involved in the sensing of sweeteners by entero-endocrine cells. This study investigated the role of gustducin-mediated sweet taste receptor signaling on ghrelin secretion in a gastric ghrelinoma cell line, tissue segments and mice. The monosaccharide d-glucose and low-intensity sweetener oligofructose (OFS) decreased (p < 0.001) ghrelin secretion while the high-intensity sweetener sucralose increased (p < 0.001) ghrelin secretion in vitro. These effects were not mediated via the sweet taste receptor or glucose transporters (the sodium-dependent glucose cotransporter SGLT-1 and GLUT2). The effect of these compounds was mimicked ex vivo in gastric and jejunal segments from both wild type (WT) and α-gustducin knockout (α-gust−/−) mice. In vivo, the sensing of d-glucose was polarized since intragastric but not intravenous administration of d-glucose decreased (p < 0.05) ghrelin levels in an α-gustducin independent manner which involved inhibition of duodenal ghrelin release. In contrast, neither OFS nor sucralose affected ghrelin secretion in vivo. In conclusion, α-gustducin-mediated sweet taste receptor signaling does not play a functional role in the sensing of carbohydrates, or low- or high-intensity sweeteners by the ghrelin cell.

Gut Hormones and Regulation of Food Intake in Birds.

Gut hormones act as appetite regulatory hormones in mammals. For example, the hunger hormone ghrelin, which is released from the stomach before food intake, stimulates appetite. In contrast, satiety hormones such as cholecystokinin, glucagon-like peptide-1, and peptide YY, which are released from the intestines after food intake, suppress appetite. The effects of these peptides on food intake have been shown to be similar in both mammals and fishes. However, evidence suggests that the physiological roles of these gut hormones may be different between birds and other vertebrates. This review summarizes the current information on the roles of gut hormones in the regulation of food intake in birds, especially in chickens.

Interactive effects of ghrelin and ketamine on forced swim performance: Implications for novel antidepressant strategies

The efficacy of ketamine to alleviate depressive symptoms has promoted a wealth of research exploring alternate therapeutic targets for depression. Given the caveats of ketamine treatment taken together with the increasingly greater emphasis on combinatorial therapeutic approaches to depression, we sought to asses whether the hypothalamic “hunger hormone”, ghrelin, would augment the effects of ketamine. Indeed, ghrelin has recently been found to possess antidepressant potential and may be especially effective against the metabolic and feeding deficits observed with depression. Two studies were performed: 1. mice were given an intraperitoneal injection of ghrelin (80μg/kg) or saline, followed by a saline or a low or high dose of ketamine (5 or 10mg/kg) and 2. mice received 10mg/kg of ketamine together with saline or the ghrelin receptor antagonist JMV2959 (3 or 6mg/kg) and Forced Swim Test (FST) performance was assessed. In both studies, ketamine alone reduced FST immobility. Similarly, ghrelin alone reduced swim immobility suggesting an antidepressant-like response. However, ghrelin did not augment the impact of ketamine when co-administered and in fact, it appeared to antagonize its actions at the lower dose. As well, JMV2959 did not significantly influence FST performance. These data confirm the antidepressant-like effects of ketamine and further suggest that ghrelin might have similar properties. Yet, our results caution against combinatorial treatment with these agents, probably owing to unexpected allosteric or other antagonist actions.

Butyrylcholinesterase Deficiency Promotes Adipose Tissue Growth and Hepatic Lipid Accumulation in Male Mice on High-Fat Diet.

Despite numerous reports of relationships between weight gain and butyrylcholinesterase (BChE), this enzyme's role in the genesis of obesity remains unclear, but recent research points to strong links with ghrelin, the "hunger hormone." The availability of BChE knockout (KO) mice provides an opportunity to clarify the causal relationship between BChE and obesity onset. We now find that young KO mice have abnormally high plasma ghrelin levels that slowly decline during long-term high-fat feeding and ultimately drop below those in wild-type mice. On such a diet, the KO mice gained notably more weight, more white fat, and more hepatic fat than wild-type animals. In addition to a greater burden of hepatic triglycerides, the livers of these KO mice show distinctly higher levels of inflammatory markers. Finally, their energy expenditure proved to be lower than in wild-type mice despite similar activity levels and increased caloric intake. A gene transfer of mouse BChE with adeno-associated virus vector restored nearly all aspects of the normal phenotype. Our results indicate that BChE strongly affects fat metabolism, has an important impact on fat accumulation, and may be a promising tool for combating obesity.

Ghrelin treatment prevents development of activity based anorexia in mice

Stimulation of feeding is necessary for treatment of pathological conditions of chronic malnutrition due to anorexia. Ghrelin, a hunger hormone, is one of the candidate for pharmacological treatments of anorexia, but because of its instability in plasma has limited efficacy. We previously showed that plasmatic IgG protect ghrelin from degradation and that IgG from obese subjects and mice may increase ghrelin׳s orexigenic effect. In this study we tested if ghrelin alone or combined with IgG may improve feeding in chronically food-restricted mice with or without physical activity-based anorexia (ABA) induced by free access to a running wheel. Mice received a single daily intraperitoneal injection of ghrelin (1nM) together or not with total IgG (1nM) from obese ob/ob or lean mice before access to food during 8 days of 3h/day feeding time. We found that both ghrelin and ghrelin combined with IgG from obese, but not lean mice, prevented ABA, however, they were not able to diminish body weight loss. Physical activity was lower during the feeding period and was increased shortly after feeding in mice receiving ghrelin together with IgG from obese mice. In food-restricted mice without ABA, ghrelin treatments did not have significant effects on food intake. Thus, this study supports pharmacological use of ghrelin or ghrelin combined with IgG from obese animals for treatment of anorexia accompanied by elevated physical activity. The utility of combining ghrelin with protective IgG should be further determined in animal models of anorexia with unrestricted access to food.

Unexpected Reaction Pathway for butyrylcholinesterase-catalyzed inactivation of "hunger hormone" ghrelin.

Extensive computational modeling and simulations have been carried out, in the present study, to uncover the fundamental reaction pathway for butyrylcholinesterase (BChE)-catalyzed hydrolysis of ghrelin, demonstrating that the acylation process of BChE-catalyzed hydrolysis of ghrelin follows an unprecedented single-step reaction pathway and the single-step acylation process is rate-determining. The free energy barrier (18.8 kcal/mol) calculated for the rate-determining step is reasonably close to the experimentally-derived free energy barrier (~19.4 kcal/mol), suggesting that the obtained mechanistic insights are reasonable. The single-step reaction pathway for the acylation is remarkably different from the well-known two-step acylation reaction pathway for numerous ester hydrolysis reactions catalyzed by a serine esterase. This is the first time demonstrating that a single-step reaction pathway is possible for an ester hydrolysis reaction catalyzed by a serine esterase and, therefore, one no longer can simply assume that the acylation process must follow the well-known two-step reaction pathway.

Centrally Administered Ghrelin Acutely Influences Food Choice in Rodents.

We sought to determine whether the orexigenic hormone, ghrelin, is involved in the intrinsic regulation of food choice in rats. Ghrelin would seem suited to serve such a role given that it signals hunger information from the stomach to brain areas important for feeding control, including the hypothalamus and reward system (e.g. ventral tegmental area, VTA). Thus, in rats offered a choice of palatable foods (sucrose pellets and lard) superimposed on regular chow for 2 weeks, we explored whether acute central delivery of ghrelin (intracerebroventricular (ICV) or intra-VTA) is able to redirect their dietary choice. The major unexpected finding is that, in rats with high baseline lard intake, acute ICV ghrelin injection increased their chow intake over 3-fold, relative to vehicle-injected controls, measured at both 3 hr and 6 hr after injection. Similar effects were observed when ghrelin was delivered to the VTA, thereby identifying the VTA as a likely contributing neurobiological substrate for these effects. We also explored food choice after an overnight fast, when endogenous ghrelin levels are elevated, and found similar effects of dietary choice to those described for ghrelin. These effects of fasting on food choice were suppressed in models of suppressed ghrelin signaling (i.e. peripheral injection of a ghrelin receptor antagonist to rats and ghrelin receptor (GHSR) knock-out mice), implicating a role for endogenous ghrelin in the changes in food choice that occur after an overnight fast. Thus, in line with its role as a gut-brain hunger hormone, ghrelin appears to be able to acutely alter food choice, with notable effects to promote “healthy” chow intake, and identify the VTA as a likely contributing neurobiological substrate for these effects.

Physiological roles for butyrylcholinesterase: A BChE-ghrelin axis

Butyrylcholinesterase (BChE) has long been regarded as an “orphan enzyme” with no specific physiological role other than to metabolize exogenous bioactive esters in the diet or in medicines. Human beings with genetic mutations that eliminate all BChE activity appear completely normal, and BChE-knockout mice have been described as “lacking a phenotype” except for faster weight gain on high-fat diets. However, our recent studies with viral gene transfer of BChE in mice reveal that BChE hydrolyzes the so-called “hunger hormone,” ghrelin, at a rate which strongly affects the circulating levels of this peptide hormone. This action has important consequences for weight gain and fat metabolism. Surprisingly, it also impacts emotional behaviors such as aggression. Overexpression of BChE leads to low ghrelin levels in the blood stream and reduces aggression and social stress in mice. Under certain circumstances these combined effects contribute to increased life-span in group-housed animals. These findings may generalize to humans, as recent clinical studies by multiple investigators indicate that, among patients with severe cardiovascular disease, longevity correlates with increasing levels of plasma BChE activity.

Stress and Overeating

Submit Manuscript | http://medcraveonline.com Numerous studies showed that physical and emotional distress increases the intake of high sugary and high fatty foods in personal preferences list.These foods in this condition served as COMFORT FOODS for these people. High cortisol level in combination of high insulin levels increases one’s appetite including motivation towards eating.These hormones also contribute fat deposition around the waist line. That’s why two indicators of chronic stress: low socioeconomic status and job pressures have been strongly associated with abdominal obesity. Some studies show a significant role of Ghrelin a hunger hormone in it also. There is a mark Gender difference in Stress coping behavior, as women are more likely to turn to foods and men towards alcohol and smoking [1,6,7].

Central ghrelin increases food foraging/hoarding that is blocked by GHSR antagonism and attenuates hypothalamic paraventricular nucleus neuronal activation.

The stomach-derived "hunger hormone" ghrelin increases in the circulation in direct response to time since the last meal, increasing preprandially and falling immediately following food consumption. We found previously that peripheral injection of ghrelin potently stimulates food foraging (FF), food hoarding (FH), and food intake (FI) in Siberian hamsters. It remains, however, largely unknown if central ghrelin stimulation is necessary/sufficient to increase these behaviors regardless of peripheral stimulation of the ghrelin receptor [growth hormone secretagogue receptor (GHSR)]. We injected three doses (0.01, 0.1, and 1.0 μg) of ghrelin into the third ventricle (3V) of Siberian hamsters and measured changes in FF, FH, and FI. To test the effects of 3V ghrelin receptor blockade, we used the potent GHSR antagonist JMV2959 to block these behaviors in response to food deprivation or a peripheral ghrelin challenge. Finally, we examined neuronal activation in the arcuate nucleus and paraventricular hypothalamic nucleus in response to peripheral ghrelin administration and 3V GHSR antagonism. Third ventricular ghrelin injection significantly increased FI through 24 h and FH through day 4. Pretreatment with 3V JMV2959 successfully blocked peripheral ghrelin-induced increases in FF, FH, and FI at all time points and food deprivation-induced increases in FF, FH, and FI up to 4 h. c-Fos immunoreactivity was significantly reduced in the paraventricular hypothalamic nucleus, but not in the arcuate nucleus, following pretreatment with intraperitoneal JMV2959 and ghrelin. Collectively, these data suggest that central GHSR activation is both necessary and sufficient to increase appetitive and consummatory behaviors in Siberian hamsters.

Sleeve gastrectomy effects on hunger, satiation, and gastrointestinal hormone and motility responses after a liquid meal test

The relation between hunger, satiation, and integrated gastrointestinal motility and hormonal responses in morbidly obese patients after sleeve gastrectomy has not been determined. The objective was to assess the effects of sleeve gastrectomy on hunger, satiation, gastric and gallbladder motility, and gastrointestinal hormone response after a liquid meal test. Three groups were studied: morbidly obese patients (n = 16), morbidly obese patients who had had sleeve gastrectomy (n = 8), and nonobese patients (n = 16). The participants fasted for 10 h and then consumed a 200-mL liquid meal (400 kcal + 1.5 g paracetamol). Fasting and postprandial hunger, satiation, hormone concentrations, and gastric and gallbladder emptying were measured several times over 4 h. No differences were observed in hunger and satiation curves between morbidly obese and nonobese groups; however, sleeve gastrectomy patients were less hungry and more satiated than the other groups. Antrum area during fasting in morbidly obese patients was statistically significant larger than in the nonobese and sleeve gastrectomy groups. Gastric emptying was accelerated in the sleeve gastrectomy group compared with the other 2 groups (which had very similar results). Gallbladder emptying was similar in the 3 groups. Sleeve gastrectomy patients showed the lowest ghrelin concentrations and higher early postprandial cholecystokinin and glucagon-like peptide 1 peaks than did the other participants. This group also showed an improved insulin resistance pattern compared with morbidly obese patients. Sleeve gastrectomy seems to be associated with profound changes in gastrointestinal physiology that contribute to reducing hunger and increasing sensations of satiation. These changes include accelerated gastric emptying, enhanced postprandial cholecystokinin and glucagon-like peptide 1 concentrations, and reduced ghrelin release, which together may help patients lose weight and improve their glucose metabolism after surgery. This trial was registered at clinicaltrials.gov as NCT02414893.

Blockade of growth hormone secretagogue receptor 1A signaling by JMV 2959 attenuates the NMDAR antagonist, phencyclidine-induced impairments in prepulse inhibition.

RationaleSchizophrenic-spectrum patients commonly display deficits in preattentive information processing as evidenced, for example, by disrupted prepulse inhibition (PPI), a measure of sensorimotor gating. Similar disruptions in PPI can be induced in rodents and primates by the psychotomimetic drug phencyclidine (PCP), a noncompetitive inhibitor of the NMDA receptor. Mounting evidence suggests that the hunger hormone ghrelin and its constitutively active receptor influences neuronal circuits involved in the regulation of mood and cognition.ObjectivesIn the present series of experiments, we investigated the effects of ghrelin and the growth hormone secretagogue receptor (GHS-R1A) neutral antagonist, JMV 2959, on acoustic startle responses (ASR), PPI, and PCP-induced alterations in PPI.ResultsIntraperitoneal (i.p.) administration of ghrelin (0.033, 0.1, and 0.33 mg/kg) did not alter the ASR or PPI in rats. Conversely, i.p. injection of JMV 2959 (1, 3, and 6 mg/kg), dose dependently decreased the ASR and increased PPI. Pretreatment with JMV 2959 at a dose with no effect on ASR or PPI per se, completely blocked PCP-induced (2 mg/kg) deficits in PPI while pretreatment with the highest dose of ghrelin did not potentiate or alter PPI responses of a sub-threshold dose of PCP (0.75 mg/kg).ConclusionThese findings indicate that the GHS-R1A is involved in specific behavioral effects of PCP and may have relevance for patients with schizophrenia.

Hunger in pregnant sows: Effects of a fibrous diet and free access to straw

Fibrous diets and the provision of straw have been suggested to reduce feeding motivation in pregnant sows. The present experiment investigated the separate and interactive effects of a fibrous diet and ad libitum access to straw on feeding motivation, oral behaviour and plasma levels of metabolites and hormones in pregnant sows. Ten groups of three pregnant sows were housed in pens with concrete floor where a limited amount of chopped straw (approx. 330g/sow) was provided daily. In 5 of the 10 groups sows had free access to uncut straw in racks in addition to the chopped straw (Ad libitum straw), while the remaining 5 groups did not (Limited straw). The experimental period (week 2–9 of pregnancy) was divided into two 4-week periods and in a cross-over design sows within groups were fed a standard control diet (18% dietary fibre) during one period and a fibrous diet containing sugar beet pulp (35% dietary fibre) during the other period. Both diets were offered restrictively at 22MJ net energy per day and throughout the experimental period sows were fed twice daily at 0800 and 1500h. At the end of each 4-week period the undisturbed behaviour of the sows was recorded during two 24h periods. Furthermore, the sows’ feeding motivation was assessed during behavioural tests, and blood samples were draw via a jugular vein catheter, at 0700, 0900, 1200 and 1900h in a balanced design. Feeding motivation was not affected by diet or straw. However, feeding motivation was highest 1h before morning feeding indicated by a higher number of rewards earned during the entire test (P<0.01) and during the first 5min of the test (P<0.001). In the period where sows were fed the fibrous diet they manipulated the floor less frequently (P<0.02) and drank water less frequently (P<0.02) than in the period they were fed the control diet. Sows with limited access to straw manipulated equipment less frequently during the period they were fed the fibre diet, while no effect of diet was seen among sows with ad libitum straw (diet×straw interaction P<0.001). In conclusion, feeding motivation was not reduced by a fibrous diet or by ad libitum provision of straw. However, a fibrous diet did reduce frequency of drinking and floor directed explorative behaviour suggesting some alleviation of the adverse effects of hunger as supported by higher plasma levels of short-chain fatty acids and lower levels of the hunger hormone Ghrelin. Ad libitum straw did not reduce feeding motivation, but more lateral lying in sows with ad libitum straw suggests that the straw provided increased lying comfort.

Brain circuits mediating the orexigenic action of peripheral ghrelin: narrow gates for a vast kingdom.

Fil: Cabral, Agustina Soledad. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - La Plata. Instituto Multidisciplinario de Biologia Celular. Provincia de Buenos Aires. Gobernacion. Comision de Investigaciones Cientificas. Instituto Multidisciplinario de Biologia Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biologia Celular; Argentina

Ghrelin-reactive immunoglobulins and anxiety, depression and stress-induced cortisol response in adolescents. The TRAILS study.

Ghrelin, a hunger hormone, has been implicated in the regulation of stress-response, anxiety and depression. Ghrelin-reactive immunoglobulins (Ig) were recently identified in healthy and obese humans showing abilities to increase ghrelin's stability and orexigenic effects. Here we studied if ghrelin-reactive Ig are associated with anxiety and depression and with the stress-induced cortisol response in a general population of adolescents. Furthermore, to test the possible infectious origin of ghrelin-reactive Ig, their levels were compared with serum IgG against common viruses. We measured ghrelin-reactive IgM, IgG and IgA in serum samples of 1199 adolescents from the Dutch TRAILS study and tested their associations with 1) anxiety and depression symptoms assessed with the Youth Self-Report, 2) stress-induced salivary cortisol levels and 3) IgG against human herpesvirus 1, 2, 4 and 6 and Influenza A and B viruses. Ghrelin-reactive IgM and IgG correlated positively with levels of antibodies against Influenza A virus. Ghrelin-reactive IgM correlated negatively with antibodies against Influenza B virus. Ghrelin-reactive IgM correlated positively with anxiety scores in girls and ghrelin-reactive IgG correlated with stress-induced cortisol secretion, but these associations were weak and not significant after correction for multiple testing. These data indicate that production of ghrelin-reactive autoantibodies could be influenced by viral infections. Serum levels of ghrelin-reactive autoantibodies probably do not play a role in regulating anxiety, depression and the stress-response in adolescents from the general population.

The role of ghrelin signalling for sexual behaviour in male mice.

Ghrelin, a gut-brain signal, is well known to regulate energy homeostasis, food intake and appetite foremost via hypothalamic ghrelin receptors (GHS-R1A). In addition, ghrelin activates the reward systems in the brain, namely the mesolimbic dopamine system, and regulates thereby the rewarding properties of addictive drugs as well as of palatable foods. Given that the mesolimbic dopamine system mandates the reinforcing properties of addictive drugs and natural rewards, such as sexual behaviour, we hypothesize that ghrelin plays an important role for male sexual behaviour, a subject for the present studies. Herein we show that ghrelin treatment increases, whereas pharmacological suppression (using the GHSR-1A antagonist JMV2959) or genetic deletion of the GHS-R1A in male mice decreases the sexual motivation for as well as sexual behaviour with female mice in oestrus. Pre-treatment with L-dopa (a dopamine precursor) prior to treatment with JMV2959 significantly increased the preference for female mouse compared with vehicle treatment. On the contrary, treatment with 5-hydroxythyptohan (a precursor for serotonin) prior to treatment with JMV2959 decreased the sexual motivation compared to vehicle. In separate experiments, we show that ghrelin and GHS-R1A antagonism do not affect the time spent over female bedding as measured in the androgen-dependent bedding test. Collectively, these data show that the hunger hormone ghrelin and its receptor are required for normal sexual behaviour in male mice and that the effects of the ghrelin signalling system on sexual behaviour involve dopamine neurotransmission.

Effect of aerobic exercise on hunger feelings and satiety regulating hormones in obese teenage girls.

Exercise is implicated in modifying subsequent energy intake (EI) through alterations in hunger and/or satiety hormones. Our aim was to examine the effects of aerobic exercise on hunger, satiety regulatory peptides, and EI in obese adolescents. Nine obese girls (age: 13-18 years old, BMI: 33.74 ± 4.04 kg/m2) participated in this randomized controlled crossover study. Each participant randomly underwent 2 experimental protocols: control (seated for 150 min) and exercise (exercised for 30 min on a treadmill performed at ventilatory threshold [VT] intensity and then remained seated for 120 min). Leptin, peptide YY(3-36) (PYY(3-36)), and subjective hunger were measured at baseline as well as 30 min and 150 min, followed by 24-hr EI measurement. Exercise session resulted in an acute increase in PYY(3-36) (p < .01) without changes in leptin and/or hunger scores. The control session increased hunger scores (p < .01) and decreased circulating leptin levels (p = .03). There was a strong effect size for carbohydrate intake (d = 2.14) and a modest effect size for protein intake (d = 0.61) after the exercise compared with the control session. Exercise performed at VT intensity in this study appears to provoke a state of transient anorexia in obese girls. These changes may be linked to an increase in circulating PYY3-36 and maintenance of leptin levels.