-
Nutrients Apr 2023There is evidence that reduced sleep duration increases hunger, appetite, and food intake, leading to metabolic diseases, such as type 2 diabetes and obesity. However,... (Randomized Controlled Trial)
Randomized Controlled Trial
OBJECTIVE
There is evidence that reduced sleep duration increases hunger, appetite, and food intake, leading to metabolic diseases, such as type 2 diabetes and obesity. However, the impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. We aimed to evaluate the impact of sleep loss during the late vs. early part of the night on the regulation of hunger, appetite, and desire for food.
METHODS
Fifteen normal-weight ([mean ± SEM] body-mass index: 23.3 ± 0.4 kg/m) healthy men were studied in a randomized, balanced, crossover design, including two conditions of sleep loss, i.e., 4 h sleep during the first night-half ('late-night sleep loss'), 4 h sleep during the second night-half ('early-night sleep loss'), and a control condition with 8h sleep ('regular sleep'), respectively. Feelings of hunger and appetite were assessed through visual analogue scales, and plasma ghrelin and leptin were measured from blood samples taken before, during, and after night-time sleep.
RESULTS
Ghrelin and feelings of hunger and appetite, as well as the desire for food, were increased after 'late-night sleep loss', but not 'early-night sleep loss', whereas leptin remained unaffected by the timing of sleep loss.
CONCLUSIONS
Our data indicate that timing of sleep restriction modulates the effects of acute sleep loss on ghrelin and appetite regulation in healthy men. 'Late-night sleep loss' might be a risk factor for metabolic diseases, such as obesity and type 2 diabetes. Thereby, our findings highlight the metabolic relevance of chronobiological sleep timing.
Topics: Male; Humans; Appetite Regulation; Leptin; Ghrelin; Diabetes Mellitus, Type 2; Sleep; Obesity
PubMed: 37432152
DOI: 10.3390/nu15092035 -
European Review For Medical and... Dec 2023Anorexia nervosa (AN), a severe psychiatric disorder primarily affecting adolescents and young adults, is characterized by extreme dietary restriction and distorted body...
OBJECTIVE
Anorexia nervosa (AN), a severe psychiatric disorder primarily affecting adolescents and young adults, is characterized by extreme dietary restriction and distorted body image. While the psychological aspects of AN are well-documented, its intricate metabolic underpinnings remain less explored. We think that metabolomic analysis of hair samples emerges as a promising tool to unveil the complex physiological alterations in AN. This study aims to comprehensively profile amino acid concentrations in hair samples from AN patients and healthy controls. Additionally, it seeks to elucidate potential correlations between amino acid alterations and appetite dysregulation in AN, thereby shedding light on the physiological basis of this debilitating disorder.
PATIENTS AND METHODS
A total of 25 AN patients and 25 age-matched healthy controls were recruited for this study. Hair samples were collected, and metabolites were extracted and analyzed using high-resolution liquid chromatography-mass spectrometry. Clinical data and biochemical markers were also gathered to characterize participants' demographic and clinical profiles.
RESULTS
Metabolomic analysis revealed significant alterations in amino acid concentrations in AN patients compared to healthy controls. Notably, deficiencies in essential amino acids (EAAs) and branched-chain amino acids (BCAAs) were observed, highlighting potential contributors to muscle wasting and appetite dysregulation. Further analysis identified specific amino acids as robust biomarkers capable of distinguishing AN patients with high sensitivity and specificity.
CONCLUSIONS
This study unveils the complex metabolic disturbances associated with AN and underscores the role of amino acid dysregulation in the disorder's pathophysiology. The identified biomarkers hold promise for diagnostic screening and potential therapeutic interventions, opening avenues for personalized approaches in AN treatment. Ultimately, this research contributes to our understanding of chronic disorders through the lens of metabolomics and the chemosensory underpinnings of appetite regulation.
Topics: Adolescent; Young Adult; Humans; Amino Acids; Anorexia Nervosa; Appetite Regulation; Metabolomics; Biomarkers
PubMed: 38112949
DOI: 10.26355/eurrev_202312_34691 -
Physiology & Behavior Sep 2011Obesity is a serious and growing public health problem in the United States and the world. While weight loss is associated with significant benefits in obesity-related... (Review)
Review
Obesity is a serious and growing public health problem in the United States and the world. While weight loss is associated with significant benefits in obesity-related co-morbidities, successful long-term weight loss maintenance is extremely difficult. This limited success is primarily due to biologic mechanisms that clearly favor weight regain. The weight-reduced state is associated with not only reductions in energy expenditure and changes in substrate metabolism but also in increased energy intake. Measures of appetite (increased hunger, reduced satiety) clearly change with weight loss. These changes in appetite may be mediated by alterations of peripheral appetite-related signals, such as leptin and meal-related gut peptides, promoting energy intake. Furthermore, significant changes in the neuronal response to food-related cues in the weight-reduced state have also been shown, stressing the importance of the interactions between homeostatic and non-homeostatic regulation of energy intake. In summary, the weight-reduced state is clearly associated with a dysregulation of energy balance regulation, resulting in a milieu promoting weight regain, and thus being one of the major obstacles of "treating" obesity and reducing its comorbidities. This paper will review the adaptations in the central regulation of energy intake that occur after weight-loss or in the weight-reduce state in humans, including changes in peripheral appetite-related signals and neuroimaging studies examining the brain's response to weight loss.
Topics: Adaptation, Biological; Appetite Regulation; Brain; Energy Intake; Humans; Models, Biological; Obesity; Weight Gain; Weight Loss
PubMed: 21496461
DOI: 10.1016/j.physbeh.2011.04.003 -
Frontiers in Endocrinology 2023N-lactoylphenylalanine (Lac-Phe) is a new form of "exerkines" closely related to lactate (La), which may be able to inhibit appetite. Blood flow restriction (BFR) can... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
N-lactoylphenylalanine (Lac-Phe) is a new form of "exerkines" closely related to lactate (La), which may be able to inhibit appetite. Blood flow restriction (BFR) can lead to local tissue hypoxia and increase lactate accumulation. Therefore, this study investigated the effects of combining Moderate-intensity Continuous Exercise (MICE) with BFR on Lac-Phe and appetite regulation in obese adults.
METHODS
This study employed the cross-design study and recruited 14 obese adults aged 18-24 years. The participants were randomly divided into three groups and performed several tests with specific experimental conditions: (1) M group (MICE without BFR, 60%VO, 200 kJ); (2) B group (MICE with BFR, 60%VO, 200 kJ); and (3) C group (control session without exercise). Participants were given a standardized meal 60 min before exercise and a ad libitum 60 min after exercise. In addition, blood and Visual Analogue Scale (VAS) were collected before, immediately after, and 1 hour after performing the exercise.
RESULTS
No significant difference in each index was detected before exercise. After exercise, the primary differential metabolites detected in the M and B groups were xanthine, La, succinate, Lac-Phe, citrate, urocanic acid, and myristic acid. Apart from that, the major enrichment pathways include the citrate cycle, alanine, aspartate, and glutamate metabolism. The enhanced Lac-Phe and La level in the B group was higher than M and C groups. Hunger of the B group immediately after exercise substantially differed from M group. The total ghrelin, glucagon-like peptide-1 and hunger in the B group 1 hour after exercise differed substantially from M group. The results of calorie intake showed no significant difference among the indexes in each group.
CONCLUSIONS
In conclusion, this cross-design study demonstrated that the combined MICE and BFR exercise reduced the appetite of obese adults by promoting the secretion of Lac-Phe and ghrelin. However, the exercise did not considerably affect the subsequent ad libitum intake.
Topics: Adult; Humans; Appetite Regulation; Blood Flow Restriction Therapy; Citrates; Ghrelin; Lactates; Obesity
PubMed: 38116312
DOI: 10.3389/fendo.2023.1289574 -
Acta Biochimica Et Biophysica Sinica Mar 2009Ghrelin, a 28 amino acid gut brain peptide, acts as an endogenous ligand for its receptor, the growth hormone secretagogue receptor, to exercise a variety of functions... (Review)
Review
Ghrelin, a 28 amino acid gut brain peptide, acts as an endogenous ligand for its receptor, the growth hormone secretagogue receptor, to exercise a variety of functions ranging from stimulation of growth hormone secretion, regulation of appetite and energy metabolism, and cell protection to modulation of inflammation. This review summarizes the advance in the regulation of ghrelin expression and secretion. We introduce the structure of ghrelin promoter, the processing and modification of ghrelin precursor, and the regulation mechanism in these processes. Then we discuss factors found to be important in the regulation of ghrelin production, including nutrients, hormones, and autonomic nervous system. Finally, we outline the alteration in the level of ghrelin in certain physiological and pathological status.
Topics: Animals; Appetite Regulation; Autonomic Nervous System; Eating; Energy Metabolism; Ghrelin; Humans; Inflammation; Peptide Hormones; Receptors, Ghrelin
PubMed: 19280057
DOI: 10.1093/abbs/gmp001 -
International Journal of Molecular... Jan 2017Ghrelin is the only known peripherally-derived orexigenic hormone, increasing appetite and subsequent food intake. The ghrelinergic system has therefore received... (Review)
Review
Ghrelin is the only known peripherally-derived orexigenic hormone, increasing appetite and subsequent food intake. The ghrelinergic system has therefore received considerable attention as a therapeutic target to reduce appetite in obesity as well as to stimulate food intake in conditions of anorexia, malnutrition and cachexia. As the therapeutic potential of targeting this hormone becomes clearer, it is apparent that its pleiotropic actions span both the central nervous system and peripheral organs. Despite a wealth of research, a therapeutic compound specifically targeting the ghrelin system for appetite modulation remains elusive although some promising effects on metabolic function are emerging. This is due to many factors, ranging from the complexity of the ghrelin receptor (Growth Hormone Secretagogue Receptor, GHSR-1a) internalisation and heterodimerization, to biased ligand interactions and compensatory neuroendocrine outputs. Not least is the ubiquitous expression of the GHSR-1a, which makes it impossible to modulate centrallymediated appetite regulation without encroaching on the various peripheral functions attributable to ghrelin. It is becoming clear that ghrelin's central signalling is critical for its effects on appetite, body weight regulation and incentive salience of food. Improving the ability of ghrelin ligands to penetrate the blood brain barrier would enhance central delivery to GHSR-1a expressing brain regions, particularly within the mesolimbic reward circuitry.
Topics: Animals; Appetite Regulation; Brain; Eating; Gastric Mucosa; Ghrelin; Humans; Receptors, Ghrelin
PubMed: 28134808
DOI: 10.3390/ijms18020273 -
International Journal of Molecular... Apr 2020Obesity is one of the major social and health problems globally and often associated with various other pathological conditions. In addition to unregulated eating... (Review)
Review
Obesity is one of the major social and health problems globally and often associated with various other pathological conditions. In addition to unregulated eating behaviour, circulating peptide-mediated hormonal secretion and signaling pathways play a critical role in food intake induced obesity. Amongst the many peptides involved in the regulation of food-seeking behaviour, somatostatin (SST) is the one which plays a determinant role in the complex process of appetite. SST is involved in the regulation of release and secretion of other peptides, neuronal integrity, and hormonal regulation. Based on past and recent studies, SST might serve as a bridge between central and peripheral tissues with a significant impact on obesity-associated with food intake behaviour and energy expenditure. Here, we present a comprehensive review describing the role of SST in the modulation of multiple central and peripheral signaling molecules. In addition, we highlight recent progress and contribution of SST and its receptors in food-seeking behaviour, obesity (orexigenic), and satiety (anorexigenic) associated pathways and mechanism.
Topics: Animals; Appetite; Appetite Regulation; Eating; Energy Metabolism; Feeding Behavior; Humans; Obesity; Peptides; Somatostatin
PubMed: 32272767
DOI: 10.3390/ijms21072568 -
Physiology & Behavior May 2020The prevention and management of chronic diseases, particularly overweight and obesity, relies on multidisciplinary strategies mainly combining dietary approaches with...
The prevention and management of chronic diseases, particularly overweight and obesity, relies on multidisciplinary strategies mainly combining dietary approaches with physical activity. Recently, the timing of exercise (time of the day as well as delay/position relative to a meal) has been suggested as an important parameter to consider when prescribing physical activity. Some studies have for instance shown the interest of the timing of exercise on the glycemia, sleep and body composition regulation. However, the impact of exercise-timing on appetite control and energy intake remains unclear. This is why, the present paper questions whether physical exercise, depending on its timing during the day and related to a meal, can affect energy intake, appetite sensations and food reward. Although evidences remain actually limited, exercising during the morning; and particularly close to lunch, might have a better impact on overall energy balance through reduced subsequent energy intake, without leading to compensatory intakes at the following meals. Importantly, dealing with the timing of exercise to optimize energy balance (and affect energy intake and appetite) does not only require to consider its time during the day (morning vs. afternoon or evening), but also and maybe mainly its order/position (pre vs. post) and delay regarding meals. While the actual literature remains limited in this area, the present paper tends to highlight the importance of considering the timing of exercise to optimize our impact on the overall energy balance, and to encourage the elaboration of further studies to better understand and determine the potential effect of this timing of exercise, in order to find the best combination between the different exercise characteristics, intensity, duration, modality, to empower these effects.
Topics: Appetite; Appetite Regulation; Energy Intake; Energy Metabolism; Exercise; Meals
PubMed: 31707067
DOI: 10.1016/j.physbeh.2019.112733 -
Journal of Diabetes Investigation Nov 2016The hypothalamus is a center of food intake and energy metabolism regulation. Information signals from peripheral organs are mediated through the circulation or the... (Review)
Review
The hypothalamus is a center of food intake and energy metabolism regulation. Information signals from peripheral organs are mediated through the circulation or the vagal afferent pathway and input into the hypothalamus, where signals are integrated to determine various behaviors, such as eating. Numerous appetite-regulating peptides are expressed in the central nervous system and the peripheral organs, and interact in a complex manner. Of such peptides, gut peptides are known to bind to receptors at the vagal afferent pathway terminal that extend into the mucosal layer of the digestive tract, modulate the electrical activity of the vagus nerve, and subsequently send signals to the solitary nucleus and furthermore to the hypothalamus. All peripheral peptides other than ghrelin suppress appetite, and they synergistically suppress appetite through the vagus nerve. In contrast, the appetite-enhancing peptide, ghrelin, antagonizes the actions of appetite-suppressing peptides through the vagus nerve, and appetite-suppressing peptides have attenuated effects in obesity as a result of inflammation in the vagus nerve. With greater understanding of the mechanism for food intake and energy metabolism regulation, medications that apply the effects of appetite-regulating peptides or implantable devices that electrically stimulate the vagus nerve are being investigated as novel treatments for obesity in basic and clinical studies.
Topics: Afferent Pathways; Animals; Appetite Regulation; Diabetes Mellitus; Gastrointestinal Tract; Humans; Hypothalamus; Neurons; Obesity; Peptides; Signal Transduction; Vagus Nerve
PubMed: 27180615
DOI: 10.1111/jdi.12492 -
Journal of Internal Medicine Oct 2005In the clinic, obesity and anorexia constitute prevalent problems whose manifestations are encountered in virtually every field of medicine. However, as the command... (Review)
Review
In the clinic, obesity and anorexia constitute prevalent problems whose manifestations are encountered in virtually every field of medicine. However, as the command centre for regulating food intake and energy metabolism is located in the brain, the basic neuroscientist sees in the same disorders malfunctions of a model network for how integration of diverse sensory inputs leads to a coordinated behavioural, endocrine and autonomic response. The two approaches are not mutually exclusive; rather, much can be gained by combining both perspectives to understand the pathophysiology of over- and underweight. The present review summarizes recent advances in this field including the characterization of peripheral metabolic signals to the brain such as leptin, insulin, peptide YY, ghrelin and lipid mediators as well as the vagus nerve; signalling of the metabolic sensors in the brainstem and hypothalamus via, e.g. neuropeptide Y and melanocortin peptides; integration and coordination of brain-mediated responses to nutritional challenges; the organization of food intake in simple model organisms; the mechanisms underlying food reward and processing of the sensory and metabolic properties of food in the cerebral cortex; and the development of the central metabolic system, as well as its pathological regulation in cancer and infections. Finally, recent findings on the genetics of human obesity are summarized, as well as the potential for novel treatments of body weight disorders.
Topics: Animals; Anorexia; Appetite Regulation; Brain; Eating; Energy Metabolism; Hormones; Humans; Models, Animal; Neoplasms; Obesity; Signal Transduction; Vagus Nerve
PubMed: 16164570
DOI: 10.1111/j.1365-2796.2005.01553.x