Forum of Nutrition最新文献

{"title":"Cortical mechanisms of human eating.","authors":"Morten L Kringelbach,&nbsp;Alan Stein","doi":"10.1159/000264404","DOIUrl":"https://doi.org/10.1159/000264404","url":null,"abstract":"<p><p>The hedonic component of eating is an underexplored topic within neuroscience, which is surprising given its importance for our survival and general well-being, as well as the obvious links to obesity and eating disorders. Based on findings from neuroimaging, this review gives an overview of the established principles, neural mechanisms and functional neuroanatomy of the primate and human brain processing systems involved in controlling eating. Four main processing principles underlying these processes are discussed: (1) motivation-independent discriminative processing of identity and intensity, (2) formation of learning-dependent multimodal sensory representations, (3) reward representations using mechanisms including selective satiation, and (4) representations of hedonic experience, monitoring/learning or direct behavioural change.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"164-175"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000264404","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28543821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic variation in dopaminergic reward in humans.","authors":"Eric Stice,&nbsp;Alain Dagher","doi":"10.1159/000264405","DOIUrl":"https://doi.org/10.1159/000264405","url":null,"abstract":"<p><p>Dopamine-based reward circuitry appears to play a role in encoding reward from eating and incentive sensitization, whereby cues associated with food reward acquire motivational value. Data suggest that low levels of dopamine D2 receptors and attenuated responsivity of dopamine-target regions (e.g. the striatum) to food and food cues are associated with elevated weight. There is mixed evidence that genotypes that appear to be associated with reduced signaling of dopamine circuitry, including DRD2, DRD4 and DAT, are correlated with obesity. In addition, there is emerging fMRI evidence that reduced responsivity in brain regions implicated in food reward increase risk for future weight gain among individuals who appear to be at genetic risk for attenuated dopamine signaling by virtue of DRD2 and DRD4 genotypes. However, it is vital for these relations to be replicated in larger, independent prospective studies and to use positron emission tomography to better characterize parameters of dopamine signaling, including dopamine receptor density, basal dopamine levels, and phasic dopamine release. Improved understanding of the role of dopamine-based reward circuitry and genotypes that influence the functioning of this circuitry may inform the design of more effective preventive and treatment interventions for obesity.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"176-185"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000264405","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28543822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction - obesity and food intake: basic and clinical approaches.","authors":"Annette D De Kloet,&nbsp;Stephen C Woods","doi":"10.1159/000264391","DOIUrl":"https://doi.org/10.1159/000264391","url":null,"abstract":"Background This introduction considers the current status of research on obesity and therapeutic strategies for it, including their relationships to the physiology of eating. Given the immense research effort currently targeting overweight and obesity, this summary is necessarily only a snapshot of a large and rapidly evolving area. It is nonetheless of immense importance since there is no sign that the obesity epidemic is abating, and because obesity per se carries so great a risk for numerous co-morbidities, such as type-2 diabetes mellitus (T2DM), several cardiovascular disorders and certain cancers. The topic is at the heart of the theme of this volume, given that obesity cannot exist unless energy intake (i.e. eating) chronically surpasses energy expenditure and since tackling aspects of eating represents, at least at present, the more approachable limb of the energy equation. As noted below, even the most successful therapeutic method now available, gastric bypass surgery, ultimately owes its efficacy to reduced energy intake. Generally speaking, obesity refers to a state of excessive body fat and implies an unhealthy or undesirable body condition. Depending on one’s perspective, obesity can be considered a symptom that carries an increased risk for numerous serious medical conditions or co-morbidities; a disease that warrants confrontation by governments, national health agencies, private benevolent groups, and third-party (health insurance) providers; or merely a warning that one should consider changing his or her lifestyle by consuming fewer calories each day [1]. Especially now that obesity has become a major focus of many health-care organizations, much new information has been forthcoming in the past few years and is beginning to influence the practice of medicine. It is important to realize that obesity is not a novel human condition; rather, evidence points to its existence in prehistoric times. What is novel is the persistent creep upward in the incidence of overweight and obesity in most human populations, a trend that is now widely considered an epidemic.","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000264391","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28544518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overview of the physiological control of eating.","authors":"Wolfgang Langhans,&nbsp;Nori Geary","doi":"10.1159/000264392","DOIUrl":"https://doi.org/10.1159/000264392","url":null,"abstract":"In this chapter we discuss the physiology of eating, with a particular focus on its relevance to the present obesity epidemic. The physiology of eating comprises the functional organization of eating behavior, the types of exteroceptive and interoceptive information that affect eating, the neural and endocrine sensory mechanisms relaying this information to the central nervous system (CNS), and the CNS neural networks that process and integrate this and other information to control eating (fig. 1). We emphasize the role of eating in the regulation of body weight. These topics have taken on new importance with the obesity epidemic. It is well recognized that overeating together with reduced exercise are the proximal causes of obesity. Therefore, better understanding of the physiology of eating and its role in body weight regulation, or dysregulation, should lead to new and hopefully more effective approaches for the therapeutic control of eating in obese persons or persons at special risk for obesity and obesity-related diseases.","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"9-53"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000264392","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28544519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leptin-signaling pathways and leptin resistance.","authors":"Heike Münzberg","doi":"10.1159/000264400","DOIUrl":"10.1159/000264400","url":null,"abstract":"<p><p>Leptin acts as an anorexigenic hormone in the brain, where the long form of the leptin receptor (LRb) is widely expressed in hypothalamic and extra-hypothalamic sites that are known to participate in diverse feeding circuits. The important role of leptin in energy homeostasis is demonstrated by the profound hyperphagia and morbid obesity in humans and rodents null for leptin or LRb. However, common forms of obesity are associated with high leptin levels and a failure to respond effectively to exogenous leptin; indicating a state of leptin resistance. Leptin resistance is thought to be an important component in the development of obesity. Several defects may contribute to the leptin resistant state, including a defective leptin transport across the blood-brain barrier, which reduces the availability of leptin at its receptor. Furthermore, defects in LRb signal transduction involving reduced LRb expression or the induction of feedback inhibitors have been found in leptin resistance; these defects are commonly termed cellular leptin resistance,. Finally, reduced leptin action can result in the disruption of proper neuronal interactions, by altering neuronal wiring. Interestingly, some leptin functions remain intact in the leptin-resistant state, such as cardiovascular leptin effects. The appearance of selective leptin resistance is mirrored by the observation that cellular leptin resistance has been found only in some subpopulations of hypothalamic LRb neurons. Current efforts to dissect leptin function in specific populations of LRb neurons will increase our understanding of these complexities of leptin physiology.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"123-132"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11129273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28543817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of amylin in satiation, adiposity and brain development.","authors":"Thomas A Lutz","doi":"10.1159/000264394","DOIUrl":"https://doi.org/10.1159/000264394","url":null,"abstract":"<p><p>Amylin plays an important role in the control of nutrient fluxes. It is cosecreted with insulin and reduces eating by promoting meal-ending satiation. This effect seems to depend on a stimulation of amylin receptors in the area postrema. Subsequent to area postrema activation, the neural signal is conveyed to the forebrain via distinct relays in the nucleus of the solitary tract and the lateral parabrachial nucleus to the lateral hypothalamic area and other hypothalamic nuclei; the functional roles of these relays in amylin's eating inhibitory effect have not been fully investigated. Amylin may also play a role in the regulation of adiposity. Plasma levels of amylin are increased in adiposity, although the precise relation is unknown. Furthermore, chronic infusion of amylin into the brain reduced body weight gain and adiposity, and chronic infusion of an amylin receptor antagonist increased body adiposity. Both these animal data and pre-clinical research in humans indicate that amylin is a promising option for anti-obesity therapy, especially in combination with leptin. Finally, recent findings indicate that amylin may also be necessary for normal brain development; it acts as a neurotrophic factor for the development of brainstem pathways involved in the control of eating. How this may be relevant under physiological conditions requires further studies, but these findings substantiate the concept that amylin plays an integrative role in the development and operation of neural circuits involved in the control of eating and energy homeostasis.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"64-74"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000264394","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28544521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Do leptin and insulin signal adiposity?","authors":"Jacquelien J G Hillebrand,&nbsp;Nori Geary","doi":"10.1159/000264399","DOIUrl":"https://doi.org/10.1159/000264399","url":null,"abstract":"<p><p>The physiological regulation of adiposity is supposed to depend on endocrine 'adiposity signals' that inform the brain about the mass of the adipose tissue. Basal levels of insulin and leptin are widely accepted to be adiposity signals, and amylin, ghrelin and peptide YY have been hypothesized to be. Support for these ideas comes from associations between basal hormone levels and levels of adiposity, from demonstrations of receptors for these hormones in neural circuits supposed to regulate energy homeostasis, from neuropharmacological manipulations of the hormones' actions on eating and energy expenditure, and from the effects on energy balance in animals or people bearing mutations in these endocrine signaling pathways. This chapter focuses on only the first of these four types of evidence and only on insulin and leptin. We ask whether circulating levels of either hormone indeed encodes the necessary information to act as an adiposity signal. In considering this question, we emphasize the distinction between regulation of AT mass in steady versus dynamic states. We argue that the best experimental designs for identifying potentially effective adiposity signals involve situations in which the level of adiposity is changing as the organism responds to imposed perturbations. Traditionally, this is the type of design that most convincingly supports the idea that adiposity is actively regulated. Unfortunately, there are few of such studies for any of the hypothesized endocrine adiposity signals, and the evidence that is available does not strongly support the hypotheses. Therefore, we conclude that the question of how adiposity is signaled to the brain remains an open frontier in the physiology of energy homeostasis.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"63 ","pages":"111-122"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000264399","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28543816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise and food factors.","authors":"Wataru Aoi","doi":"10.1159/000212747","DOIUrl":"https://doi.org/10.1159/000212747","url":null,"abstract":"<p><p>Habitual exercise is beneficial to health as it improves metabolism, reduces the risk of cardiovascular disease, and maintains the immune system. Appropriate nutrition contributes to acceleration of health promotion due to exercise. Recommended daily allowance is elevated by physical activity and intake of various food factors such carbohydrates, proteins, vitamins, minerals, and other phytochemicals is required to avoid their shortage. Additional dietary food factors are effective not only in supplementation to satisfy the allowance but also in further acceleration of the benefits of fitness. Dietary nutrition is also important to maintain active function in the elderly by preventing aging-induced muscle atrophy and avoiding intense exercise-induced disorders. Recently, several food components have been found to show physiological effects, and some of them are considered to be useful for promoting or alternating the beneficial effects of exercise, maintaining homeostasis, and preventing muscle aging. However, some of these food factors should only be used when there is clear scientific evidence. Also, it is important to understand the physiological changes caused by exercise to use them correctly. This article describes various food factors that have been reported to be effective for improving health promotion, along with the relevant physiological changes that occur during exercise.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"147-155"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212747","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28108800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress-induced posttranslational modification of proteins as a target of functional food.","authors":"Yuji Naito,&nbsp;Toshikazu Yoshikawa","doi":"10.1159/000212737","DOIUrl":"https://doi.org/10.1159/000212737","url":null,"abstract":"<p><p>In lifestyle-related diseases including metabolic syndrome, atherosclerosis, and cancer, oxidative stress is indicated by several markers, among which are lipid peroxides, aldehydes, and nitrotyrosine. We hypothesized that identification of proteins that are posttranslationally modified due to oxidative stress would lead to a greater understanding of some of the potential molecular mechanisms involved in degeneration and inflammation in these disorders. Proteomics is an emerging method for identification of proteins and their modification residues, and its application to food factor science is just beginning. Especially, we can obtain several monoclonal antibodies to detect specifically oxidized proteins, which can be applied to analysis by immunostaining or immunoblot. In this review, we present the use of these monoclonal antibodies in several diseases, from which new insights have emerged into mechanisms of metabolism and inflammation in these disorders that are associated with oxidative stress.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"39-54"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212737","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28183569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemoprevention by isothiocyanates: molecular basis of apoptosis induction.","authors":"Yoshimasa Nakamura","doi":"10.1159/000212749","DOIUrl":"https://doi.org/10.1159/000212749","url":null,"abstract":"<p><p>An important and promising group of compounds that have a cancer-chemopreventive property are organosulfur compounds, such as isothiocyanates (ITCs). Various ITCs are effective chemoprotective agents against chemical carcinogenesis in experimental animals. Several epidemiological studies also indicated that the dietary consumption of ITCs or ITC-containing foods inversely correlates with the risk of developing lung, breast, and colon cancers, providing evidence that they have a potential to prevent cancer in humans. Mechanistically, ITCs are capable of inhibiting both the formation and development of a cancer cell through multiple pathways; i.e. the inhibition of carcinogen-activating cytochrome P450 mono-oxygenases, induction of carcinogen-detoxifying phase 2 enzymes, induction of apoptosis, and inhibition of cell cycle progression. We have clarified the molecular mechanisms underlying the relationship between cell cycle regulation and apoptosis induced by benzyl ITC (BITC), a major ITC compound isolated from papaya (Carica papaya) fruit. We identified phosphorylated Bcl-2 as a key molecule linking p38 MAPK-dependent cell cycle regulation with the c-Jun N-terminal kinase activation by BITC. We also established that BITC exerts the cytotoxic effect more preferentially in the proliferating cells than in the quiescent cells. Furthermore, p53 was found to be a potential negative regulator of apoptosis induction by BITC in normal epithelial cells through inhibition of cell cycle progression at the G(0)/G(1) phase. In contrast, treatment with an excessive concentration of BITC resulted in necrotic cell death in an ATP-dependent manner. This review addresses the biological impact of cell death induction by BITC as well as other ITCs and the involved molecules regulating signal pathways.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"170-181"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212749","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28108802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}