ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewObesity continues to increase around the globe, and creates a major health problem because of its comorbidities such as diabetes and cardiovascular disease. Considering that the major cause of most human obesities is the modern lifestyle in a rapidly changing environment, this suggests that the battle is between brain areas controlling internal metabolic homeostasis and those dealing with cognitive and emotional processing of external information. Thus, this review is intended to bridge this apparent neural dichotomy and highlight possible ways of interactions between these homeostatic and nonhomeostatic systems.Recent findingsRapid progress has been made in identifying the molecular mechanisms underlying the neural circuits regulating food intake and energy balance. Specific populations of peptidergic neurons in the medial hypothalamus can be considered metabolic integrators sensing both short and long-term availability of fuels. These cell groups in turn connect with various other brain regions to orchestrate adaptive responses through changes in food intake, as well as endocrine and autonomic responses. Alternatively, the impact of the environmental changes on ingestive behavior have been documented, and many of the underlying cortico-limbic pathways are starting to be identified. It has been proposed that a switch from instinctual control of energy balance to a more cognitive control will be necessary to stop the obesity epidemic.SummaryThe realization that there is nothing wrong with the homeostatic regulatory system in common obesity suggests that a systematic investigation of pathways that link the ‘cognitive’ with the ‘metabolic’ brain might be a more promising area of research. Such an investigation would reveal new molecular and cellular mechanisms providing new drug targets, leading to behavioral therapies that are directed more towards the causes of common obesity.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewFood intake is critical for survival and is a complex behavior with multiple levels of control. Short-term, meal-related signals arise from many sources including the gastrointestinal tract, the environment, and higher centers in the brain. As described in this review, inputs from the gastrointestinal tract can exert potent effects on meal initiation, meal termination, and meal frequency. The complex array of signals generated from the gastrointestinal system and from adipose tissue, which participate in the regulation of food intake, and specifically how these signals relate to satiety and hunger, is the focus of this review.Recent findingsLiterature on the role of the well-studied gastrointestinal peptide, cholecystokinin, in satiety, in addition to its interaction with long-term adiposity signals in mediating food intake will be reviewed. In addition, literature on the gastrointestinal hormones glucagon-like-peptide 1, apolipoprotein A-IV and peptide YY, and how they may act to regulate satiety, is described. Finally, the newly discovered hormone, ghrelin, and how it relates to meal initiation and hunger is discussed.SummaryA better understanding of these systems and how they relate to body adiposity will prove to have important clinical applications. The available data suggest that interventions directed at multiple targets in the energy homeostasis system may be necessary to achieve and maintain weight loss.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewGiven the global rates of obesity and the potential link to dietary fat intake, understanding the role of fat in the regulation of food intake is critical. Some short-term, laboratory-based studies demonstrate poor compensation for manipulation of fat content, leading to passive overconsumption, while others demonstrate compensation to levels similar to other macronutrients. The observation of compensation in the short term does not concur with long-term rates of obesity increase. This review discusses factors that may explain at a physiological level these discrepancies, in particular fat structure, dietary adaptation, and palatability.Recent findingsMedium-chain triglycerides have been demonstrated to be more satiating and promote weight loss. Recent data suggest different gastrointestinal transduction mechanisms elicit vagal afferent firing for fatty acids of different chain length. Dietary adaptation to fat can influence the sensitivity of the feedback response, which appears to be nutrient specific and relate to gastric emptying rates and hormonal feedback. Fat content has been found to influence palatability of foods. Recently it has been demonstrated that increasing palatability can partially override the satiating effects of covertly manipulated macronutrient preloads. Recent data suggest that hormonal influences may also affect the palatability response.SummaryIt is becoming increasingly clear that although energy density of diets is a major factor determining intake, macronutrient structure, subject, dietary and taste differences can all play an important modulatory influence on the final response on food intake. Further understanding of these factors and interactions may provide strategies to help aid weight regulation.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewTo highlight the underexposed but important role of protein in food intake and body weight regulation.Recent findingsProtein plays a key role in food intake regulation through satiety related to diet-induced thermogenesis. Protein also plays a key role in body weight regulation through its effect on thermogenesis and body composition. A high percentage of energy from dietary protein limits body weight (re)gain through its satiety and energy inefficiency related to the change in body composition.SummaryProtein is more satiating than carbohydrate and fat in the short term, over 24 h and in the long term. Thermogenesis plays a role in this satiety effect, but the role of satiety hormones still needs to be elucidated. On the short-term ‘fast’ proteins are more satiating than ‘slow’ proteins, and animal protein induces a higher thermogenesis than vegetable protein. In the longer term the higher postabsorptive satiety and thermogenesis are sustained irrespective of the protein source. High-protein diets affect body weight loss positively only under ad-libitum energy intake conditions, implying also a decreased energy intake. Body composition and metabolic profile are improved. Additional protein consumption results in a significantly lower body weight regain after weight loss, due to body composition, satiety, thermogenesis, and energy inefficiency, while the metabolic profile improves. Implications from these findings are: for practice, recommendations for increasing the percentage of energy from protein while reducing energy intake; for clinical research, assessment of the paradox of increasing the percentage energy from a highly satiating macronutrient; of the potential roles of protein in a negative and positive energy balance; assessment of possibilities of replacing dietary protein by effective amino acids or peptides that may show a similar impact on body weight regulation.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewAlcohol is commonly consumed around mealtimes, and both the immediate pharmacological actions of ethanol and the energy generated by metabolism of alcohol have the potential to modify food intake. Effects of moderate alcohol consumption on food intake in humans will be reviewed, and potential mechanisms considered.Recent findingsUnlike other macronutrients, there is minimal evidence for any reduction in food intake to compensate for the potential energy in alcohol. In contrast, moderate alcohol consumption prior to a test meal leads to a short-term increase in food intake. This stimulatory effect of alcohol is not apparent beyond acute administration, but the inability to reduce voluntary energy intake in response to energy from alcohol metabolism is evident over extended periods. Alcohol suppresses fatty acid oxidation, increases short-term thermogenesis and stimulates a number of neurochemical and peripheral systems implicated in appetite control, including inhibitory effects on leptin, glucagon-like peptide-1, and serotonin, and enhancement of γ-aminobutyric acid, endogenous opioids and neuropeptide Y. All of these effects could lead to overeating, and mechanisms underlying appetite stimulation through alcohol require further substantiation.SummaryAlcohol is a complex component of the diet, and appears to have multiple effects on appetite. Failure to reduce food intake in response to energy from alcohol makes moderate alcohol consumption a risk factor for obesity. Further integration of evidence from nutrition and neuroscience will be crucial to our understanding of effects of alcohol on appetite.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewTea is considered to be one of the most promising dietary chemopreventive agents and, consequently, it is being studied extensively worldwide. Despite the fact that tea has proved very efficient in affording protection against chemical-induced cancer in animal models of the disease, epidemiological studies do not always support the laboratory findings, so that the value of tea as a human anticarcinogen may be considered as ‘not proven’. A major mechanism of the anticarcinogenic activity of tea in animals is impairment of the interaction of carcinogens with DNA leading to mutations. The antimutagenic activity of tea as well as the underlying mechanisms will be reviewed, and the role of polyphenols, the postulated bioactive components, and caffeine will be critically evaluated.Recent findingsIn rats, exposure to tea modulated the disposition of heterocyclic amines, a major group of food-borne carcinogens, stimulating the pathways that lead to deactivation, and this is concordant with the established ability of tea to modulate the carcinogen-metabolizing enzyme systems. These observations provide a rational mechanism for the anticarcinogenic activity of tea in animals.SummaryThe beneficial activities of tea have always been attributed to the polyphenols, as these are present in tea at substantial concentrations and are endowed with antioxidant activity. It is becoming increasingly evident, however, that the bioavailability of these compounds is poor as a result of limited absorption and presystemic metabolism by mammalian and microbial enzymes. We propose that the biological activity of tea may be mediated by caffeine and microbial metabolites of polyphenols.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThis review presents the latest experimental and clinical research focussing on the relationship between the intake of tomato products and lycopene supplementation and carcinogenesis, with the aim of drawing conclusions for concepts of clinical nutritional support.Recent findingsApart from the preventative role of tomato products/lycopene intake there is evidence that oral supplementation of these compounds in cancer patients may also improve the biomarkers of carcinogenesis and reduce tumour growth. New experimental studies in animal models provide insights concerning the potential mechanism(s).SummaryAlthough the first clinical trials are promising, it is too early to make final recommendations for nutritional therapy in cancer patients. Whether the bioactive compound in tomatoes is lycopene or whether other substrates contribute to the beneficial physiological effects is still unclear.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewTo review pharmaceutical and pharmacological issues relating to the benefits and risks associated with the use of naturally sourced nutraceuticals when administered singly or in combinations.Recent findingsThe application of vegetable extracts or dietary supplementation with selenium or antioxidant vitamins results in positive benefits on immunity and other phenomena associated with chronic diseases, ageing and cancer. However, there appear to be no cardiovascular benefits from vitamin mixtures, which may in fact cause harm. Therefore, although recent publications have increased our understanding of the metabolic actions of nutraceuticals, learning to use them to the best advantage is going to require products with uniform and consistent quality. Unfortunately, a single purified substance will not always have the same antioxidant activity, nor provide the same clinical benefits as nutraceutical mixtures and combinations occurring in natural extracts. In order to perform first-class clinical studies to determine safety and efficacy, the stability, compatibility and other pharmaceutical variables inherent in many of these combination products will have to be better controlled.SummaryNutraceuticals have potent biological actions. Their use is increasing dramatically, and there is growing evidence of clinical benefits. No medicinal products are completely safe so their risks need to be characterized and controlled. Imposing pharmaceutical levels of control and regulation would increase costs and reduce patient access to new products, but the evidence is compelling that closer monitoring of raw materials, processing and formulation will be required to maximize the benefits and minimize the risks.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID