摘要:

Purpose of reviewAnorexia and reduced food intake are important issues in the management of cancer patients. This article discusses the currently proposed hypothesis of its pathogenesis, and reviews the available and future therapeutic options as they relate to the pathogenic mechanisms.Recent findingsCurrently available data suggest that the pathogenesis of cancer anorexia is multifactorial, and involves most of the hypothalamic neuronal signaling pathways modulating energy intake. Thus, a number of factors have been proposed as putative mediators of cancer anorexia, including hormones (e.g. leptin), neuropeptides (e.g. neuropeptide Y), cytokines (e.g. IL‐1, IL‐6, tumor necrosis factor) and neurotransmitters (e.g. serotonin and dopamine). It is unlikely, however, that they represent separate and distinct pathogenic mechanisms, rather it appears that close interrelationships may exist among them. In line with this reasoning, consistent experimental and human data suggest that hypothalamic monoaminergic neurotransmission may represent a major target on which different anorexia‐related factors converge.SummaryIn the pathogenesis of cancer anorexia, cytokines appear to play a key role. Their increased expression during tumor growth inhibits the hypothalamus to appropriately respond to peripheral signals, by persistently activating the melanocortin system and inhibiting the neuropeptide Y neuronal pathway. Hypothalamic monoaminergic neurotransmission may significantly contribute to these effects. Thus, interfering pharmacologically with cytokine expression or hypothalamic monoaminergic neurotransmissions is an effective therapeutic strategy in anorectic cancer patients.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewDespite much current debate regarding central and peripheral neural mechanisms which may be responsible for the onset of fatigue during prolonged exercise, maintenance of nutritional and hydration status remains critical for successful participation in ultra‐endurance exercise. This review focuses on substrate and fluid homeostasis during ultra‐endurance exercise and the use of nutritional supplementation both as ergogenic aid and to attenuate exercise‐induced immunosuppression.Recent findingsCurrent evidence continues to support mandatory high carbohydrate intakes (1) before the event to maximize muscle glycogen stores, (2) during the event to prevent hypoglycaemia and (3) after the event to optimize post‐event repletion of endogenous carbohydrate stores. No consistent performance benefit has yet been shown following a high‐fat diet. Greater utilization of intrafascicular triglyceride stores appears to account for additional fat utilization in females. Recent trends towards excessive fluid intake have resulted in frequent reports of hyponatraemic hyperhydration in ultra‐distance athletes, with greater incidence in women than in men. Carbohydrate supplementation during the event attenuates immunosuppressive hormonal and cytokine responses to ultraendurance exercise, but may impair vitamin C absorption, while the ergogenic value of caffeine supplementation in ultra‐endurance performance is currently being questioned.SummaryMeeting macronutrient and fluid intake demands remains an important priority for ultra‐endurance athletes. Yet these athletes are reported to present with a high incidence of disordered eating patterns during periods of training, and excessive fluid replacement strategies have resulted in an increased incidence of water intoxication with resultant central nervous system dysfunction.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewTo summarize the current knowledge of the effects of physical activity on muscular dystrophies.Recent findingsAlthough the usefulness of exercise training in muscular dystrophy patients has been debated for many years, only a limited number of articles addressing this issue have been published to date. Existing studies on the effects of strength training in patients with muscular dystrophies have shown promising results, but interpretations are hampered by several methodological shortcomings.SummaryThe scientific basis for solid recommendations of different exercise regimens in muscular dystrophies is poor, but existing data suggest beneficial effects of adopting an active lifestyle. Low‐ to moderate‐intensity resistance and aerobic training may be recommended in slowly progressive myopathic disorders. To date, there is no evidence to support the recommendation of high‐resistance exercise regimens over low‐moderate intensity exercise. In rapidly progressive myopathies, which are due to aberrant structural proteins such as Duchenne muscular dystrophy, the use of high‐resistance and eccentric training should be avoided. There is still, however, no evidence that physical training can influence the evolution of muscular dystrophies in the long term.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThe liver plays an important role in glucose tolerance. A number of studies have suggested fructose improves glucose tolerance especially in insulin resistant settings. This review summarizes the recent work suggesting that fructose enhances glucose tolerance by augmenting liver glucose uptake. This increase may be mediated by the translocation and activation of hepatic glucokinase.Recent findingsCatalytic quantities of fructose (<10% of total carbohydrate flux) enhance liver glucose uptake in a dose dependent manner. The primary fate of the glucose is glycogen synthesis. The ability of fructose to augment liver glucose uptake is not impaired by the presence of marked insulin resistance such as in type 2 diabetes or infection. In addition, it is able to further enhance liver glucose uptake in the normal adapted setting of total parenteral nutrition and reverse the infected‐induced decrease in liver glucose uptake. Studies also demonstrate that the beneficial effects of fructose on liver glucose uptake during chronic nutritional support do not persist.SummaryFructose is a potent acute regulator of liver glucose uptake and glycogen synthesis. Inclusion of catalytic quantities of fructose in a carbohydrate meal improves glucose tolerance. This improvement is primarily mediated by the activation of hepatic glucokinase and consequent facilitation of liver glucose uptake. The improvement in glucose tolerance is most evident in insulin resistant settings (e.g. Type 2 diabetes and infection). The beneficial effect of fructose on hepatic glucose disposal, however, does not persist if fructose is given continuously such as in total parenteral nutrition.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThis review depicts recent developments concerning the role of the liver in control of carbohydrate and lipid utilization from ingestion to storage; it covers the liver's influence on food intake, post‐absorptive nutrient metabolism and body weight. The mechanisms involved have implications for the pathogenesis of obesity and type II diabetes.Recent findingsRecent studies have identified some of the molecular and biochemical mechanisms which control whole body and hepatic carbohydrate and lipid metabolism, thus providing the basis of the liver's role in the control of food intake, metabolism, and body weight. Fatty acids are known to effect gene transcription in various ways. Advances in our understanding of the control of glucose and lipid utilization by the liver include (1) a better functional characterization of some newly discovered transcription factors, (2) new discoveries concerning the physiological and pathophysiological role of hepatic glucokinase and of the glycogen‐targeting subunits of protein phosphatase‐1, and (3) the demonstration of substantial overlap in the molecular control mechanisms of glucose‐lipid utilization. Also, impaired insulin signaling due to a certain gene (Foxo1) has emerged as a possible unifying mechanism for various common metabolic abnormalities of type II diabetes. Finally, recent findings confirm and extend previous knowledge about the important role of hepatic nerves in the control of liver and whole body glucose‐lipid utilization.SummaryThe identification of new molecular and neural mechanisms of the hepatic control of glucose‐lipid utilization and body weight provides a focus for future studies and may eventually help to develop new treatments for obesity and type II diabetes.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewPost‐liver transplant patients present a vast array of metabolic changes in the early and late phase which impact on their morbidity and mortality. The development of obesity and diabetes in these patients has been widely described in the literature with several hypotheses suggested: liver donor, nutritional and metabolic state, and immunosuppressive drugs.Recent findingsMost that is known about the development of these metabolic derangements has been attributed to the drugs used, especially the corticosteroids. When these have been used in higher doses for longer periods to treat rejection, the incidence of diabetes and obesity seems to be higher. However cyclosporine and to a lesser extent tacrolimus are also related to these alterations.SummaryAs long‐term survival improves in liver transplant patients, cardiovascular complications associated with dyslipidemia, obesity, and diabetes are emerging as risk factors for late morbidity and mortality. Therefore, it is important to assess the potential risk factors related to these complications, in order to prevent or decrease their incidence. From what has been seen, immunossupressive drugs seem to be the greatest risk factor for the development of metabolic derangements in post‐transplantation patients. However other risk factors might also be involved, such as non‐healthy eating habits and lack of exercise. The latter can be preventable if counseling policies are targeted at these patients in the pre‐transplantation phase and continued after the operation.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThe gastrointestinal hormones glucagon‐like peptide 1 and glucose‐dependent insulinotropic polypeptide are emerging as essential regulators of insulin secretion and glucose homeostasis. These peptides, termed incretins, are the key intermediaries in a system that links the absorption of nutrients in the gut with important metabolic processes in substrate assimilation. New findings indicate that the enteroinsular system mediated by the incretins is relevant to both the pathophysiology and treatment of diabetes.Recent findingsImportant advances have been made in the understanding of mechanisms fundamental to incretin function such as their release from the intestine during meals, their actions on &bgr;‐cell secretion, and extrapancreatic effects. In addition, the regulation of islet growth by glucagon‐like peptide 1 and glucose‐dependent insulinotropic polypeptide is a novel area with considerable support from recent studies. Abnormalities of incretin function are present in patients with diabetes and current research has implicated specific defects of both glucagon‐like peptide 1 and glucose‐dependent insulinotropic polypeptide action in diabetes. Finally, several pharmacological applications of the incretin signaling pathways are under active investigation for the treatment of diabetes.SummaryWith the intensified research of the last several years the physiologic importance of the incretins has been clarified. Enteroinsular signaling is an essential component of the metabolic processes that govern carbohydrate, and likely other nutrient metabolism. As a pathophysiology of the incretins emerges, glucagon‐like peptide 1 and glucose‐dependent insulinotropic polypeptide will have increasing clinical relevance. This is currently exemplified by the development of therapeutics for diabetes that work through the incretin signaling pathways.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewCold response can be insulative (drop in peripheral temperature) or metabolic (increase in energy expenditure). Nonshivering thermogenesis by sympathetic, norepinephrineinduced mitochondrial heat production in brown adipose tissue is a well known component of this metabolic response in infants and several animal species. In adult humans, however, its role is less clear. Here we explore recent findings on the role and variability of nonshivering thermogenesis in adults.Recent findingsLarge individual differences exist in mild cold response with respect to the relative contribution of the insulative response and the metabolic (nonshivering) response. In search for the possible explanations of this variation, recent studies on potential mechanisms of nonshivering thermogenesis in humans are presented. Emphasis is given to the role of uncoupling proteins, mitochondrial ATP‐synthase, and calcium cycling. The potential contribution of human skeletal muscle to nonshivering thermogenesis is discussed. The differences in nonshivering thermogenesis can partly be attributed to factors such as age, gender, physical fitness, adaptation, and diet. There are indications that genetic variation affect cold response.SummaryThe implications of the observed large individual variation in cold response is that a low metabolic response to cold can partly explain increased risk to develop obesity. Both the effect of environmental factors and genetic factors on nonshivering thermogenesis require more well controlled studies. With extended knowledge on these factors it can be ascertained if a pharmacological regimen is possible which would mimic the effects of chronic cold or elevated catecholamine levels, without attendant side effects.

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