Food reinforcement and eating: A multilevel analysis.

Eating represents a choice among many alternative behaviors. The purpose of this review is to provide an overview of how food reinforcement and behavioral choice theory are related to eating and to show how this theoretical approach may help organize research on eating from molecular genetics through treatment and prevention of obesity. Special emphasis is placed on how food reinforcement and behavioral choice theory are relevant to understanding excess energy intake and obesity and how they provide a framework for examining factors that may influence eating and are outside of those that may regulate energy homeostasis. Methods to measure food reinforcement are reviewed, along with factors that influence the reinforcing value of eating. Contributions of neuroscience and genetics to the study of food reinforcement are illustrated by using the example of dopamine. Implications of food reinforcement for obesity and positive energy balance are explored, with suggestions for novel approaches to obesity treatment based on the synthesis of behavioral and pharmacological approaches to food reinforcement. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Parental socialization of child and adolescent physical activity: A meta-analysis.

Meta-analysis was used to integrate research on the relations between parental socialization behavior and child and adolescent physical activity (PA) levels. Four major databases were examined: PubMED, ERIC, Web of Science, and PsychLit (1960 -2005). Thirty studies met the following inclusion criteria: (a) child age (2-18 years) and (b) statistical information permitting calculation of an effect size between parent socialization behavior and child PA. Mean age of participants across studies ranged from 2.54 to 15.5 years. The unweighted mean and median effect sizes (as indexed by r) were .17 and .13, respectively, indicating that a moderate positive relation exists between parental support and modeling behavior and child and adolescent PA levels. The moderating effect of type of parental socialization behavior, population characteristics, and methodological factors were investigated. Theoretical and methodological implications concern the inclusion of mediated models of parental influence and the use of longitudinal investigations in determining causal direction. From an applied viewpoint, these results are useful for the design of future, more effective childhood obesity prevention programs by suggesting child-age-appropriate parental influences. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice

Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217^+/−) mice were constructed. Zfp217^+/− mice and Zfp217^+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217^+/− mice had less weight gain than Zfp217^+/+ mice. Histological observations revealed that Zfp217^+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217^+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217^+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217^+/+ mice compared to Zfp217^+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity.     

Dietary variety, energy regulation, and obesity.

Increased variety in the food supply may contribute to the development and maintenance of obesity. Thirty-nine studies examining dietary variety, energy intake, and body composition are reviewed. Animal and human studies show that food consumption increases when there is more variety in a meal or diet and that greater dietary variety is associated with increased body weight and fat. A hypothesized mechanism for these findings is sensory-specific satiety, a phenomenon demonstrating greater reductions in hedonic ratings or intake of foods consumed compared with foods not consumed. Nineteen studies documenting change in preference, intake, and hedonic ratings of food after a food has been eaten to satiation in animals and humans are reviewed, and the theory of sensory-specific satiety is examined. The review concludes with the relevance of oral habituation theory as a unifying construct for the effects of variety of sensory-specific satiety, clinical implications of dietary variety and sensory-specific satiety on energy regulation, and suggestions for future research. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Overview: Can psychologists help the obese child?

To submit personal problems to psychological analysis is no longer to imply that one is emotionally immature. Psychological intervention can be justified rather differently. Since achieving such a negative energy balance necessitates a change in one's behaviour, the behaviour modifier (of whatever psychological persuasion) does have a role to play. The negative energy balance proposition that I have suggested as the basic assumption for psychological intervention may be a sufficient argument for having psychologists involved in weight management; but with benefit of archival records of more than 15 years of an applied psychology of obesity, our contributors are able to delineate many complexities that are now seen to characterize the experience of fatness in children. Donna White discusses the implications for children of our using Stunkard's categorization of levels of obesity. Michael LeBow examines the evidence on the basic question of whether it is dangerous to be an obese child and then proceeds to consider whether it is dangerous to be treated for obesity. Erik Woody reviews the evidence on these and related issues and shows that much of our clinical lore about the obese child is in need of serious revision. And Coates and Thoreson (1981) will encourage us to return more often to a careful individual functional analysis as the basis for design of a client's weight management programme. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Inflammasome NLRP3 Potentially Links Obesity-Associated Low-Grade Systemic Inflammation and Insulin Resistance with Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia. Metabolic disorders including obesity and type 2 diabetes mellitus (T2DM) may stimulate amyloid β (Aβ) aggregate formation. AD, obesity, and T2DM share similar features such as chronic inflammation, increased oxidative stress, insulin resistance, and impaired energy metabolism. Adiposity is associated with the pro-inflammatory phenotype. Adiposity-related inflammatory factors lead to the formation of inflammasome complexes, which are responsible for the activation, maturation, and release of the pro-inflammatory cytokines including interleukin-1β (IL-1β) and interleukin-18 (IL-18). Activation of the inflammasome complex, particularly NLRP3, has a crucial role in obesity-induced inflammation, insulin resistance, and T2DM. The abnormal activation of the NLRP3 signaling pathway influences neuroinflammatory processes. NLRP3/IL-1β signaling could underlie the association between adiposity and cognitive impairment in humans. The review includes a broadened approach to the role of obesity-related diseases (obesity, low-grade chronic inflammation, type 2 diabetes, insulin resistance, and enhanced NLRP3 activity) in AD. Moreover, we also discuss the mechanisms by which the NLRP3 activation potentially links inflammation, peripheral and central insulin resistance, and metabolic changes with AD.     

High-Fat Diet Alters Serum Fatty Acid Profiles in Obesity Prone Rats: Implications for In Vitro Studies

High‐fat diets (HFD) are commonly used in rodents to induce obesity, increase serum fatty acids and induce lipotoxicity in various organs. Invitro studies commonly utilize individual free fatty acids (FFA) to study lipid exposure in an effort to model what is occurring in vivo; however, these approaches are not physiological as tissues are exposed to multiple fatty acids in vivo. Here we characterize circulating lipids in obesity‐prone rats fed an HFD in both fasted and fed states with the goal of developing physiologically relevant fatty acid mixtures for subsequent in vitro studies. Rats were fed an HFD (60 % kcal fat) or a control diet (10 % kcal fat) for 3 weeks; liver tissue and both portal and systemic blood were collected. Fatty acid profiles and absolute concentrations of triglycerides (TAG) and FFA in the serum and TAG, diacylglycerol (DAG) and phospholipids in the liver were measured. Surprisingly, both systemic and portal serum TAG were ~40 % lower in HFD‐fed compared to controls. Overall, compared to the control diet, HFD feeding consistently induced an increase in the proportion of circulating polyunsaturated fatty acids (PUFA) with a concomitant decline in monounsaturated fatty acids (MUFA) and saturated fatty acids (SFA) in both serum TAG and FFA. The elevations of PUFA were mostly attributed to increases in n‐6 PUFA, linoleic acid and arachidonic acid. In conclusion, fatty acid mixtures enriched with linoleic and arachidonic acid in addition to SFA and MUFA should be utilized for in vitro studies attempting to model lipid exposures that occur during in vivo HFD conditions.     

2010年广西正常体重成年人中心型肥胖流行状况分析

目的：了解广西正常体重人群中心型肥胖流行状况及分布特点。方法利用中国慢性病及其危险因素监测项目问卷调查及身体测量获得的数据,分析广西6个监测点18岁以上体重正常人群2244人中心型肥胖的流行情况,以及体重正常人群中心型肥胖与心血管疾病危险因素聚集的关系。结果体重正常成人中,按照腰围、腰围身高比划分的中心型肥胖率分别为7.3％和16.6％,均为女性高于男性（P值均＜0.01）并随着年龄的增加而上升;按照腰围划分,城市地区中心型肥胖率（10.5%）高于农村（6.1%）,而按照腰围身高比划分则两者差别不大,城市、农村地区分别为17.9%和16.1%。在调整了年龄、性别、受教育程度、城乡等因素后,正常体重人群中心型肥胖者心脑血管疾病危险因素聚集的比例是非中心型肥胖者的2.272倍。结论体重正常人群中约有17%为中心型肥胖,并伴有心脑血管疾病危险因素聚集的风险升高。建议在开展肥胖干预时,不仅要强调维持健康体重和腰围,更要结合腰围身高比指标,倡导通过控制饮食和增加身体活动来控制肥胖。