Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.

BRIEF COMMUNICATION ARISING: Gut hormone PYY3-36 physiologically inhibits food intake

Objective: The recent obesity epidemic has been accompanied by a parallel growth in chronic sleep deprivation. Physiologic studies suggest sleep deprivation may influence weight through effects on appetite, physical activity, and/or thermoregulation. This work reviews the literature regarding short sleep duration as an independent risk factor for obesity and weight gain.

Short sleep duration and weight gain : a systematic review

This article reviews scientific advances in the prevention and treatment of substance-use disorder and related developments in public policy. In the past two decades, research has increasingly supported the view that addiction is a disease of the brain. Although the brain disease model of addiction has yielded effective preventive measures, treatment interventions, and public health policies to address substance-use disorders, the underlying concept of substance abuse as a brain disease continues to be questioned, perhaps because the aberrant, impulsive, and compulsive behaviors that are characteristic of addiction have not been clearly tied to neurobiology. Here we review recent advances in the neurobiology of addiction to clarify the link between addiction and brain function and to broaden the understanding of addiction as a brain disease. We review findings on the desensitization of reward circuits, which dampens the ability to feel pleasure and the motivation to pursue everyday activities; the increasing strength of conditioned responses and stress reactivity, which results in increased cravings for alcohol and other drugs and negative emotions when these cravings are not sated; and the weakening of the brain regions involved in executive functions such as decision making, inhibitory control, and self-regulation that leads to repeated relapse. We also review the ways in which social environments, developmental stages, and genetics are intimately linked to and influence vulnerability and recovery. We conclude that neuroscience continues to support the brain disease model of addiction. Neuroscience research in this area not only offers new opportunities for the prevention and treatment of substance addictions and related behavioral addictions (e.g., to food, sex, and gambling) but may also improve our understanding of the fundamental biologic processes involved in voluntary behavioral control. In the United States, 8 to 10% of people 12 years of age or older, or 20 to 22 million people, are addicted to alcohol or other drugs. 1 The abuse of tobacco, alcohol, and illicit drugs in the United States exacts more than $700 billion annually in costs related to crime, lost work productivity, and health care. 2-4 After centuries of efforts to reduce addiction and its related costs by punishing addictive behaviors failed to produce adequate results, recent basic and clinical research has provided clear evidence that addiction might be better considered and treated as an acquired disease of the brain (see Box 1 for definitions of substance-use disorder and addiction). Research guided by the brain disease model of addiction has led to the development of more effective methods of prevention and treatment and to more informed public health policies. Notable examples include the Mental Health Parity and Addiction Equity Act of 2008, which requires medical insurance plans to provide the same coverage for substance-use disorders and other mental illnesses that is provided for other illnesses, 5 and the proposed bipartisan Senate legislation that From the National Institute on Drug Abuse (N.D.V.) and the National Institute of Alcohol Abuse and Alcoholism (G.F.K.) — both in Bethesda, MD; and the Treatment Research Institute, Philadelphia (A.T.M.). Address reprint requests to Dr. Volkow at the National Institute on Drug Abuse, 6001 Executive Bld., Rm. 5274, Bethesda, MD 20892, or at nvolkow@ nida . nih . gov.

Review Article: Neurobiologic Advances from the Brain Disease Model of Addiction

For some time now councils with social services responsibilities (CSSRs) have been required to conduct surveys of user’s experience of social services. These have taken place nationally in three-yearly cycles. In 2002/03 the survey was for older people, in 2003/04 it was for younger adults with physical and sensory impairments, and in 2004/05 it was for children. 2005/06 marked the beginning of the second wave of the cycle. The mandate for conducting surveys of user’s experiences and satisfaction with services was first given in the white paper Modern Local Government: in Touch with the People (Department for the Environment, Trade and the Regions, 1998). In 2002 the Office of National Statistics (ONS) and SPRU developed a set of questionnaires for this purpose (Qureshi and Rowlands, 2004). Subsequent national surveys have drawn on this work to identify a set of compulsory questions for each round. User experience surveys (UESs) are regarded as an important part of the overall performance framework for social care and, providing councils with information about how they might improve services locally. Local authorities are required to submit their results to government bodies so that the relative performance of the CSSRs can be judged. This report is composed of five sections. The aims and objectives of the report are outlined in the second section and the method used to gather the data is outlined in section 3. In section 4 we report on the findings from the fieldwork and draw some conclusions and recommendations for the national survey in section 5. The topic guides for the focus groups and interviews are included in the appendices along with a brief discussion of the findings from the focus groups and a copy of the final extended questionnaire.

Younger Adults' Understanding of Questions for a Service User Experience Survey. Funded/commissioned by: The Health and Social Care Information Centre

How does a lack of sleep affect our brains? In contrast to the benefits of sleep, frameworks exploring the impact of sleep loss are relatively lacking Importantly, the effects of sleep deprivation (SD) do not simply reflect the absence of sleep and the benefits attributed to it; rather, they reflect the consequences of several additional factors, including extended wakefulness With a focus on neuroimaging studies, we review the consequences of SD on attention and working memory, positive and negative emotion, and hippocampal learning We explore how this evidence informs our mechanistic understanding of the known changes in cognition and emotion associated with SD, and the insights it provides regarding clinical conditions associated with sleep disruption

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The sleep-deprived human brain

In view of the increasing numbers in overweight and obesity, insight in food intake regulation is necessary. Food intake is regulated by sensory, cognitive, post-ingestive, and post-absorptive processes. Food properties, such as energy density, macronutrient composition, volume, and form, influence the satiating capacity of a food. This chapter focuses on the role of food texture in food intake regulation. Texture is an essential part of the whole spectrum of sensory properties of a food. Several studies showed that liquid foods elicit weaker suppressive appetite responses and a weaker compensatory response in energy intake than solid or semisolid foods. The mechanisms underlying the effect of texture on satiety are not well understood. Beverages might engage thirst mechanisms and not hunger mechanisms. Food properties such as viscosity and texture could affect chewing, oro-gastric handling of foods, and absorption. Other factors that play a role are beliefs about the satiating capacity of a food, sensory specific satiety, eating rate, gastric emptying, and learned associations between texture and metabolic consequences. One of the mechanisms involved could be the oral sensory exposure time. A longer oral exposure time gives the sensory receptors in the oral cavity more time to respond to the food. Liquid calories facilitate energy intake. This knowledge can be useful in both the overweight and underweight situation.

Texture and diet related behavior: a focus on satiation and satiety. Handbook of Behavior, Food and Nutrition, Part 2 Preedy VR, Watson RR, Martin CR 133-142

Pleunie S. Hogenkamp

Papers

Texture and diet related behavior: a focus on satiation and satiety. Handbook of Behavior, Food and Nutrition, Part 2 Preedy VR, Watson RR, Martin CR 133-142

Changes in expected satiation after repeated consumption of a low- or high-energy-dense soup

Eating rate and viscosity in learned satiation

Associations of self-reported sleep disturbance and duration with academic failure in community-dwelling Swedish adolescents