Amylin Uncovered: A Review on the Polypeptide Responsible for Type II Diabetes.

Amylin Uncovered: A Review on the Polypeptide Responsible for Type II Diabetes.

Biomed Res Int. 2013; 2013: 826706
Pillay K, Govender P

Amylin is primarily responsible for classifying type II diabetes as an amyloid (protein misfolding) disease as it has great potential to aggregate into toxic nanoparticles, thereby resulting in loss of pancreatic ?-cells. Although type II diabetes is on the increase each year, possibly due to bad eating habits of modern society, research on the culprit for this disease is still in its early days. In addition, unlike the culprit for Alzheimer’s disease, amyloid ?-peptide, amylin has failed to receive attention worthy of being featured in an abundance of review articles. Thus, the aim of this paper is to shine the spotlight on amylin in an attempt to put it onto the top of researchers’ to-do list since the secondary complications of type II diabetes have far-reaching and severe consequences on public health both in developing and fully developed countries alike. This paper will cover characteristics of the amylin aggregates, mechanisms of toxicity, and a particular focus on inhibitors of toxicity and techniques used to assess these inhibitors. HubMed – eating


Weight suppression in bulimia nervosa: Relationship with cognitive behavioral therapy outcome.

Int J Eat Disord. 2013 Apr 20;
Dawkins H, Watson HJ, Egan SJ, Kane RT

OBJECTIVE: In light of prior inconsistent findings, this study revisits the relationship between weight suppression and treatment outcome in bulimia nervosa. Aside from differences in methodology, we propose that moderator effects may assist the field in interpreting previous inconsistency. In this study, we considered moderators that might place individuals at risk of broad cognitive and biobehavioral mechanisms implicated in weight (dys)regulation and binge eating, and that within the context of a history of weight suppression, might be associated with especially poor outcomes. METHOD: Participants were 117 female outpatients aged 16-54 years (M?=?25.5) with bulimic disorders treated with enhanced cognitive behavioral therapy. RESULTS: Logistic regression indicated that higher pretreatment weight suppression did not predict drop-out or poor treatment outcome (nonabstinence from binging and purging). Moderators of parental history of overweight, childhood body shape, pretreatment body mass index, and the difference between highest and lowest ever adult body weight were analyzed, but no moderator effects were apparent. DISCUSSION: This study, along with other negative studies, calls into question the association between weight suppression and treatment outcome. We maintain that moderators may account for inconsistencies, but no candidates were identified in this study. Moderator models could assist us to refine conceptualizations of why some patients high in weight suppression may be vulnerable to poor treatment adherence and outcome and to establish clinical interventions that enhance prognosis. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013). HubMed – eating


Early Onset Binge Eating and Purging Eating Disorders: Course and Outcome in a Population-Based Study of Adolescents.

J Abnorm Child Psychol. 2013 Apr 19;
Allen KL, Byrne SM, Oddy WH, Crosby RD

This study aimed to describe the course of early onset eating disorders in a population-based sample followed from 14 to 20 years; identify variables that could account for the persistence of eating disorders from 14 to 20 years; and describe outcome of early onset eating disorders with reference to general and psychological functioning at age 20. Participants (N?=?1,383; 49 % male) were drawn from the Western Australian Pregnancy Cohort (Raine) Study, which has followed children from pre-birth to young adulthood. Eating disorder symptoms were assessed using an adapted version of the Eating Disorder Examination-Questionnaire, at ages 14, 17 and 20. At age 14, 70 participants met DSM-IV criteria for a binge eating or purging eating disorder. Nearly half (44 %) of these adolescents ceased to meet criteria for an eating disorders at ages 17 and 20, whilst one-quarter still met criteria for an eating disorder at age 20 and one-fifth met criteria for an eating disorder at all three time points. Purging at age 17 and externalising behaviour problems at age 14 were the strongest predictors of eating disorder persistence to age 20. Participants who experienced a persistent eating disorder were less likely to complete high school than other participants, and reported pronounced depressive and anxiety symptoms at age 20. This study provides new data the course and outcome of early onset eating disorders at a population level. Behavioural difficulties in early adolescence and purging in middle adolescence may predict persistent eating pathology to young adulthood. HubMed – eating


Circadian clocks and mood-related behaviors.

Handb Exp Pharmacol. 2013; 217: 227-39
Albrecht U

Circadian clocks are present in nearly all tissues of an organism, including the brain. The brain is not only the site of the master coordinator of circadian rhythms located in the suprachiasmatic nuclei (SCN) but also contains SCN-independent oscillators that regulate various functions such as feeding and mood-related behavior. Understanding how clocks receive and integrate environmental information and in turn control physiology under normal conditions is of importance because chronic disturbance of circadian rhythmicity can lead to serious health problems. Genetic modifications leading to disruption of normal circadian gene functions have been linked to a variety of psychiatric conditions including depression, seasonal affective disorder, eating disorders, alcohol dependence, and addiction. It appears that clock genes play an important role in limbic regions of the brain and influence the development of drug addiction. Furthermore, analyses of clock gene polymorphisms in diseases of the central nervous system (CNS) suggest a direct or indirect influence of circadian clock genes on brain function. In this chapter, I will present evidence for a circadian basis of mood disorders and then discuss the involvement of clock genes in such disorders. The relationship between metabolism and mood disorders is highlighted followed by a discussion of how mood disorders may be treated by changing the circadian cycle. HubMed – eating