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      Hyperphagia: Current concepts and future directions proceedings of the 2nd international conference on hyperphagia : Hyperphagia Directions

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          Abstract

          Hyperphagia is a central feature of inherited disorders (e.g., Prader-Willi Syndrome) in which obesity is a primary phenotypic component. Hyperphagia may also contribute to obesity as observed in the general population, thus raising the potential importance of common underlying mechanisms and treatments. Substantial gaps in understanding the molecular basis of inherited hyperphagia syndromes are present as are a lack of mechanistic of mechanistic targets that can serve as a basis for pharmacologic and behavioral treatments.

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          Highly efficient neural conversion of human ES and iPS cells by dual inhibition of SMAD signaling

          Stuart Chambers, Christopher Fasano, Eirini P. Papapetrou … (2009)
          Current neural induction protocols in human ES cells (hESCs) rely on embryoid body formation, stromal feeder co-culture, or selective survival conditions; each strategy displaying significant drawbacks such as poorly defined culture conditions, protracted differentiation and low yield. Here we report that the synergistic action of two inhibitors of SMAD signaling, Noggin and SB431542, is sufficient for inducing rapid and complete neural conversion of hESCs under adherent culture conditions. Temporal fate analysis reveals a transient FGF5+ epiblast-like stage followed by PAX6+ neural cells competent of rosette formation. Initial cell density determines the ratio of CNS versus neural crest progeny. Directed differentiation of human iPSCs into midbrain dopamine and spinal motoneurons confirm robustness and general applicability of the novel induction protocol. Noggin/SB431542 based neural induction should greatly facilitate the use of hESC and hiPSCs in regenerative medicine and disease modeling and obviate the need for stromal feeder or embryoid body based protocols.
          Article 0 comments Cited 525 times – based on 0 reviews     Review now
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            Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals.

            Rudolf Jaenisch, Adrian P. Bird (2003)
            Cells of a multicellular organism are genetically homogeneous but structurally and functionally heterogeneous owing to the differential expression of genes. Many of these differences in gene expression arise during development and are subsequently retained through mitosis. Stable alterations of this kind are said to be 'epigenetic', because they are heritable in the short term but do not involve mutations of the DNA itself. Research over the past few years has focused on two molecular mechanisms that mediate epigenetic phenomena: DNA methylation and histone modifications. Here, we review advances in the understanding of the mechanism and role of DNA methylation in biological processes. Epigenetic effects by means of DNA methylation have an important role in development but can also arise stochastically as animals age. Identification of proteins that mediate these effects has provided insight into this complex process and diseases that occur when it is perturbed. External influences on epigenetic processes are seen in the effects of diet on long-term diseases such as cancer. Thus, epigenetic mechanisms seem to allow an organism to respond to the environment through changes in gene expression. The extent to which environmental effects can provoke epigenetic responses represents an exciting area of future research.
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              Preliminary validation of the Yale Food Addiction Scale.

              Ashley Gearhardt, William Corbin, Kelly D. Brownell (2009)
              Previous research has found similarities between addiction to psychoactive substances and excessive food consumption. Further exploration is needed to evaluate the concept of "food addiction," as there is currently a lack of psychometrically validated measurement tools in this area. The current study represents a preliminary exploration of the Yale Food Addiction Scale (YFAS), designed to identify those exhibiting signs of addiction towards certain types of foods (e.g., high fat and high sugar). Survey data were collected from 353 respondents from a stratified random sample of young adults. In addition to the YFAS, the survey assessed eating pathology, alcohol consumption and other health behaviors. The YFAS exhibited adequate internal reliability, and showed good convergent validity with measures of similar constructs and good discriminant validity relative to related but dissimilar constructs. Additionally, the YFAS predicted binge-eating behavior above and beyond existing measures of eating pathology, demonstrating incremental validity. The YFAS is a sound tool for identifying eating patterns that are similar to behaviors seen in classic areas of addiction. Further evaluation of the scale is needed, especially due to a low response rate of 24.5% and a non-clinical sample, but confirmation of the reliability and validity of the scale has the potential to facilitate empirical research on the concept of "food addiction".
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                Author and article information

                Journal
                Title: Obesity
                Abbreviated Title: Obesity
                Publisher: Wiley
                ISSN: 19307381
                Publication date Created: February 2014
                Publication date (Print): February 2014
                Publication date (Electronic): February 26 2014
                Volume: 22
                Issue: S1
                Pages: S1-S17
                Affiliations
                [1 ]Pennington Biomedical Research Center; Louisiana State University System; Baton Rouge Louisiana USA
                [2 ]Department of Psychiatry; University of Florida College of Medicine; Gainesville Florida USA
                [3 ]Diabetes Molecular Genetics Section; Phoenix Epidemiology and Clinical Research Branch, NIDDK, NIH; Phoenix Arizona USA
                [4 ]College of Physicians and Surgeons; Columbia University; New York New York USA
                [5 ]Kansas University Medical Center; Kansas City Kansa USA
                [6 ]Division of Genetics and Metabolism, Department of Pediatrics; University of Florida College of Medicine; Gainesville Florida USA
                [7 ]New York Stem Cell Foundation; New York New York USA
                [8 ]UT Southwestern Medical Center; Dallas Texas USA
                [9 ]The Pittsburgh Partnership; Pittsburgh Pennsylvania USA
                [10 ]Metabolic & Molecular Imaging Group, MRC Clinical Sciences Centre; Imperial College London; UK
                [11 ]Section on Growth and Obesity; National Institute of Child Health and Human Development, NIH; Bethesda Maryland USA
                [12 ]Prader-Willi Syndrome Association (USA); Sarasota Florida USA
                [13 ]The Genetics of Obesity and Related Metabolic Traits Program; The Charles Bronfman Institute for Personalized Medicine, The Mindich Child Health and Development Institute, The Icahn School of Medicine at Mount Sinai; New York New York USA
                [14 ]Division of Pediatric Gastroenterology; Nutrition and Hepatology at Johns Hopkins School of Medicine; Baltimore Maryland USA
                [15 ]Center for Integrative Brain Research; Seattle Children's Research Institute; Seattle Washington USA
                [16 ]Center of Excellence in Obesity and Diabetes; University of Cincinnati; Cincinnati Ohio USA
                [17 ]Pediatrics and Medical Genetics; University of Iowa College of Medicine; Iowa City Iowa USA
                [18 ]Department of Endocrinology; Hôpital des Enfants and Paul Sabatier Université; Toulouse France
                [19 ]University of California, San Francisco, School of Medicine; San Francisco California USA
                [20 ]USDA/ARS Children's Nutrition Research Center, Department of Pediatrics and Molecular & Human Genetics; Baylor College of Medicine; Houston Texas USA
                [21 ]Department of Medical Genetics; University of Alberta; Edmonton Canada
                [22 ]McDermott Center for Human Growth and Development; UT Southwestern Medical Center; Dallas Texas USA
                Article
                DOI: 10.1002/oby.20646
                PubMed ID: 24574081
                SO-VID: c8ce4971-30bd-4d15-82b7-efe58ddfc367
                Copyright © © 2014
                License:

                http://doi.wiley.com/10.1002/tdm_license_1.1

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