Vol. 11, Supplement 1, May 2018 Official Organ of Affiliated with EASO DAG IFSO-EC

364 Pages·2017·16.16 MB·English

Vol. 11, Supplement 1, May 2018
Official Organ of Affiliated with
EASO DAG IFSO-EC
European Association Deutsche International Federation
for the Study of Obesity Adipositas-Gesellschaft for the Surgery of Obesity
Editorial Representatives Editorial Representative and Metabolic Disorders –
European Chapter
Hermann Toplak, Graz Matthias Blüher, Leipzig
Editorial Representative
Martin Fried, Prague
Editor-in-Chief Assistant Editor
Hans Hauner, MD Else Kroener-Fresenius Center for Nutritional Nora Klöting, MD I ntegrated Research and Treatment Center
Medicine, Klinikum rechts der Isar, Technical (IFB) AdiposityDiseases, University of
University of Munich, Munich, Germany Leipzig, Leipzig, Germany
Associate Editors
Jennifer Lyn Baker, Institute of Preventive Medicine, Frederiksberg John G. Kral, MD Department of Surgery, SUNY Downstate
MD Hospital, Frederiksberg, Denmark Medical Center, Brooklyn, NY, USA
Ellen E. Blaak, MD Department of Human Biology, NUTRIM Lauren Lissner, Department of Public Health and Community
School of Nutrition and Translational Research MD Medicine, Institute of Medicine, Sahlgrenska
in Metabolism, Maastricht University Medical Academy, University of Gothenburg,
Center, Maastricht, The Netherlands Gothenburg, Sweden
Matthias Blüher, MD Department of Medicine, Endocrinology and Bernhard Ludvik, MD D epartment of Medicine 1, Rudolfstiftung
Diabetes, University of Leipzig, Leipzig, Germany Hospital, Vienna, Austria
John E. Blundell, PhD School of Psychology, Faculty of Medicine and Dragan Micic, MD S chool of Medicine, University of Belgrade,
Health, University of Leeds, Leeds, UK Belgrade, Serbia
Karine Clément, MD Institute of Cardiometabolism and Nutrition, Manfred J. Müller, MD I nstitute of Human Nutrition and Food Science,
Assistance Publique-Hôpitaux de Paris, Faculty of Agricultural and Nutritional Sciences,
Pitié-Salpétrière Hospital, Paris, France Christian-Albrechts-University, Kiel, Germany
Carl-Erik Flodmark, Department of Pediatrics, Skåne University Yves Schutz, MD D ivision of Physiology, Department of Medicine,
MD Hospital Malmö, Malmö, Sweden University of Fribourg, Fribourg, Switzerland
Martin Fried, MD OB Klinika – Centre for Treatment of Obesity Hermann Toplak, MD L ipid Clinic, Department of Medicine, Medical
and Metabolic Disorders, 1st Faculty of Medicine, University of Graz, Graz, Austria
Charles University, Prague, Czech Republic Matthias Tschöp, MD H elmholtz Diabetes Center and Helmholtz
Vojtech Hainer, MD Obesity Management Centre, Institute of Pioneer Campus, Helmholtz Zentrum München,
Endocrinology, Prague, Czech Republic German Center for Diabetes Research (DZD),
Berit L. Heitmann, Research Unit for Dietary Studies, The Parker Technical University of Munich, Neuherberg,
MD Institute, Frederiksberg Hospital, Copenhagen, Germany
Denmark Haijun Wang, PhD D epartment of Child, Adolescent and Women’s
Anja Hilbert, PhD Integrated Research and Treatment Center (IFB) Health, School of Public Health, Peking
AdiposityDiseases, Behavioral Medicine, Univer- University, Beijing, China
sity of Leipzig, Leipzig, Germany Kurt Widhalm, MD A ustrian Academic Institute for Clinical
Anke Hinney, PhD Department of Child and Adolescent Psychiatry, Nutrition, Vienna, Austria
University Hospital Essen, University of Tommy Visscher, PhD W indesheim University of Applied Sciences,
Duisburg-Essen, Essen, Germany Zwolle, The Netherlands
Christina Holzapfel, University Hospital Klinikum rechts der Isar,
PhD Technical University of Munich, Munich,
Germany
S. Karger GmbH P.O. Box, 79095 Freiburg, Germany Founding Editor Johannes Hebebrand, Essen
Editorial Office Sven Riestenpatt, PhD;
[email protected]
Basel · Freiburg · Paris · London · New York · Chennai · New Delhi ·
Bangkok · Beijing · Shanghai · Tokyo · Kuala Lumpur · Singapore · Sydney
Editorial Board Members
Hans-Rudolf Berthoud, Pennington Biomedical Research Center, Paul T. Pfluger, MD H elmholtz Diabetes Center and Helmholtz
MD Louisiana State University System, Baton Pioneer Campus, Helmholtz Zentrum München,
Rouge, LA, USA German Center for Diabetes Research (DZD),
Stefan Engeli, MD I nstitute for Clinical Pharmacology, Hanover Technical University of Munich, Neuherberg,
Medical School, Hanover, Germany Germany
Gema Frühbeck, MD, Department of Endocrinology and Gabriela Roman, Clinical Center of Diabetes, Nutrition,
PhD Nutrition, Clínica Universidad de Navarra, MD, PhD Metabolic Diseases, 'Iuliu Hatieganu' University
University of Navarra, CIBEROBN, IdiSNA, of Medicine & Pharmacy, Cluj-Napoca, Romania
Pamplona, Spain Stephan Rössner, MD Professor emeritus, Karolinska Institutet, Apple
Susanna Hofmann, MD H elmholtz Center Munich, Institute of Diabetes Bay Obesity Research Centre, Bromma, Sweden
and Regeneration Research, Neuherberg, Jacob C. Seidell, PhD Department of Health Sciences, Faculty of Earth
Germany and Life Sciences, VU University Amsterdam,
Martin Klingenspor, Chair of Molecular Nutritional Medicine, Else Amsterdam, The Netherlands
MD Kröner-Fresenius Center, Technical University of Antonio J. Torres, MD D epartment of Surgery, Hospital Clinico San
Munich, Freising-Weihenstephan, Germany Carlos, Complutense University of Madrid,
Julian G. Mercer, MD T he Rowett Institute, University of Aberdeen, Madrid, Spain
Foresterhill, UK Christian Vaisse, Diabetes Center and Department of Medicine,
Vidya Mohamed-Ali, Adipokines and Metabolism Research Group, MD, PhD University of California San Francisco,
MD Centre for Clinical Pharmacology, BHF Labs San Francisco, CA, USA
University College London, London, UK Philippe Valet, PhD I nstitut des Maladies Metaboliques et Cardio-
Dénes Molnár, MD D epartment of Pediatrics, University of Pécs vasculaires, I2MC, Inserm – University Paul
Medical School, Pécs, Hungary Sabatier UMR 1048, Toulouse, France
Rubén Nogueiras, MD D epartment of Physiology, School of Medicine, Volkan Demirhan Division of Endocrinology, Metabolism and
University of Santiago de Compostela, Santiago Yumuk, MD Diabetes, Istanbul University Cerrahpaşa
de Compostela, Spain Medical Faculty, Istanbul, Turkey
Jean-Michel Oppert, Department of Nutrition, Pitié-Salpétrière
MD Hospital (AP-HP), Paris, France
Andreas F.H. Pfeiffer, Department of Clinical Nutrition, German
MD Institute of Human Nutrition Potsdam-
Rehbruecke, Nuthetal, Germany
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Vol. 11, Supplement 1,
May 2018
25th European Congress on
Obesity
Vienna, Austria, May 23–26, 2018
ABSTRACTS
Basel · Freiburg · Paris · London · New York · Chennai · New Delhi ·
Bangkok · Beijing · Shanghai · Tokyo · Kuala Lumpur · Singapore · Sydney
Committee
Obesity Facts 2018;11(suppl 1):IV
PROGRAMME ORGANISING COMMITTEE (POC)
EASO EC
President Hermann Toplak (Graz)
President Elect Nathalie Farpour-Lambert (Geneva)
Secretary Ellen Blaak (Maastricht)
Treasurer Jason Halford (Liverpool)
Regional VP North Johannes Hebebrand (Essen)
Regional VP Middle Dana Mullerova (Pilsen)
Regional VP South Volkan Yumuk (Istanbul)
COTF Co-Chair Jennifer Baker (Copenhagen)
COTF Co-Chair Jens-Christian Holm (Copenhagen)
OMTF Co-Chair Luca Busetto (Padua)
OMTF Co-Chair Dror Dicker (Tel Aviv)
PPHTF Chair Harry Rutter (Oxford)
SAB Co-Chair Gijs Goossens (Maastricht)
Paul Christinsen (Liverpool)
Dragan Micic (Belgrade)
Lauren Lissner (Gothenburg)
Gema Frühbek (Navarra)
Austrian Colleagues
LOC Berhard Ludvik (Vienna)
LOC Karin Schindler (Vienna)
LOC Johanna Brix (Vienna)
LOC Thomas Scherer (Vienna)
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Contents
Obesity Facts 2018;11(suppl 1):V
PLENARY SESSIONS
Wednesday, 23 May 2018
PL1 – Personalised versus person centred approaches 1
Thursday, 24 May 2018
PL2 – Is obesity a trigger for puberty? 1
PL3 – Novel aspects in neuroendocrine and energy homeostasis regulation
by peripheral signals acting through the CNS. Implications for obesity
therapeutics 1
PL4 – Global food policy and obesity 2
Friday, 25 May 2018
PL5 – Large-scale regulatory changes focused on obesity prevention:
Current state of knowledge in Europe and beyond 2
Saturday, 26 May 2018
PL7 – The Pink Adipocyte 2
SCIENTIFIC SESSIONS
Wednesday, 23 May 2018
S1 – Joint Session with TOS: Integrating obesity research from
across the globe 3
S2 – Psychological mechanisms and successful interventions:
‘what kind of eater are you?’ 5
S3 – How to overcome stigma and discrimination 6
S4 – The role of gut microbiota: from basic science to clinical practice 7
S5 – Does the obesity paradox really exist? 8
Thursday, 24 May 2018
S6 – Signals and Messaging 8
S7 – WHO/EASO Session: Food marketing in the digital age –
immersive, influential, unstoppable? 10
S8 – Individualised prescription of physical activity: prevention to treatment 10
S9 – Joint Session with IFSO-EC: How to build an effective and safe clinical
pathway for bariatric surgery patients 11
S10 – Joint Session with WCRF: Obesity and Cancer 12
S11 – Joint Session with IFSO-EC: How to tackle specific post-bariatric clinical
problems 13
S12 – Food addiction: searching for the culprit 14
S13 – Short and long term consequences of childhood obesity 15
S14 – Where do we want to be in 2030? 17
S15 – Obesity in children: science vs reality 17
Friday, 25 May 2018
S17 – EASO Nutrition Working Group: Evidence and Efficacy 19
S18 – Assessing body composition for better understanding of risks related
to childhood obesity and designing effective interventions 20
S19 – Innovative approaches to improving health in low income areas 22
S20 – Understanding human appetite control – are we making progress? 22
S22 – Physiology of obesity: From mechanisms to medicine 24
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Contents
Obesity Facts 2018;11(suppl 1):VI
Saturday, 24 May 2018
S23 – Hunger, dieting and cognitive control of food intake 25
S24 – What is the current state of childhood obesity management? 26
S25 – Obesity and reproductive health 27
S26 – Public health interventions: how to set them up and keep them going 28
S27 – The NoHoW Project 29
ORAL SESSIONS
Wednesday, 23 May 2018
O1 – Pathophysiological mechanisms behind weight loss 30
O2 – Nutritional aspects in childhood obesity 32
O3 – Energy Homeostasis 34
Thursday, 24 May 2018
O4 – Energy balance and activity 37
O5 – Adipose tissue biology 39
Friday, 25 May 2018
O6 – Epidemiology and lifestyle 42
O7 – Bariatric surgery 45
O8 – New directions in obesity management 48
O9 – Psychological determinants and outcomes 51
O10 – Nutrition and the food environment 53
O11 – Lifecourse effects of childhood obesity 55
Saturday, 26 May 2018
O12 – Obesity trajectories in children 58
O13 – Policy in action 61
O14 – Glucose and lipid homeostasis 64
POSTER SESSIONS
T1 – Basic and Experimental Science 66
T2 – Health, Behavior and Environment 119
T3 – Childhood and Adolescent Obesity 187
T4 – Management and Intervention 235
LATE-BREAKING ABSTRACTS
T1 – Basic and Experimental Science 320
T2 – Health, Behavior and Environment 324
T3 – Childhood and Adolescent Obesity 332
T4 – Management and Intervention 334
Imprint II
Author Index 341
Author Index Late-Breaking Abstracts 357
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1
Abstracts
Obesity Facts 2018;11(suppl 1):1–358
Doi:10.1159/000489691
PLENARY SESSIONS*
Wednesday, 23 May 2018 Thursday, 24 May 2018
PL1 – Personalised versus person centred approaches PL2 – Is obesity a trigger for puberty?
PL1.1 PL2.1
Personalised approaches Is obesity a trigger for puberty?
Orer, H. S. Ong, K. K.
Pharmacology, Koç University School of Medicine, Istanbul/Turkey MRC Epidemiology Unit & Department of Paediatrics, University of Cambridge,
Cambridge/United Kingdom
Introduction: The use of patient-specific information to tailor precise
treatments is the essence of the personalized medicine. The ultimate aim Introduction: The timing of puberty, the transition from child to adult,
is to have interventions as efficient as possible without adverse reactions. varies widely between individuals. This wide variation is implicated in
Methods: A systematic review of the literature was made to evaluate the psychological concerns and risk-taking behaviours during adolescence,
current status of genomic medicine with relation to obesity. and it also has important relevance for long-term health. In general, ear-
Results: The emergence of evidence-based medicine marks the culmi- lier timing of puberty is associated with higher risks for premature mor-
nating point of the modern (or analog) era where randomized controlled tality and health outcomes, such as obesity, type 2 diabetes, cardiovascular
trials are the backbone of the clinical research. However, with the advent disease and sex steroid-sensitive cancers.
of molecular biology in the late 20th century, genomics has fast taken cen- Methods: This talk will highlight findings from cohort studies, trials and
ter stage of the treatment. Pharmacogenomic studies showed that not all population genetics studies.
drugs act the same way in all individuals, even though the diagnosis is the Results: A major role of childhood obesity in promoting earlier timing
same. As the gene-wide analyses become affordable, genetic profiling has of puberty is supported by many epidemiological studies, particularly in
become an essential part of the patient management in targeted therapy girls. On the contrary, obese boys are sometimes reported to have delayed
protocols. Gene-based technologies also have a predictive value, an un- puberty. Secular trends towards earlier puberty timing appear to coincide
precedented opportunity to develop biomarkers. The acknowledgment of with population-level markers of nutritional sufficiency, but it is curious
patient heterogeneity compromises the statistical power of randomized that the secular trends have slowed in settings where childhood obesity
controlled trials. New measures to assess efficacy and safety of the new is still rising. Genome-wide association studies (GWAS), which genotype
drugs are emerging. Exceptional responders, or “outliers” who were once hundreds of thousands of common genetic variants located across the
excluded from data analyses or concealed in the background noise, are entire genome, have identified hundreds of specific genetic determinants
now seen as an opportunity to pinpoint unique mechanisms of action of of pubertal timing. These findings substantiate strong mechanistic links
drugs. However, such a precision renders the data generalization prob- between obesity and earlier timing of puberty, as well as between earlier
lematic and the development of the new therapy modalities too costly. timing of puberty and later disease risks. While many genomic loci im-
Until now, rare diseases and cancers are the two main avenues of research plicate genes that regulate the hypothalamo-pituitary-gonadal axis, many
to implement personalized medicine. In the future, complex disorders and others implicate genes that regulate energy homeostasis and weight gain,
other conditions, including obesity will increasingly enter into its scope. as well as obesity-independent pathways to later disease.
Conclusion: Both inherited genetic and environmentally-modified epi- Conclusion: Puberty timing is an important outcome to be considered
genetic factors contribute to the development of obesity, and the compli- in the evaluation of interventions that aim to avoid or reduce childhood
cations emerge in many years. Therefore, it is difficult to establish a direct obesity.
link between obesity and organ dysfunctions. Gene networks that serve as
an on-off switch in the presence of appropriate epigenetic factors are im-
portant drug targets. Besides the therapy focus, prevention will also be an
important area of research in the coming years. Especially, genomic risk PL3 – Novel aspects in neuroendocrine and energy
assessment and associated lifestyle changes may be of value to prevent the homeostasis regulation by peripheral signals acting
obesity preemptively. Financial bottlenecks fast become a significant lim- through the CNS. Implications for obesity therapeutics
itation to the development of personalized treatments. A major problem
in obesity management may be that by putting too much emphasis on the
genetic constituency, one may fail to engage the patients in lifestyle chang- PL3.1
es. Moreover, in such a lucrative field, marketing efforts may overtake the Novel aspects in neuroendocrine and energy homeostasis
science, and ethically questionable practices may prevail. regulation by peripheral signals acting through the CNS.
Implications for obesity therapeutics
Mantzoros, C.
Harvard, Boston/USA
Introduction: In the mid-1990s, the discovery of the hormone leptin
raised hopes that researchers had finally found a treatment for obesity.
With its name based on the Greek word “leptos” (meaning thin), leptin
secreted by fat cells appeared to switch off the urge to eat in preclinical
animal studies.
© 2018 S. Karger GmbH, Freiburg * Please note: By default, authors did not disclose any conflicts of
interest unless explicitly stated in the abstract.
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Methods: While those findings did not translate to humans who are over- ing of the rapid shifts in our diets, eating behaviors and the factors un-
weight or obese, subsequent work by Mantzoros and his colleagues in the derlying these changes. While we also need healthy activity patterns and
field resulted in the paradigm-shifting concept that fat tissue is not an in- need to work on ways to improve physical activity, we have learned that
ert energy storage organ but an active endocrine organ – a concept that we must shift toward much healthier eating patterns to prevent and even
revolutionized the way endocrinologists view metabolic disorders and has reduce obesity. But in all cases, we are at a very early stage of understand-
contyributed to our understanding of neuroendocrine regulation, obesity, ing for each type of action what works, what are the limitations and how
insulin resistance, and their consequences which include diabetes, cardio- can we improve our actions. I review what we know in the areas of fiscal
vascular disease, and malignancies. In more recent studies, actions, marketing controls, front-of-the-package profiling.
Results: Mantzoros and colleagues are using, neuroanatomical, neuro- Methods: Use of an array of longitudinal commercial datasets on food
cognitive and neuroimaging studies to examine how environmental and purchases, food retail data, commercial sales, employment and price data
dietary factors interact with hormones to alter activity in the brain and along with self-collected in-depth data on each food product, including
thus neuroendocrine regulation of human physiology and eating behav- ingredients, nutrition facts panels, bar codes and much other data on each
ior. package. Longitudinal fixed and random effects statistical models based
Conclusion: Novel physiology findings will be presented along with on counterfactual designs where we look at how policies shift trends[tra-
translational research contributions that propel forward our understand- jectories] of food purchases. Many other methods are also being used to
ing of the physiology and therapeutic utility on leptin and adipokines in look at overall food urchase pattner shifts . For fiscal evaluation this is
humans, the development of novel treatments for neuroendocrine and combined with other sales, employment, price and demographic data. For
metabolic disease, and the physiology of other key molecules and hor- marketing evaluations, commercial data on audiences and all TV shows
mones secreted by muscle and the gastrointestinal tract such as incretins are used to select representative samples of synthetic multiple weeks of TV
that regulate appetite and obesity in humans. viewing. For package characters and other claims, coding of all materials
on packages is used. Cohorts of children in various ages are used to pro-
Conflicts of Interest: Shareholder: Coherus, Pangea and Pnoe, Consulting or
vide exposure to various TV shows to which they are linked for advertis-
grant fees through my Institution: Novo, Esai, Aegerion, Intarcia
ing exposure in addition to data on knowledge and attitude changes and
ultimately dietary behavior.
Results: My review focuses more on current evaluations underway in
PL4 – Global food policy and obesity Mexico, Chile, the US and limited work done in Europe. Other studies are
just in the initial stages and discussed briefly. Fiscal actions appear now to
be one of the most promising areas. We know that increased relative costs,
PL4.1 especially if significant for that specific population, can reduce intake of
Global Food Policy and Obesity the taxed product, be it sugary beverages or various categories of what we
might term nonessential junk food. In the marketing area our knowledge
Brownell, K.
of the inability of voluntary efforts to make any impact on behavior is
Sanford School of Public Policy, Duke University, Durham, NC/USA great but we are only now learning about the effort of more comprehen-
sive regulatory efforts, led by Chile. Similarly, in the front-of-the-package
Understanding the conditions that make obesity so prevalent, and iden-
profiling area, knowledge is scarce, but several evaluations provide some
tifying opportunities for prevention, requires knowledge of policies and
sense of potentially effective options. All these efforts have focused at the
practices that affect food systems overall. Food assistance programs in the
large-scale level on limited aspects of what constitutes our overall food
context of international development, for example, are intended to ad-
system. I discuss some of the gaps and how we need to begin to think
dress world hunger but affect broader food systems in ways that likely in-
about the next generation of interventions. We cannot limit ourselves to
fluence obesity. Intersections will be discussed around four food policy ar-
the three major clusters of current actions but must move far beyond. We
eas: obesity; food insecurity; agriculture and environment; and food safety
have major gaps in food system interventions that require experimenta-
and defense. There is considerable depth of expertise in each area, but
tion and major pushes. And we are far from learning how to create a cul-
too little interaction across areas. Coordinated food policies could lead
ture of healthy eating.
to wins across areas, stronger coalitions of groups supporting particular
Conclusion: While there is much to cheer, we must recognize we have
policies, and better anticipation of unintended consequences. A model for
many decades of major challenges ahead. We are in the very early stages of
coordination of world policy will be presented, with special attention to
learning what works and must undertake thoughtful evaluations of what
implications for addressing obesity.
works as well as constantly learn of ways to address the industrial forces
fighting against healthy dietary policies in the coming decades.
Friday, 25 May 2018
Saturday, 26 May 2018
PL5 – Large-scale regulatory changes focused on
obesity prevention: Current state of knowledge in
PL7 – The pink adipocyte
Europe and beyond
PL7.1
PL5.1 The pink adipocyte
Large-scale regulatory changes focused on obesity
prevention: Current state of knowledge Cinti, S.
University of Ancona, Ancona/Italy
Popkin, B. M.
Nutrition, Gillings School of Global Public Health, University of North Carolina at Introduction: Most of white and brown adipocytes, in spite of their well
Chapel Hill, Chapel Hill, NC/USA known different functions: i.e. storing energy (white) and thermogene-
sis (brown), are contained together in visceral and subcutaneous depots
Introduction: In Europe and globally we have seen increases in obesity, (adipose organ) in all mammals including humans (S Cinti The Adipose
particularly child obesity. This appears to be the decade when countries Organ, Kurtis Milan 1999, A Frontini et al Cell Metab 2010). A grow-
are finally beginning to take on major fiscal and regulatory efforts to ad- ing body of evidence suggests that the reason for this anatomical mixture
dress this problem. We are beginning to gain a much greater understand- could reside in the fact that adipocytes have peculiar plastic properties
2 Obes Facts 2018;11(suppl 1):1–358 Abstracts
allowing them to convert directly each other under appropriate stimuli (S transdifferentiate to brown adipocytes, highlighting a hitherto unappreci-
Cinti Am J Physiol EM 2009). Under chronic cold exposure white convert ated feature of mouse adipose organ plasticity (Giordano et al Cell Physiol
into brown to support the need for thermogenesis and under obesogenic 2017).
diet brown convert into white to satisfy the need of energy storing. Adi- Methods: Data have been obtained mainly with morphology, immuno-
pocyte population in the mammary gland offers another striking example histochemistry and lineage tracing techniques.
of adipocyte plasticity: during pregnancy and lactation adipocytes trans- Results: We recently showed by transmission electron microscopy that in
differentiate into milk-producing epithelial cells (we propose to call them: the post-lactating mammary gland interscapular multilocular adipocytes
pink adipocytes) and vice versa in the post-lactation period (Morroni M found close to the mammary alveoli contain milk protein granules. Lin-
et al PNAS 2004, DeMatteis R et al Stem Cells 2009, Prokesch et al Stem eage tracing system allowed showing that the involuting mammary gland
Cells 2014). The white into brown transdifferentiation is of great medical of whey acidic protein-Cre/R26R mice, whose secretory alveolar cells ex-
interest because the brown phenotype of the adipose organ is associat- press the lacZ gene during pregnancy, contains some X-Gal-stained and
ed with obesity resistance and drugs inducing the brown phenotype curb uncoupling protein 1 immunoreactive interscapular multilocular adipo-
obesity and related disorders (Giordano et al Nature Rev Drug Discov cytes. These data suggest that during mammary gland involution some
2016). We recently showed by transmission electron microscopy that in milk- secreting epithelial cells in the anterior subcutaneous depot may
the post-lactating mammary gland interscapular multilocular adipocytes transdifferentiate to brown adipocytes, highlighting a hitherto unappreci-
found close to the mammary alveoli contain milk protein granules. Lin- ated feature of mouse adipose organ plasticity (Giordano et al Cell Physiol
eage tracing system allowed showing that the involuting mammary gland 2017).
of whey acidic protein-Cre/R26R mice, whose secretory alveolar cells ex- Conclusion: In conclusion the plasticity of adipose organ is further sup-
press the lacZ gene during pregnancy, contains some X-Gal-stained and ported by the reversible physiologic transdifferentiation of white to pink
uncoupling protein 1 immunoreactive interscapular multilocular adipo- adipocytes and by pink to brown. These data open new avenues for future
cytes. These data suggest that during mammary gland involution some treatment of obesity-type 2 diabetes and allow a better understanding of
milk- secreting epithelial cells in the anterior subcutaneous depot may mammary gland physiology.
SCIENTIFIC SESSIONS*
Wednesday, 23 May 2018 Hunan province, along with stronger similarity in microbes in the urban
(versus rural) Chinese as individuals in the Human Microbiome Project
S1 – Joint Session with TOS: Integrating obesity cohort of American subjects. Furthermore, using whole metagenome se-
quencing, we found that urbanization was associated with a loss of micro-
research from across the globe
bial diversity along with increased gene diversity and antibiotic resistance
and virulence strongly correlated with Escherichia and Shigella.
S1.1 Conclusion: Urbanization in China is associated with changes in be-
Urbanization in China in Relation to Obesity: Diet, Omics, and haviours, weight status, and cardiometabolic diseases but at differences
Cardiometabolic Disease in pace of change across more and less urbanized areas and with differ-
ent pathways to disease. Our data suggest that urbanization has produced
Gordon-Larsen, P. convergent evolution of the gut microbial composition in American and
Professor and Vice Chair For Research, Nutrition University of North Carolina at urban Chinese populations, resulting in similar compositional patterns
Chapel Hill, Chapel Hill, NC/USA of abundant microbes through similar lifestyles on different continents.
Introduction: Urbanization is associated with increased risk for obesity,
diabetes, and other chronic diseases, yet we know little about the pathways S1.2
through which urbanization bears its influence. Partially these gaps relate Fast food restaurants and obesity: guilty as charged or falsely
to lack of data across molecular to behavioural to environment levels. accused?
Methods: We hypothesised that urbanization in China accompanies
Speakman, J. R.1; Mazidi, M. 2
changes in the microbiome and metabolome, which in turn relate to di-
etary behaviours, obesity, and cardiometabolic diseases. In this study, we 1State Key Laboratory of Molecular Developmental Biology, Institute of Genetics
used data from the China Health and Nutrition Survey and compared the and Developmental Biology, Chinese Academy of Sciences, Beijing/China
2University of the Chinese Academy of Sciences, Beijing/China
gut microbiome, plasma metabolome, dietary habits and health biomark-
ers of rural and urban people from a single Chinese province. We used Introduction: In the USA the obesity epidemic has been mirrored by
16S ribosomal RNA (rRNA) sequencing of faecal samples, as well as whole expansions in the numbers of, and portion sizes at, fast food restaurants
genome sequencing data to assess the gut microbial community of our (FFR), leading many to lay the blame for the epidemic at the door of the
subjects and plasma metabolomics to characterize circulating metabolites restaurant industry. If FFR do cause obesity, greater per capita densities of
in the host bloodstream. We used 24-hour dietary recall data to character- FFR should correlate with greater obesity levels.
ize the dietary intake of the participants. We used pathway-based models Methods: We used county level data for obesity prevalence across the
to examine pathways from urbanization through diet behaviours to car- mainland USA in 2012 and matched this to county level per capita densi-
diometabolic disease and we used mixed linear models to examine dif- ties of FFR and FSR in the same year. Multiple linear regression was used
ferences in urban versus rural status with microbial and metabolite data. to determine the relation between prevalence of obesity and densities of
Results: We found increases in many markers of Westernized diet across FFR and FSR after adjustment for confounding factors.
time and with urbanization, with strongest effects in individuals of low Results: Contrary to expectations obesity prevalence was highly signifi-
and moderate urbanization whereas individuals living in highly urbanized cantly negatively related to the densities of both FFR and FSR (combined
areas had slower pace of increase. Indirect pathways from urbanization effect R2 = 0.195). This was principally because greater numbers of both
through baseline and change in traditional and Western markers of diet as FFR and FSR were located in areas where individuals were on average
well as baseline occupational activity were associated with BMI at follow richer and more educated. When we normalised for these factors (and
up. We identified significant differences in the microbiota and microbio- additional socioeconomic variables) the associations between restaurant
ta-related plasma metabolites in rural versus recently urban subjects from densities and obesity effectively disappeared, (pooled R2 = 0.008). Esti-
Abstracts Obes Facts 2018;11(suppl 1):1–358 3
* Please note: By default, authors did not disclose any conflicts of
interest unless explicitly stated in the abstract.
mates of the proportion of calories consumed out of the home indicate on age, gender or hormones, have explained only a small percentage of the
average 15.9% of calories are consumed in FFR and FSR. variability. However, novel insights suggest an interaction between diet
Conclusion: Variations in the density of FFR and FSR are not correlat- composition and the individual obese patient’s glucose metabolism, open-
ed with the prevalence of obesity in the USA. This is likely because food ing up for prescription of personalized diets with a much greater success
consumed in these establishments is responsible for less than a one fifth rate than previous “one diet fits all” concept.
of total energy intake. This has implications for policy decisions regarding Methods: We hypothesise that the acute satiating effect of carbohydrates
how we aim to tackle the obesity epidemic. depends on glucose uptake in insulin-dependent tissue (brain, muscle
and liver), whilst the satiating effect of fat and protein depends more on
the release of gastrointestinal hormones with neurohumoral signalling to
S1.3
the brain (CCK, GLP-1 and PYY). There is evidence that the “gluco-static
A comparative analysis of explicit weight bias in the UK and
concept” is an important regulator of satiation and determinant of spon-
eight other countries
taneous energy intake during meals. With increasing insulin resistance
Kyle, T.K.1; Nadglowski, J.2 Ramos Salas, X.3; Thomas, D.4; Puhl, R.M.5; and failure to compensate with enhanced postprandial insulin secretion,
Watts, K.4 the satiating effects of carbohydrates are attenuated due to reduced glu-
cose uptake in the brain, and possibly in other tissues. Consequently, the
1ConscienHealth, Pittsburgh, PA, USA;
2Obesity Action Coalition, Tampa, FL, USA; satiating effect of carbohydrate is weakened in obese individuals with type
3Canadian Obesity Network, Edmonton, Alberta, Canada; 2 diabetes or pre-diabetics with low insulin secretion. Carbohydrate-rich
4US Military Academy, West Point, NY, USA; diets are thus effective in normoglycemic obese individuals, but type 2
5Rudd Center for Food Policy and Obesity, University of Connecticut, Hartford, diabetics lose more weight on carbohydrate-restricted diets rich in protein
CT, USA and fat. We tested this hypothesis by reanalysing randomized controlled
trials of diets for weight loss.
Introduction: Weight bias (WB) is an important source of harm to peo-
Results: In seven different trials we found that some pre-treatment in-
ple with obesity (PwO) and a barrier to progress in reducing its health
dices for insulin resistance and secretion are powerful predictors of in-
impact. Although WB has been documented in many different countries,
dividual weight loss responsiveness to diets with different carbohydrate
few studies have examined the extent of WB and trends across multiple
contents. For example, a randomized energy-restricted diet comparison
countries. The present research measured explicit attitudes about PwO
of a low-fat, high-carbohydrate versus a low-carbohydrate, higher-fat diet
and beliefs about the causes of obesity in 9 countries: Australia (AU),
(NUGENOB), found no difference in weight loss (7.5 kg in both arms).
Brazil (BR), Canada (CA-En, CA-Fr), Germany (DE), Italy (IT), Mexico
In a reanalysis, type 2 diabetics lost 2.0 kg more on the low-carbohy-
(MX), Sweden (SE), UK, and US.
drate, higher-fat diet than on the low-fat, high-carbohydrate diet, whereas
Methods: Random samples of 90,573 adults completed anonymous, vol-
normoglycemic individuals lost a mean of 0.4 kg more on the low-fat,
untary online surveys beginning in the fall of 2016. Participants indicated
high-carbohydrate diet (group difference 2.5 kg). With diets high versus
their agreement (using 5-point Likert scales) with 4 narratives regarding
low in glycaemic load, fibre and whole grain, the difference between nor-
causes of obesity, as well as perceptions of blame, laziness, self-discipline,
moglycemic and prediabetic obese individuals in responsiveness is sub-
and social acceptance of PwO. Cumulative logit models were fit to each
stantial. In the Diogenes trial prediabetic individuals regained a mean
survey question within each category with responses on 5-point Likert
of 5.8 kg more on a high–glycaemic load diet than on a low–glycaemic
scales as outcome variables. Explanatory variables for the models were
load diet, whereas normoglycemic individuals regained only 1.4 kg more
gender, age intervals, and country and interaction terms.
(group difference 4.4 kg). Responsiveness in prediabetic obese to high-fi-
Results: In all nine countries, respondents agreed with addiction to junk
bre diets seems also to depend on microbiota, e.g. the ratio of Prevotella
food and sugary drinks as an explanation for obesity, consistently rating
to bacteroides, which suggests that the production of short-chain fatty ac-
it as high or higher than personal irresponsibility, environment, or medi-
ids such as butyrate by certain bacteria may stimulate satiety, potentially
cal narratives. BR, CA-Fr, and IT favored the addiction narrative over all
through an insulin sensitizing mechanism.
other narratives. Only US and UK respondents expressed beliefs in irre-
Conclusion: Personalized diets matching macronutrient composition and
sponsibility as strong as their beliefs in other narratives. UK respondents
fibre content of diets to glucose metabolism and microbiota can improve
tended to reject a medical narrative as a cause for obesity. MX respondents
weight loss outcome.
were likely to agree that PwO are lazy and deserve blame. AU respondents
were likely to agree with blaming and socially rejecting PwO. Across all Conflicts of Interest: Arne Astrup is co-inventor of patents owned by UCPH,
measures, UK respondents expressed harsh bias while CA-Fr respondents and is co-owner of UCPH spin-out Personalized Weight Management Research
expressed less bias. Consortium/Gluco-diet.dk. He is advisor to & member of advisory board for
Conclusion: Patterns of explicit bias about obesity and PwO differ signifi- Gelesis, USA. Recent research funded by Gelesis. Full disclosure on the NEXS,
UCPH website.
cantly among the countries studied. Even though food addiction remains
a matter of scientific controversy, public opinion seems to favor this con-
cept as an explanation for obesity. In some countries, such as the UK, bias S1.5
appears to be an especially important factor to consider for advancing sci- Regulatory efforts in Mexico & Chile: impacts of taxation on
ence-based approaches to reducing obesity. Continued tracking of these obesity. Comparisons with taxation efforts in the US
attitudes over time may offer important insights into cultural differences
in weight bias and strategies to address this problem. Barquera, S.; Colchero, A; Sánchez-Bazán, K.
Nutrition and Health Research Center (CINyS), National Institute of Public
Health (INSP), Mexico City/Mexico
S1.4
Personalized dietary management of obesity based on simple Introduction: Fiscal policies have been used to reduce the consumption
biomarkers of goods with harmful effects on health such as tobacco, alcohol and, re-
cently, sugar-sweetened beverages (SSB). In 2014, Mexico implemented
Astrup, A.
an excise tax of a 1 peso per liter to all non-alcoholic beverages with added
Department of Nutrition, Exercise and Sports, University of Copenhagen, sugars. In 2014, Chile increased an existing tax to SSB from 13 to 18% for
Copenhagen/Denmark beverages with a sugar concentration of at least 6.25grms/100ml and those
below that cut-off point decreased to 10%. In 2015, the city Berkeley in the
Introduction: Slimming diets produce variable responses, ranging from
USA implemented a one cent ($0.01) per ounce excise tax to all non-alco-
major weight loss, to almost no loss, or even weight gain. Efforts to iden-
holic beverages with caloric sweeteners added. The objective of the study
tify responders based on pre-treatment biomarkers such as initial BMI,
4 Obes Facts 2018;11(suppl 1):1–358 Abstracts