Brain vs Gut

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Brain vs Gut

Monday, May 2, 2011

The New York Academy of Sciences

Energy balance over one's life-span varies within a narrow range in most people, yet it reflects an incessant competition between countervailing energy-storing (anabolic) and (less abundant) energy-using (catabolic) processes. Concomitantly there is a conflict between autonomic/metabolic and cognitive/behavioral processes rendering labor-saving Homo sapiens physiologically maladaptive, embodied in the chronic overnutrition syndrome, obesity. This symposium brings together pre-clinical and clinical scientists to present an update on diverse aspects of energy balance, from nutrient sensing and appetite regulation to eating disorders and bariatric surgery, and constructively discuss current minimally invasive interventions to restore healthy energy balance.

This event will also be broadcast as a webinar.

Please note: Transmission of presentations via the webinar is subject to individual consent by the speakers. Therefore, we cannot guarantee that every speaker's presentation will be broadcast in full via the webinar. To access all speakers' presentations in full, we invite you to attend the live event in New York City, where possible

Networking reception to follow.

Grant Support

This meeting is part of our Translational Medicine Initiative, sponsored by the Josiah Macy Jr. Foundation and The Mushett Family Foundation.

This event is funded in part by the Life Technologies™ Foundation.

Agenda

*Presentation times are subject to change.


8:00 AM

Registration & Continental Breakfast

8:30 AM

Welcome & Opening Remarks
Jennifer S. Henry, PhD, The New York Academy of Sciences
John G. Kral, MD, PhD, SUNY Downstate Medical Center

SESSION I

Moderator: John G. Kral

8:45 AM

The Evolution of Metabolic Surgery
John G. Kral, MD, PhD, SUNY Downstate Medical Center

9:15 AM

Bariatric Surgery
Philip R. Schauer, MD, Bariatric and Metabolic Institute, Cleveland Clinic

9:45 AM

NOTES for Appetite
Christopher C. Thompson, MD, MSc, Brigham and Women's Hospital

10:05 AM

Questions and Discussion

10:20 AM

Coffee Break

SESSION II

Moderator: Gary J. Schwartz

10:45 AM

Appetitive Peptides
Timothy H. Moran, PhD, Johns Hopkins University School of Medicine

11:30 AM

Incretins
Blandine Laferrère, MD, Columbia University—St. Luke's Roosevelt Hospital Center

11:55 AM

Human Foregut Endocrine Cells
Walter J. Pories, MD, East Carolina University

12:15 PM

Lunch

SESSION III

Moderator: Gary J. Schwartz

1:15 PM

Neurobiology of Motivation to Eat
Allen S. Levine, PhD, University of Minnesota

2:00 PM

From Mouth to Gut: Sweet Taste Receptors and the Vagus
Karen L. Teff, PhD, Monell Chemical Senses Institute and University of Pennsylvania

2:30 PM

Nutrient Sensing and Appetitive Behavior
Anthony Sclafani, PhD, CUNY, Brooklyn College

3:00 PM

Questions and Discussion

3:15 PM

Coffee Break

SESSION IV

Moderator: Gary J. Schwartz

3:35 PM

Appetitive Neuroimaging in Human
Gene-Jack Wang, MD, Brookhaven National Laboratories

4:00 PM

Eating Behavior in Eating Disorders
B. Timothy Walsh, Columbia University

4:25 PM

Panel Discussion: Research Needs
All speakers and Gary J. Schwartz, PhD, Albert Einstein College of Medicine
Moderator: John G. Kral

5:00 PM

Networking Reception

6:00 PM

Adjourn

Speakers

Organizers

John G. Kral, MD, PhD

SUNY Downstate Medical Center

With an MA in Behavioral Neuroscience (Psychology) Dr. Kral attended medical school at the University of Göteborg, Sweden where he completed residencies in Surgery and Medicine and PhD studies on adipose tissue and lipid and carbohydrate metabolism. He initiated the program for obesity surgery in Göteborg and, in 1981 the Division of Surgical Metabolism at St. Luke’s-Roosevelt Hospital Center, Columbia U., New York. Apart from studies of body composition, adipose tissue receptors and lipid and carbohydrate metabolism his career-long interests have included ingestive behavior and genetic and epigenetic determinants of the chronic inflammatory insulin resistant over-nutrition syndrome termed “obesity”. In 1983 he was a co-founder of the American Society for Bariatric Surgery and co-organized the 1991 NIH Consensus Development Conference: Gastrointestinal Surgery for Severe Obesity. Dr Kral studied the effects of intestinal diversion on hyperinsulinemia, gastric emptying, intestinal adaptation, microflora and mucosal immunity and performed the first clinical studies of vagotomy for the treatment of obesity. His most recent publications describe early-life stress as a precursor of insulin resistance in monkeys and the importance of the intrauterine environment for the development of adolescent obesity and insulin resistance in humans.

Andrew G. Swick, PhD

Nutrition Research Institute, University of North Carolina

Dr Andrew G. Swick has over 20 years of experience in obesity and metabolic diseases research with expertise in relevant cell and animal models and a keen understanding of translational research. He joined the University of North Carolina at Chapel Hill Department of Nutrition and the Nutrition Research Institute in August of 2010 where he is currently an associate professor and Director of Obesity and Eating Disorders Research. Dr Swick’s two main areas of research are 1) gut metabolism as it relates to obesity and metabolic diseases and 2) body weight and energy expenditure in humans with an emphasis on variability in energy metabolism in response to diet, exercise, nutriceuticals and pharmaceuticals etc. Dr Swick earned a BS in Animal Science from the University of Florida in 1981 followed by an MS in Nutrition from the University of Nebraska in 1982. While in Lincoln, he worked on the effects of dietary fiber and fat on serum lipid levels. He then moved on to the University of Wisconsin where he conducted research on diet-induced-thermogenesis and brown adipose tissue metabolism and function. After earning his PhD in 1987, Andy pursued postdoctoral research at the Lineberger Cancer Research Institute at the University of North Carolina where he studied transcriptional regulation of the dihydrofolate reductase gene and the effects of chemotherapeutic agents on transcription and gene amplification. In 1990, Andy joined Dan Lane's lab in the Department of Biological Chemistry at Johns Hopkins University Medical Center where he conducted research on the regulation of adipocyte gene expression and differentiation. In 1992, Dr Swick joined Pfizer Global Research and Development as a Senior Research Scientist in Cardiovascular and Metabolic Diseases working on diabetes and obesity and rose to become Senior Director of Cardiovascular, Metabolic and Endocrine Diseases (CVMED). His efforts were concentrated on target validation, biomarker discovery, animal models and translational research focusing on the molecular mechanisms that regulate body weight and obesity-associated comorbidities with an eye on the translation of preclinical results to the clinical situation. Dr Swick was a key member of the CVMED Leadership Team, Obesity Disease Area Strategy Team, CVMED Translational Research Team and Obesity Development Team. While at Pfizer Andy was responsible for the delivery of more than a dozen compounds to clinical development, including biologicals and small molecules spanning multiple mechanisms across obesity and diabetes, covering Phases 1, 2 and 3. In 2009, Dr Swick formed Illuminate BioPharma Consulting LLC to provide expert advice to Biotechnology, Pharmaceutical and Venture Capital companies and non-profit organizations on Drug Discovery Research and Development. Andy is an elected member of several professional organizations and currently serves on the New York Academy of Sciences Diabetes and Obesity Steering Committee.

Jennifer S. Henry, PhD

The New York Academy of Sciences


Moderator

Gary J. Schwartz, PhD

Albert Einstein College of Medicine

Gary J. Schwartz, PhD, is a Professor of Medicine and Neuroscience at the Albert Einstein College of Medicine of Yeshiva University.  His basic research focuses on the neurobiology of feeding behavior, energy balance, and glucose homeostasis in obesity and diabetes.  He has published extensively on the role of gut-brain communication in the control of food intake and  metabolism, and is an Associate Editor of the American Journal of Physiology, Endocrinology & Metabolism section.  He is a senior member and Core leader for the Albert Einstein Diabetes Research and Training Center and the New York Obesity Research Center, and is the Director of the Skirball Institute for Nutrient Sensing.


Speakers

Blandine Laferrère, MD

Columbia University—St. Luke's Roosevelt Hospital Center

Blandine Laferrère, MD, is Associate Professor of Medicine at St Luke's Roosevelt Hospital, Columbia University College of Physicians and Surgeons, Attending Physician is the Division of Endocrinology and Diabetes, and Member of the New York Obesity Nutrition Research Center (NYONRC) and the Diabetes Endocrinology Research Center. Dr Laferrère trained as a Endocrinologist Diabetologist both in France and in the United States. She is a full time Attending physician in the Division of Endocrinology, Diabetes and Metabolism at St Luke's Roosevelt Hospital where she is co-Director of the fellowship program. The focus of her research at the NYONRC is the relation between weight changes and diabetes risk. Her laboratory has contributed to the understanding of the mechanisms of diabetes remission after bariatric surgery by showing a role of the incretins. The focus of her current research is to understand the mechanisms of the differential metabolic response between diet and surgical weight loss, the mechanisms of incretin release after GBP and the long-term effect of surgical weight loss on beta-cell function.

Allen S. Levine, PhD

University of Minnesota

Allen Levine is Dean of the College of Food, Agricultural and Natural Resource Sciences at the University of Minnesota. Prior to this position, he was Head of the Department of Food Science and Nutrition. He was the Associate Director of Research and a Senior Career Scientist at the Minneapolis VA Medical Center. He is also Director of the Minnesota Obesity Center, a National Institutes of Health funded collaborative research group of over 55 federally funded investigators from the University, the Mayo Clinic, the Minneapolis VA Medical Center, Health Partners, and Hennepin County Medical Center. His research focus for the past 25 years has been on neural regulation of food intake, particularly related to the opioid peptides and Neuropeptide Y. He has published over 285 scientific papers and over 90 review articles, editorials and book reviews. Dr. Levine has served on a variety of Editorial Boards and National Organizations; including American Journal of Clinical Nutrition, Journal of Nutrition, NAASO (ethics committee chair), SSIB (currently President; treasurer), ASNS, APA, and ILSI. He has been on the advisory groups of various food and pharmaceutical corporations including the Dannon Institute, Best Foods, and the International Life Sciences Institute. He also has experience with non-profit corporations having been on the Boards and served as President or Executive Director of five non-profit organizations. Dr. Levine is a Professor in the Departments of Food Science and Nutrition, Psychiatry, Neuroscience, Medicine, and is a member of the nutrition, food science, and the neuroscience graduate faculties at the University of Minnesota.

Timothy H. Moran, PhD

Johns Hopkins University School of Medicine

Dr. Moran received his PhD in Biopsychology at Johns Hopkins University in 1982.  Following a postdoctoral fellowship in the Department of Psychiatry at Johns Hopkins focusing on developmental neurochemistry and neurochemical responses to brain injury, he joined the faculty in the Department of Psychiatry in 1984. He was promoted to Professor in 1992 and was named the Paul R. McHugh Professor of Motivated Behavior in 2002. He currently serves as Vice Chair and Director of Research for the Department of Psychiatry and Behavioral Sciences at the Johns Hopkins University School of Medicine. Dr. Moran has been an associate editor for the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology and for Brain Research.  He is on the Editorial Boards of multiple journals.  He has served on the board of directors, as president and as program chair for the Society for the Study of Ingestive Behavior.  He has also served as the chair of the integrated physiology track of the program committee of the Obesity Society. He is currently on the Scientific Advisory Committee for the New York Obesity Center, The Klarman Family Foundation for Eating Disorders Research, the Ingestive Behavior Research Center at Purdue and the Institure for Mental Health Research at the University of Ottawa. He has served on and chaired multiple NIH Study Sections. Dr. Moran's research program is aimed at identifying the roles of various neural signaling pathways in the controls of food intake and body weight. Work has focused on brain/gut peptides as feedback controls of meal size and how these interact with hypothalamic peptide systems involved in overall energy balance. Additional projects examine how gestational and early developmental factors can bias metabolic programming to contribute to obesity. This work has resulted in over 280 original data articles, reviews and book chapters.

Walter J. Pories, MD

East Carolina University

Walter J. Pories, MD, FACS is a Professor of Surgery, Biochemistry, Sport and Exercise Medicine in the Department of Surgery at the Brody School of Medicine at East Carolina University in Greenville, North Carolina where he serves as the Director of the Bariatric Research Program. Dr. Pories’s research has been focused on trace element metabolism, the mechanisms underlying the effects of bariatric surgery and quality control of bariatric surgery. He has been funded by the NIH for almost three decades. He served as the founding Chairman of his Department, as the President of a number of surgical societies and received a number of national awards primarily for his contributions in nutrition. He retired from the US Army as a Colonel after serving as a Commander in the First Gulf War with a Legion of Merit and a Presidential Unit Citation. He is also the recipient of the O. Max Gardner Award given annually by the Trustees of the University of North Carolina to the outstanding faculty member in the 16 university system.

Philip R. Schauer, MD

Bariatric and Metabolic Institute, Cleveland Clinic

Dr. Philip Schauer is Professor of Surgery at the Cleveland Clinic Lerner College of Medicine, Chief of Minimally Invasive General Surgery and Director of the Cleveland Clinic Bariatric and Metabolic Institute (BMI).He is past president of the American Society for Metabolic & Bariatric Surgery (ASMBS). After receiving his medical degree from the Baylor College of Medicine, Dr. Schauer completed his residency in surgery at The University of Texas, where he served as chief resident of general surgery. He then completed his fellowship in laparoscopic surgery at Duke University Medical Center. Prior to joining The Cleveland Clinic in 2004, Dr. Schauer served as director of endoscopic surgery, director of bariatric surgery and Director of the Mark Ravitch/Leon Hirsch Center for Minimally Invasive Surgery at the University of Pittsburgh Medical Center. Dr. Schauer's clinical interests include surgery for severe obesity, minimally invasive surgery (laparoscopic), and gastrointestinal surgery. He has performed more than 5000 operations for severe obesity. His research interests include the pathophysiology of obesity and related diseases, physiologic effects of laparoscopic surgery on postoperative injury and recovery, and outcomes of laparoscopic management of obesity, gastrointestinal diseases, and hernias. He has also participated in the development of new minimally invasive, endoscopic, and laparoscopic operations. New concepts in surgical training and education have been a major focus of his educational interests. He has authored more than 200 scientific papers, editorials, textbook chapters, abstracts, and video productions. He is editor of the textbook Minimally Invasive Bariatric Surgery. He has been an invited speaker for more than 100 regional, national and international lectures on the subject of obesity surgery and laparoscopic surgery. He is principal investigator the STAMPEDE trail comparing medical and surgical treatment of diabetes and an NIH funded study evaluating surgical treatment of diabetes. He is past chairman of the research and training and credentialing committees of ASMBS. He is current chairman of the Bariatric Surgery Section of the Obesity Society. He has been on the board of Governors of the Society of American Gastrointestinal and Endoscopic Surgeons. He is also a member of International Federation of Surgery for Obesity, the American Surgical Association, the Society of University Surgeons, the Society of Surgery of the Alimentary Tract, Central Surgical Society, and the Society of Clinical Surgery. He is a member of the American Board of Surgery Advisory Council and former member of the Board of Governors of the Fellowship Council. He is on the editorial board of Surgery for Obesity and Related Diseases and Obesity Surgery as well as 3 other medical journals. He has been director of more than 75 courses and workshops on advanced laparoscopic surgery and has trained more than 30 fellows in advanced laparoscopic and bariatric surgery.

Anthony Sclafani, PhD

CUNY, Brooklyn College

Dr. Anthony Sclafani earned a B.S. in Psychology at Brooklyn College and a Ph.D. in Biological Physiology at the University of Chicago in 1970. Dr. Sclafani then returned to Brooklyn College as an assistant professor of psychology in 1970. Currently, he is a distinguished professor of psychology and director of the Feeding Behavior and Nutrition Laboratory. Dr. Sclafani's laboratory examines the biopsychology of appetite, food preferences and obesity with the goal to reveal the role of flavor and post-oral nutrient effects on the appetite for high-sugar and high-fat foods. Dr. Sclafani's early research focused on hypothalamic mechanisms controlling appetite and obesity that included studies of high-fat and high-sugar diets. This led to innovative studies of diet-induced obesity in rodents and investigations on the role of taste and post-ingestive factors. Dr. Sclafani's laboratory was among the first to characterize in detail the sensory appeal of dietary fat to neonatal and adult rats, and to discover the taste for starch and starch-derived polysaccharides in rodents. This same lab has also made seminal discoveries concerning the post-oral actions of nutrients to stimulate food intake and conditioned flavor preferences. Recently this approach has been extended to the study of inbred mouse strains and genetically modified mice. This research has been supported by an NIH grant for the last 28 years. More recently, Dr. Sclafani's group has been investigating the neuropharmacology of learned flavor preferences with the support of a 5-year NIH grant and flavor conditioning by the post-ingestive actions of glutamate supported by a 2-year grant from the Ajinomoto Company.

Karen L. Teff, PhD

Monell Chemical Senses Institute and University of Pennsylvania

Karen L. Teff, Ph.D. is currently a Member of the Monell Chemical Senses Center and Director of Translational Research of the Institute for Diabetes, Obesity and Metabolism at the University of Pennsylvania. She is also Assistant Director of the Master’s in Translational Research Program and as of July 1 will be Director of the Penn Clinical and Translational Research Center at the University of Pennsylvania. Dr. Teff has a long-standing interest in the interactions among diet, the autonomic nervous system and endocrine responses. Her research program investigates the pathophysiological consequences of increased body adiposity, including impairments in neural activation, insulin resistance and inflammation. She is also conducting studies on the metabolic impairments induced by the atypical antipsychotics. Dr. Teff holds a B.Sc. in nutrition and a Ph.D. in Experimental Medicine from McGill University. She is a member of the NIDDK DDK-C Special Review Committee and has reviewed as an ad hoc member for multiple NIDDK review committees. Dr. Teff was a Program Director at NIDDK from 2004-2006 and an elected council member of the North American Society for the Study of Obesity and an elected board member of the Society for the Study of Ingestive Behavior. Dr. Teff has received funding from a variety of sources including the NIH, ADA and JDRF.

Christopher C. Thompson, MD, MSc

Brigham and Women's Hospital

Dr. Christopher C. Thompson is the Director of Therapeutic Endoscopy at Brigham and Women’s Hospital and an Assistant Professor of Medicine at Harvard Medical School. He is also on staff at the Danna Farber Cancer Institute and Children’s Hospital, and is co-director of the CIMIT/DOD funded Harvard Working Group on Endoscopic Surgery. He is an active clinician with focused interest in advanced endoscopy as it applies to post surgical complications, bariatric endoscopy, reflux, and pancreatic disease. He has also established an active animal lab geared toward device development and industry partnering. The lab currently has several active protocols for NOTES and the development of endoluminal devices. He has been active in the training of medical students, residents, and gastroenterology fellows for the past several years. He is also involved in the mentoring of advanced endoscopy fellows and post-doctoral research fellows.

B. Timothy Walsh, MD

Columbia University

B. Timothy Walsh, MD, a graduate of Princeton University and of Harvard Medical School, joined the staff of Columbia University Medical Center in 1979 and established the Eating Disorders Research Unit at New York State Psychiatric Institute. Dr. Walsh is currently the Ruane Professor of Pediatric Psychopharmacology in the Department of Psychiatry at the College of Physicians & Surgeons, Columbia University, and Director of the Division of Clinical Therapeutics at New York State Psychiatric Institute. Dr. Walsh's research group has examined biological and psychological abnormalities which contribute to the development and perpetuation of disturbances in eating behavior, and investigated both psychological and pharmacological treatments for Anorexia Nervosa, Bulimia Nervosa and Binge Eating Disorder. Dr. Walsh is a member of the DSM-5 Task Force and chairs the Eating Disorders Workgroup for DSM-5. He is a past president of the Academy for Eating Disorders, and of the Eating Disorders Research Society.

Gene-Jack Wang, MD

Brookhaven National Laboratories

Dr. Gene-Jack Wang is a board certified Nuclear Medicine physician and a senior scientist at the Brookhaven National Laboratory (BNL). In addition to performing his own research, he is the Chairman of the BNL Medical Department and holds a joint appointment as a Professor of Psychiatry at Mount Sinai School of Medicine. His research focuses on the application of PET and functional MRI to the study of various brain disorders. He is interested in using PET to study the neuro-psychiatric mechanisms and manifestations of alcoholism, drug addiction, obesity and eating disorder in humans and in animal models. Using PET, he reported similarity of brain circuits' disruption in drug addiction and in obesity. Currently, he uses PET to study the relationship between peripheral metabolic signals and brain neurotransmitters. His other interests include using functional MRI to study effect of diet control drug on brain satiety circuit and to assess cognitive function in obese subjects. He has published over 230 peer-reviewed papers on his imaging research. The National Institute of Health and pharmaceutical companies fund his ongoing research.

Sponsors

For sponsorship opportunities please contact Carmen McCaffery at cmccaffery@nyas.org or 212.298.8642.

Grant Support

This meeting is part of our Translational Medicine Initiative, sponsored by the Josiah Macy Jr. Foundation and The Mushett Family Foundation.

This event is funded in part by the Life Technologies™ Foundation.

Promotional Partners

Bariatric Times

The International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO)

Abstracts

The Evolution of Metabolic Surgery

John G. Kral, MD, PhD, SUNY Downstate Medical Center

Since antiquity corpulence and gluttony are attributed to men whereas embonpoint and voluptuousness, improving fecundity, characterize goddesses without mortal sin. The desire to remedy adiposity is recent, requiring surgeons’ skills, first as lipectomy and later foregut excisions to lessen the metabolic and psychosocial burdens of severe obesity (Latin: ob edere =overeat). The progression of anti-obesity surgery was: 1) lipectomy, 2) small bowel resection, 3) intestinal bypass, 4) gastric resection with duodenal or duodeno-jejunal bypass 5) gastro-duodenal bypass 6) stereotactic neurosurgery, 7) abdominal vagectomy, 8) gastric restriction (“gastroplasty”), 9) ileal interposition, 10) duodeno-jejunal bypass alone. Combinations abound. Mechanistically foregut operations are: A. purely gastric restrictive, B. diversionary (bypass) or C. neuroendocrine, denervating or excising gastrointestinal peptide-secreting cells (e.g. by sleeve gastrectomy), again with combinations.

The procedures differentially alter the magnitude, kinetics and sequence of volume, flow, motility, digestion and absorption thus modulating neurohumoral afferent signaling from foregut (big brain) to cerebrum (little brain) causing weight loss, concomitant metabolic effects on energy balance and changes in eating behavior. Structural and functional adaptation of tissues and behavior is a limitation, as it is with diet. It is difficult to allocate patients with genotypic and acquired defects in "satiety" and nutrient sensing and/or impulse control to methods with fundamentally different mechanisms, risks, costs, benefits and efficacy, finally influencing subjectively defined quality of life. Meanwhile, treatment of the chronic overnutrition syndrome, diabesity, requires an empiric, staged approach using progressively intensive or transformative methods tailored to disease severity. The ultimate goal must be prevention.

Bariatric Surgery

Philip R. Schauer, MD, Bariatric and Metabolic Institute, Cleveland Clinic

Bariatric surgery is a treatment for severe obesity by anatomic modification of the gastrointestinal tract resulting in significant long-term weight loss. Although mechanisms of weight loss after bariatric surgery are not well delineated, alteration in gut physiology as well as neuro-chemical pathways have been implicated. Clinical outcomes of bariatric surgery for treating severe obesity may provide key insights into potential mechanism of body weight regulation. The most common bariatric operations (gastric banding, gastric bypass, biliopancreatic diversion) yield 15% to 40% body weight reduction. Comorbidities such as type 2 diabetes, hypertension, dysplipidemia, sleep apnea, fatty liver disease, osteoarthritis, and cardiovascular disease are significantly ameliorated or resolved following surgery. More than eight controlled (non randomized) studies show a 30% or great mortality reduction after bariatric surgery. Perioperative morbidity and mortality (5%, 0.3% respectively) are reasonably low considering the generally high-risk status of the severely obese patient. Bariatric surgery is the only therapy proven to yield significant long-term weight loss and has become the stand of care treatment for severe obesity endorsed by numerous professional medical societies. Greater understanding of the mechanisms of action of bariatric surgery may lead to even more effective and safer treatment and prevention of our nation’s most serious public health concern.

Appetitive Peptides

Timothy H. Moran, PhD, Johns Hopkins University School of Medicine

Eating and the resulting presence of nutrients in the gastrointestinal tract elicits alterations in the release of a variety of peptides from the stomach, intestine and pancreas.  As well as being involved in modulating the digestive, absorptive and nutrient storage processes, these peptides can serve as feedback signals informing the brain about the type and extent of the ingested nutrients.  Three distinct actions have been identified.  The gastric peptide ghrelin stimulates food intake and is involved in meal initiation.  Plasma levels are high prior to meals and fall with the entry of nutrients into the proximal intestine.  A second class of peptide signals are involved in meal termination.  Thus, the intestinal peptide cholecystokinin, (CCK) and the pancreatic peptides amylin and glucagon have effects within the meal that stimulates their release and these are feeding inhibitory peptides that lead to meal termination.  The intestinal peptides, glucagon like peptide 1 (GLP-1) and peptide YY 3-36 (PYY3-36) are released from more distal intestinal sites and, as well as contributing to meal termination, can affect food intake beyond the meal that stimulated their release.  These gut peptides interact, either directly or indirectly through vagal afferent activity, with hypothalamic and hindbrain signaling systems that are further modulated by the adiposity signal leptin.  Interactions among these various systems play critical roles in determining food intake and overall energy balance.

Incretins

Blandine Laferrère, MD, Columbia University—St. Luke's Roosevelt Hospital Center

Bariatric surgery results in weight loss of great magnitude and sustained overtime, with remarkable improvement of type 2 diabetes. The favorable change in the incretin gut hormones after gastric bypass surgery (GBP) is thought to be responsible, in part, for diabetes remission after GBP, independent of weight loss. After GBP, the post-prandial incretin hormones plasma concentrations increase by 3-5 fold and the blunted incretin effect on insulin secretion improves rapidly in patients with diabetes. In addition to changes in incretins, insulin secretion and glucose levels, circulating branched chain amino acid decrease more after GBP compared to diet. The long term effect of the incretins on glucose metabolism and β cell function is yet unknown. Careful studies of the differential metabolic effect of matched surgical and medical weigh loss will help understand the mechanisms by which diabetes improves after GBP and may help develop less invasive treatment options for obesity and diabetes.

Human Foregut Endocrine Cells

Walter J. Pories, MD, East Carolina University

Diabetes is no longer a hopeless disease. Bariatric surgery, so named because the original intent was to induce weight loss, produce full and durable remission or type 2 diabetes (T2DM) with a reduction of mortality by 78 percent. The mechanisms for this remarkable outcome are not clear but the responses to the variations in the design of the operations, the broad effects of the procedures, the speed of remission, the effects of duration, race, gender and age of the subjects as well as the changes in gut hormones all provide tantalizing clues.

The presentation will provide the results of long and short term studies on human subjects and the troubling conclusion that the metabolic syndrome, of which T2DM is only one expression, is due to hyperinsulinemia stimulated by the neuroendocrine cells of the gut and, if that hypothesis is true, the treatment of diabetes with insulin needs early and critical review.

Neurobiology of Motivation to Eat

Allen S. Levine, PhD, University of Minnesota

Animals are motivated to eat by a variety of factors including hunger and palatability. Many neuroregulators and neural circuits are involved in feeding behavior. This talk will focus on a few peptidergic systems,forming a complex functional network, that are involved in the motivation to eat. Opioid peptides and their receptors are involved in sweet and fat consumption and so-called "addictive" feeding behavior. Evidence will be presented that, aside from increasing sugar/fat consumption, opioids silence the oxytocin-driven satiety system. The talk will also include a discussion of opioid-related hedonic deprivation. Hedonic deprivation suggests that a lack of free access to rewarding food leads to a deprivation state that resembles energy deprivation. Finally, data will be included that demonstrates interactions between food and drug reward systems. We conclude that, due to the complexity of neural and functional interactions, opioids are capable of enhancing pleasure of eating any food - palatable or aversive - making any meal into a more rewarding experience.

From Mouth to Gut: Sweet Taste Receptors and the Vagus

Karen L. Teff, PhD, Monell Chemical Senses Institute and University of Pennsylvania

At the onset of food ingestion, the sensory components of food stimulate taste receptors in the oral cavity thereby initiating a neural relay to the brain and resulting in the stimulation of vagal efferent fibers. The vagus nerve innervates most tissues involved in nutrient metabolism and promotes anabolic processes including gastric emptying, nutrient digestion and nutrient absorption. Vagal innervation of the pancreas and liver plays an important role in maintaining glucose homeostasis through the release of insulin and the inhibition of hepatic glucose production during meal ingestion. In addition, under physiological conditions which require prolonged increases in insulin secretion such as overfeeding and/or the development of insulin resistance, my laboratory has shown that vagal activation contributes to compensatory insulin secretion required to maintain euglycemia. We have demonstrated that vagal activation contributes to the temporal patterning of insulin release by eliciting pre-absorptive or cephalic phase insulin release and enhancing the magnitude of post-prandial insulin release. Exploring the sensory stimuli which elicit cephalic phase insulin and pancreatic polypeptide release provides a window into the conditions necessary for vagal activation. Using this approach, we have demonstrated that sweet nutritive and non-nutritive solutions do not elicit cephalic phase hormonal responses, in contrast to what has been demonstrated in animals. Sweet taste receptors have also been identified in the gastrointestinal tract and are co-localized in the intestinal L-cell which secretes glucagon-like peptide-1 (GLP-1). In rodents, stimulation of the sweet taste receptor elicits the release of GLP-1 while blockade or genetic deletion of the sweet taste receptor in mice attenuates post-prandial GLP-1 and insulin release. In contrast, our preliminary data suggest that blockade of the sweet taste receptor in humans enhances GLP-1 release and lowers post-prandial glucose. Thus, the relationship between the oral and intestinal sweet taste receptors and their functional responses may differ between human and rodents.

Nutrient Sensing and Appetitive Behavior

Anthony Sclafani, PhD, CUNY, Brooklyn College

Many factors influence the acceptance and preference for foods. Laboratory studies indicate that, in addition to innate taste biases (e.g., attraction to sweet taste), rodents learn to prefer the flavor of foods based on the food’s post-ingestive nutritional consequences. This is most clearly demonstrated by experiments in which the intake of a flavored solution is paired with an intragastric nutrient infusion (e.g., glucose, corn oil), and a different flavored solution is paired with a water infusion. In subsequent choice tests, animals show strong preferences for the nutrient-paired flavor. Flavor-nutrient conditioning can occur in a single training trial, in non-deprived as well as food-deprived animals, and are very resistant to extinction. The magnitude of the conditioned preference varies as a function flavor quality, nutrient type and energy density. The upper small intestine is a primary site of action for glucose conditioning as indicated by the effectiveness of duodenal and jejunal infusion sites, but not by infusions that bypass the upper intestines (ileal or hepatic-portal). The identity of the intestinal nutrient sensors that mediate flavor conditioning is not known. Intestinal sweet taste receptors are not implicated because T1R3 knockout mice are similar to wildtype mice in their robust conditioning response to IG sugar infusions. Also unknown is the gut-brain pathway that mediates nutrient conditioning. Vagal deafferentation does not block carbohydrate conditioning, which suggests hormonal mediation. Activation of brain dopamine reward circuits is critical for the acquisition but not expression of nutrient-conditioned flavor preferences.

Supported by NIH Research Grants DK-31135 and DK-071761 and the Ajinomoto Research Award Program

Appetitive Neuroimaging in Humans

Gene-Jack Wang, MD, Brookhaven National Laboratories

Multiple internal feedback signals influence food intake including gut-secreted peptides that provide information to the brain to inhibit feeding and terminate meal consumption.  Many of these signals are conveyed to the brainstem and hypothalamus via the vagus nerve. Reduced neuronal sensitivity to these signals could result in unrestrained eating and obesity. Gastric distention, as it occurs during meal ingestion, is one of the key mechanisms controlling food intake. We used functional magnetic resonance imaging to evaluate brain activation during gastric distention healthy subjects.  During slow gastric distention to maximum volumes of 700 ml, obese subjects had hypo-activation in dopaminergic innervated brain regions and hyperactivation in cerebellum and posterior insula.Inasmuch as gastric distention signals are transmitted to the brain primarily through the vagus nerve and dopamine is implicated in obesity, these findings suggest decreased sensitivity of limbic regions and enhanced sensitivity of the cerebellum and posterior insula to vagal stimulation in obesity.  In another study in obese subjects implanted with a gastric stimulator, which induces stomach expansion via electrical stimulation of the vagus nerve, we found the gastric stimulation increased metabolism in orbitofrontal cortex, striatum, and hippocampus.  The activation in the hippocampus during gastric stimulation is associated with a sensation of fullness.  These regions are involved with self-control, motivation, and memory, respectively, and were previously shown to be involved in drug craving in addicted subjects. This finding suggests that similar brain circuits underlie the enhanced motivational drive for food (and for drugs) seen in obese (and drug-addicted) subjects. These findings provide insight into the brain circuits involved in processing the vagal signals that originate from the stomach of healthy subjects. The results suggest multiple brain circuits (reward, motivation, learning, inhibitory control) are disrupted in obesity.  The results implicate the need for a multimodal approach in the treatment of obesity.

Eating Behavior in Eating Disorders

B. Timothy Walsh, MD, Columbia University

The recognized eating disorders (Anorexia Nervosa, Bulimia Nervosa, and Binge Eating Disorder) arguably provide experiments of nature in which the ability to restrain food intake can be examined. This presentation will focus on objective information about the eating behavior of individuals with eating disorders. Notably, individuals with Anorexia Nervosa impressively restrain their eating behavior on most occasions, individuals with Bulimia Nervosa alternate between binge eating and restraint, and individuals with Binge Eating Disorder appear to have difficulty restraining food intake in multiple settings. Some of the challenges of understanding the basis for these behavioral phenomena will be discussed.

*Additional abstracts coming soon.

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