Microbial Influences in Cardio–Metabolic Diseases

Microbial Influences in Cardio–Metabolic Diseases

Thursday, November 3, 2016

The New York Academy of Sciences

Presented By

Microbiome Science Discussion Group

The New York Academy of Sciences

 

The microbiota in the human colon form one of the densest natural bacterial ecosystems known. These microbial communities are integrally involved in maintaining human health. Accumulating evidence implicates the microbiome in metabolic disease: microbiota play a key role in regulating host physiological and metabolic processes, via the production of metabolites from ingested macronutrients. In parallel, the composition of the microbial population have been shown to be significantly influenced by diet, and these changes are likely to be causally related to metabolic disease including Type II diabetes, obesity, and cardiovascular disease.

This symposium focuses on the microbiota and their relationship with metabolic dysfunction. It will highlight emerging science that is furthering our understanding of causal relationships between our microbiota and disease, as well as applications for human health. This is the third in a series of symposia addressing the impact of microbiota on the whole human.

* Reception to follow.

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Member (Student / Postdoc / Resident / Fellow)$25
Nonmember (Academia)$105
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Nonmember (Non-profit)$105
Nonmember (Student / Postdoc / Resident / Fellow)$70

This event will also be broadcast as a webinar; registration is required.

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.

Webinar Pricing

Member$30
Member (Student / Postdoc / Resident / Fellow)$15
Nonmember (Academia)$65
Nonmember (Corporate)$85
Nonmember (Non-profit)$65
Nonmember (Student / Postdoc / Resident / Fellow)$45

Agenda

* Presentation titles and times are subject to change.


November 3, 2016

8:30 AM

Registration and Continental Breakfast

9:00 AM

Welcome and Opening Remarks
Sonya Dougal, PhD, The New York Academy of Sciences
John Hambor, PhD, Boehringer Ingelheim

Keynote Lecture

9:15 AM

The Role of the Early Life Microbiota in Cardio-metabolic Diseases
Martin J. Blaser, MD, New York University Langone Medical Center

Plenary Session I

10:00 AM

Human Gut Microbes Impact Host Serum Metabolome and Insulin Sensitivity
Henrik Bjørn Nielsen, PhD, Clinical-Microbiomics A/S

10:35 AM

Networking Coffee Break

11:05 AM

When Gut Microbes Talk to Organs: Impact on Metabolism
Patrice D. Cani, PhD, Universite Catholique de Louvain, LDRI

11:40 AM

Acetate Mediates a Microbiome-brain-β cell Axis Promoting the Metabolic Syndrome
Gerald I. Shulman, MD, PhD, Yale University School of Medicine

*Presenter slides will not be included as part of the Webinar broadcast

12:15 PM

Data Blitz Presentations

Oral Microbiome and Cardio-Metabolic Diseases: A Systematic Analysis of Evidence
Joseph Finkelstein, MD, PhD, Columbia University College of Dental Medicine

Defining the Bacterial Species Responsible for the Synthesis of Trimethylamine in Subjects with Chronic Kidney Disease
Danielle Fowler, Boehringer Ingelheim Pharmaceuticals, Inc.

*Presenter slides will not be included as part of the Webinar broadcast

12:35 PM

Networking Lunch Break and Poster Session

Plenary Session II

2:05 PM

Cooking Alters Gut Microbial Structure and Function
Rachel Carmody, PhD, Harvard University

2:40 PM

Gut Microbiota and Brain Interactions in Diet-induced Obesity
Marion Soto, PhD, Joslin Diabetes Center, Harvard Medical School

3:15 PM

Networking Coffee Break

3:45 PM

The Intestinal Adaptive Immune System in Obesity and Insulin Resistance: A Potential New Therapeutic Target
Daniel Winer, MD, FRCPC, University Health Network and University of Toronto

4:20 PM

Therapeutic Targeting of the Gut Microbiome for the Treatment of Cardio-metabolic Diseases
Stanley L. Hazen, MD, PhD, Cleveland Clinic

*Presenter slides will not be part of the Webinar broadcast

4:55 PM

Closing Remarks
Nilufer Seth, PhD, Pfizer

5:00 PM

Networking Reception

6:00 PM

Adjourn

Organizers

John Hambor, PhD

Boehringer Ingelheim

Dr. John Hambor is currently a Director of Research Beyond Borders at Boehringer Ingelheim where he coordinates a strategic postdoctoral research program focused on developing new therapeutic concepts in collaboration with academic investigators. Previously, Dr. Hambor was a consultant with the Cell Therapy Group, specializing in stem cell-based drug discovery. Prior to serving as CEO of CellDesign, a developer of next generation stem cell technologies, he contributed 17 years of research at Pfizer where he identified and validated new drug targets in the areas of inflammation and immunology and developed stem cell-based assays for drug efficacy and safety studies. Dr. Hambor received both a BA and MS degree in Microbiology from Miami University of Ohio, and earned a PhD in Pathology from Case Western Reserve University, followed by postdoctoral studies at Yale University in the Department of Immunobiology. He has been an Adjunct Assistant Professor at Connecticut College since 2000 where he teaches Immunology. He also serves as a member on the board of directors for the Connecticut Veterans Administration Research and Education Foundation and on the advisory committee for the Connecticut Regenerative Medicine Research Fund.

Erick Young, PhD

Boehringer Ingelheim

Erick R. R. Young obtained his PhD in synthetic bioorganic chemistry from The Pennsylvania State University and completed post-doctoral studies in natural product synthesis at The Ohio State University. Upon joining Boehringer Ingelheim Pharmaceuticals in 1998 he served as a small molecule research project leader for immunology and cardiometabolic diseases. Over time, he became increasingly involved in the generation of new target concepts and championing novel therapeutic modalities for the enablement of new target class space, areas where he has made significant contributions to the BI research strategy and portfolio. He is currently the Director of External Innovation for the newly formed Research Beyond Borders division of BI where his primary focus is the conception, identification and enablement of new therapeutic mechanisms and disease indications outside the organizations current scope or capabilities.

Nilufer Seth, PhD

Pfizer Inc

Nilufer Seth is a scientist in the Emerging Science Group in the Inflammation and Immunology Research Unit at Pfizer. She received her PhD from Medical College of Augusta in Molecular Biology and Biochemistry. She then joined the Dana-Farber Cancer Institute for her post-doctoral training where her research focused on the design and development of novel approaches to ex vivo identify and analyze antigen-specific CD4 T cells subsets in human diseases and mouse models of autoimmunity. She studied antigen specific T cells from HIV and HCV infected individuals as well as in the NOD mouse model of Type 1 Diabetes. She joined the Department of Inflammation and Immunology at Wyeth where she worked on small and large molecule therapeutic programs targeting immune cells and inflammatory cytokines. Currently at Pfizer she is leading and developing the microbiome strategy, efforts and projects. Her focus is on developing medicines that will reshape the treatment of inflammatory and autoimmune diseases by harnessing strategies and pathways used by the human gut microbiota to maintain barrier and immune homeostasis.

Sonya Dougal, PhD

The New York Academy of Sciences

Caitlin McOmish, PhD

The New York Academy of Sciences

Speakers

Henrik Bjørn Nielsen, PhD

Clinical-Microbiomics A/S

H. Bjørn Nielsen, PhD, Chief Scientific Officer at Clinical-Microbiomics A/S, has since 2008 been a frontrunner in the field of microbiome research. His participation in the MetaHit consortium led to a series of important scientific papers describing the human gut microbiome, including his pioneering work on co-abundance binning of metagenomics data into metagenomic species, bacteriophages, and other mobile genetic elements. This year Henrik has authored 4 papers published in Nature journals, including a three-pronged association study that links microbiome, serum metabolome, and clinical data in pre-diabetic Danes, and a study that reports on the largest metatranscriptomics to date. At Clinical-Microbiomics H. Bjørn heads innovation with clients and the continued adaptation and development of new analysis concepts and methods.

Martin J. Blaser, MD

New York University Langone Medical Center

Martin J. Blaser is the Muriel and George Singer Professor of Medicine, Professor of Microbiology, and Director of the Human Microbiome Program at the NYU School of Medicine. He served as Chair of the Department of Medicine at NYU from 2000–2012. A physician and microbiologist, Dr. Blaser is interested in understanding the relationships we have with our persistently colonizing bacteria. His work over 30 years focused on particular organisms, including Campylobacter species and Helicobacter pylori, which also are model systems for understanding the interactions of residential bacteria with their human hosts. Over the last 15 years, he has been actively studying the relationship of the human microbiome with health and with such important diseases as asthma, obesity, diabetes, and allergies. Over the course of his career, Dr. Blaser has served as the advisor for a large number of students, post-doctoral fellows, and junior faculty. He served as President of the Infectious Diseases Society of America, Chair of the Board of Scientific Counselors of the National Cancer Institute, Chair of the Advisory Board for Clinical Research of the National Institutes of Health, and on the Scientific Advisory Board of the Doris Duke Charitable Foundation. He was elected to the National Academy of Medicine and the American Academy for Arts and Sciences. He holds 28 U.S. patents relating to his research, and has authored over 550 original articles. Recently, he wrote "Missing Microbes," a book targeted to general audiences. He now is serving as the Chair of the Presidential Advisory Council for Combating Antibiotic-Resistant Bacteria.

Patrice D. Cani, PhD

Université Catholique de Louvain, LDRI
website

Rachel Carmody, PhD

Harvard University

Rachel Carmody is an Assistant Professor in Human Evolutionary Biology and Co-Director of the Nutritional & Microbial Ecology Laboratory at Harvard University. She received her PhD in Human Evolutionary Biology from Harvard in 2012, and recently completed a postdoctoral fellowship in Microbiology & Immunology at UCSF with Dr. Peter Turnbaugh. Dr. Carmody's research investigates the biological, behavioral, and environmental determinants of dietary energy gain, with special interests in the energetic consequences of food processing and the contributions of the gut microbiome to energy metabolism. Her past studies have shown that the adoption of cooking by human ancestors would have transformed the energy landscape, helping to support the emergence of costly traits like larger body and brain size despite reductions in tooth and gut size. Her recent research extends this story, showing that consumption of a cooked diet reshapes the gut microbiota in ways relevant to energy gain and the evolution of host-microbial interactions. Dr. Carmody is the recipient of an NSF Graduate Research Fellowship, NIDDK/NIA Keystone Scholarship, and NIH Ruth L. Kirschstein National Research Service Award.

Stanley L. Hazen, MD, PhD

Cleveland Clinic

Dr. Hazen received both his PhD in Biophysical Chemistry and Molecular Biology and medical degree at Washington University School of Medicine in St. Louis. He then performed his residency in internal medicine and specialty fellowship in endocrinology, diabetes, and metabolism at Barnes Jewish Hospital in St. Louis. He has been at the Cleveland Clinic since 1997, where he currently serves as the Chair of the Department of Cellular & Molecular Medicine at the Cleveland Clinic's Lerner Research Institute. He is also the Section Head of Preventive Cardiology & Rehabilitation at the Cleveland Clinic, and holds both the Jan Bleeksma Chair in Vascular Cell Biology and Atherosclerosis, and the Leonard Krieger Chair in Preventive Cardiology. Dr Hazen has published over 350 peer reviewed publications, including many in top tier clinical and basic science journals alike. He has been elected as member to honorary clinical and basic science societies including ASCI in 2003, the AAP in 2007, election as a Fellow to the American Association for the Advancement of Science (AAAS) in 2008, and most recently, election to the National Academy of Medicine (2017).

Dr. Hazen's laboratory focuses on understanding mechanisms through which inflammation contributes to diseases such as atherosclerosis. His work is highly innovative, and has led to numerous discoveries in multiple areas of cardiovascular disease research. His discovery of a mechanistic link between gut microbes and cardiovascular disease was an Inaugural recipient of a "Top 10 Clinical Discovery of the Year (2011)" award by the Clinical Research Forum (April, 2012), which is comprised of leadership at NHLBI, academia, and industry. His further studies on the gut microbe–cardiovascular disease connection were recognized by the American Heart Association and the American Stroke Association in 2014 as a "2013 top 10 advances in heart disease and stroke science." Dr Hazen today will speak to us about his recent advances on this exciting topic.

Gerald I. Shulman, MD, PhD

Yale University School of Medicine

Dr. Shulman is an Investigator of the Howard Hughes Medical Institute and the George R. Cowgill Professor of Physiological Chemistry, Medicine and Cellular & Molecular Physiology at Yale University. He is also Co-Director of the Yale Diabetes Research Center. Dr. Shulman completed his undergraduate studies in biophysics at the University of Michigan, and he received his MD and PhD degrees from Wayne State University. Following internship and residency at Duke University Medical Center, he did an endocrinology fellowship at the Massachusetts General Hospital / Harvard Medical School and additional postdoctoral work in molecular biophysics and biochemistry at Yale before joining the faculty at Harvard Medical School. He was subsequently recruited back to Yale and has remained there ever since. Dr. Shulman has pioneered the use of magnetic resonance spectroscopy to non-invasively examine intracellular glucose and fat metabolism in humans that has led to several paradigm shifts in our understanding of type 2 diabetes. Dr. Shulman is a Fellow of the American Association for the Advancement of Science and he has been elected to the American Society for Clinical Investigation, the Association of American Physicians, the Institute of Medicine and the National Academy of Sciences.

Marion Soto, PhD

Joslin Diabetes Center, Harvard Medical School

Dr. Soto is a senior research fellow in the C. Ronald Kahn Laboratory in the Department of Integrative Physiology and Metabolism at Joslin Diabetes Center. She earned her Ph.D. in Nutrition and Neurobiology in 2014 from AgroParisTech in France. Her research focuses on how type 2 diabetes and insulin resistance in the brain lead to defects in cognition and behavior. Dr. Soto's research interests combine both basic science investigations and translation into clinical research, using several MRI techniques in patients with type 2 diabetes to understand how this pathology affects brain function. In addition to her focus on insulin signaling in the brain, Dr. Soto is interested in the role of the microbiome in the pathogenesis of obesity and metabolic syndrome. Her studies on the interaction between the microbiome, brain, and behavior in mice led her to discover that the microbiota can regulate neurobehavioral abnormalities relevant to obesity and diabetes.

Dan Winer, MD, FRCPC

University Health Network and University of Toronto

Dr. D. Winer is a scientist at the Toronto General Research Institute at the University Health Network (UHN). He is an assistant professor in the Departments of Laboratory Medicine and Pathobiology, and Immunology at the University of Toronto, and a pathologist at UHN. His works, along with his collaborators, have identified a novel and important role for adaptive immunology in the control of metabolic diseases such as obesity, insulin resistance (IR), and type 2 diabetes. Their work was among the first to identify critical roles for T cells and B cells inside visceral adipose tissue in controlling metabolic inflammation and IR, and has helped promote the new field of immunometabolism. More recently, Dr. Winer has identified the immune system in the gut as a new regulator of whole body glucose homeostasis.

Dr. D. Winer is the recipient of several awards including the Benjamin Castleman Award for human pathology research, a Canada Research Chair in immunometabolism, and an Amgen New Investigator award. The Winer laboratory is funded by grants from the Canadian Diabetes Association, the Canadian Institutes of Health Research, the J.P. Bickell Foundation, the Banting and Best Diabetes Center, the Ontario Ministry of Innovation, and the Canadian Foundation for Innovation.

Sponsors

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Academy Friend

Clinical Microbiomics

Promotional Partner

Joslin Diabetes Center

Abstracts

When Gut Microbes Talk to Organs: Impact on Metabolism
Patrice D. Cani, PhD, Université Catholique de Louvain, Brussels

Obesity and cardiometabolic diseases are characterized by altered inter-organ communication. However, the pathophysiological mechanisms are not fully understood. Changes in gut microbiota composition and activity have been associated with several metabolic disorders such as insulin resistance, type 2 diabetes, and hepatic steatosis. We and others have discovered that both gut microbiota and host dialog operate via several mechanisms (e.g., microbial metabolites, bioactive lipids, innate immunity) to maintain symbiotic interactions. However, during nutritional disturbances such as high-fat diet feeding, low fiber intake, or other metabolic stressors, these fine-tuned interactions are altered, leading to changes in energy, lipid, and glucose homeostasis.
 
Among the key actors, we discovered that the innate immune system, the gut microbiota, and the endocannabinoid system are tightly interconnected, involving gut to brain or gut to adipose tissue axes. These findings highlight novel interactions and putatively explain pathological observations.
 
More recently, we discovered novel mechanisms of interaction between Akkermansia muciniphila and host organs. We have demonstrated that this "novel" bacterium plays a role in cardiometabolic disorders and gut barrier function in rodents. We have also found that the abundance of Akkermansia is strongly correlated with the metabolic response of obese patients upon dietary intervention. Finally, unpublished data and mechanisms of action will be discussed, using both mice and humans as model systems.

The Role of the Early Life Microbiota in Cardio–Metabolic Diseases
Martin J. Blaser, MD, New York University Langone Medical Center (NYULMC)

A major portion of the cells in the human body are microbial. We call these residential microbes—and their genes, products, and interactions with us—the human microbiome. Substantial evidence indicates that much of the human microbiome is inherited, suggesting selection for its functions. There is a growing literature of observations and experiments that indicate the importance of the microbiome in early life, with roles in the development of metabolism, immunity, and cognition. We have been studying early life exposures to antibiotics as microbiome disruptors. Antibiotics are clinically important because of their very extensive use in medical practice, especially in early life, and because they also are representative of other disruptive practices, including Cesarean sections and formula feeding affecting infants. Antibiotic exposures also are useful to model the effects of microbiome perturbation. We have studied two types of exposures: STAT (sub-therapeutic antibiotic treatment, modeled after farm practices for growth promotion), and PAT (pulsed antibiotic treatment, mimicking dosing of human children at therapeutic levels). In mouse models, we have shown that in comparison to controls, antibiotic exposures can lead to increased adiposity, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and can accelerate and increase rates of type 1 diabetes. These models show the feasibility that antibiotic exposures may indeed affect human children, and identify important relationships and pathways that can lead to improved preventions and therapies.

Therapeutic Targeting of the Gut Microbiome for the Treatment of Cardio–Metabolic Diseases
Stanley L. Hazen, MD, PhD, Cleveland Clinic

Recent studies reveal a novel mechanistic link between intestinal microbiota and the development of cardiovascular disease (CVD). Dietary nutrients with trimethyl amine groups (e.g. choline, phosphatidylcholine, and carnitine) are acted upon by gut microbes to form trimethylamine (TMA), which is then converted by host hepatic flavin monooxygenases to form the metabolite TMAO (trimethylamine-N-oxide). TMAO in animal model studies has been shown to promote atherosclerosis. Human clinical studies show TMAO strongly associates with incident risks for myocardial infarction, stroke, or death, and is generated in a gut microbiota-dependent fashion. More recent studies show that the metaorganismal TMAO pathway is linked to development and adverse prognosis in additional vulnerable populations for cardiovascular disease risks, including heart failure and chronic kidney disease patients. Moreover, the TMAO pathway is seen to be mechanistically linked to altered platelet responsiveness and enhanced thrombosis potential. A new therapeutic paradigm will be discussed and proof of concept studies presented whereby microbial pathways such as those involved in TMAO production may be targeted with non-lethal inhibitors for atherothrombotic diseases. Gut microbiota represent a novel and exciting potential therapeutic target for the treatment and prevention of CVD.

Cooking Alters Gut Microbial Structure and Function
Rachel Carmody, PhD, Department of Human Evolutionary Biology, Harvard University

Variations in the composition of the gut microbial community (microbiota) and its cumulative genetic and metabolic potential (microbiome) have been linked to risks or treatment outcomes for multiple diseases, including metabolic syndrome, inflammatory bowel disease, cardiovascular disease, and cancer. Diet has repeatedly emerged as a critical determinant of variation in gut microbial structure and function, potentially outweighing even the genetic background of the host. To date, most studies of dietary impacts on the gut microbiota have compared diets with divergent ingredient profiles, e.g. high-fat versus low-fat, animal-based versus plant-based, or with versus without additives. However the everyday practice of cooking a given food could also shape the gut microbiome through heat-induced effects on the bioavailability of nutrients and xenobiotic compounds. Using conventional and gnotobiotic mice, we show that a plant-based diet served cooked versus raw alters the membership, abundance, transcription, and physiology of the gut microbial community, with effects driven by heat-associated improvements in starch digestibility and inactivation of native foodborne antimicrobial compounds. These changes are relevant to host energy gain, with gut microbial communities conditioned on raw diets enhancing energy harvest when transplanted into germ-free recipients. Our results show that diet-driven interactions between host and microbiome depend on both the food and its form, indicating a need for careful reporting and/or controls in dietary studies of the gut microbiome.
 
Co-author: Peter Turnbaugh, UCSF

Gut Microbiota and Brain Interactions in Diet-induced Obesity
Marion Soto, PhD, Joslin Diabetes Center, Harvard Medical School

Modifications in the gut microbiota composition have been associated with a variety of pathogeneses such as obesity and type 2 diabetes. In addition to these metabolic effects, there is accumulating evidence suggesting that the microbiota may regulate brain function and behavior. To further explore the role of the gut-brain axis in obesity, we challenged C57Bl/6J mice with high fat diet (HFD) and treated them with either vancomycin, which kills gram positive bacteria, or metronidazole, which kills anaerobic bacteria. As expected, HFD-fed mice became obese and insulin resistant, and treatment with either antibiotic improved glucose metabolism. This was associated with decreased serum TNF-alpha levels and decreased inflammatory markers in different tissues, including in the brain. Neurobehavioral tasks revealed increased anxiety and depressive-like behaviors in HFD-fed mice, and both antibiotic treatments reversed this phenotype. These changes were associated with an improvement of insulin signaling at a molecular level in peripheral tissues and the brains of HFD-fed mice. These findings could be reproduced by transferring gut bacteria isolated from antibiotic-treated donors to HFD-fed mice. HFD and antibiotic treatment also changed multiple serum metabolites, including several neurotransmitters and their precursors/metabolites. Thus, antibiotic treatment modifies the gut microbiome and impacts various metabolites and inflammatory markers induced by HFD in both the periphery and the brain. This leads to improved brain insulin signaling and reversal of the HFD-induced neurobehavioral changes.
 
Coauthors: Shiho Fujisaka and C. Ronald Kahn, Joslin Diabetes Center, Harvard Medical School

The Intestinal Adaptive Immune System in Obesity and Insulin Resistance: A Potential New Therapeutic Target
Dan Winer, MD, Toronto General Research Institute (TGRI), University Health Network, Toronto; and University of Toronto

Obesity and its associated metabolic abnormalities, including insulin resistance and type 2 diabetes (T2D), represent a major global cause of morbidity and mortality. Insulin resistance precedes type 2 diabetes (T2D) in mice and humans, and is thought to be a key driving factor in the development of T2D. Multiple factors contribute to insulin sensitivity but chronic inflammation of metabolic tissues, including visceral adipose tissue (VAT) and liver, resulting in release of pro-inflammatory cytokines is known to be a major contributor. More recently, in addition to VAT and liver, growing evidence has implicated the bowel immune system as an important contributor to metabolic disease. Diet induced obesity alters the intestinal immune system at levels of innate and adaptive immunity. These alterations impact the gut microbiota, intestinal barrier function, gut hormone release, and oral tolerance to luminal antigens, with downstream implications to metabolic homeostasis. Accordingly, the gut immune system may represent a novel therapeutic target for systemic insulin resistance. This talk will outline emerging concepts in the field of intestinal immunity in obesity-related insulin resistance, with a focus on adaptive immunity, and discuss the potential for targeting the intestinal immune system as a new therapeutic approach to metabolic disease.

Human Gut Microbes Impact Host Serum Metabolome and Insulin Sensitivity
Henrik Bjørn Nielsen, PhD, Clinical-Microbiomics A/S, Copenhagen

Insulin resistance is a forerunner state of type 2 diabetes. Here we show how the human gut microbiome impacts the serum metabolome and associates with insulin resistance in 277 non-diabetic Danish individuals. The serum metabolome of insulin-resistant individuals is characterized by increased levels of branched-chain amino acids (BCAAs), which correlate with a gut microbiome that has an enriched biosynthetic potential for BCAAs and is deprived of genes encoding bacterial inward transporters for these amino acids. Prevotella copri and Bacteroides vulgatus are identified as the main species driving the association between biosynthesis of BCAAs and insulin resistance, and in mice we demonstrate that P. copri can induce insulin resistance, aggravate glucose intolerance, and augment circulating levels of BCAAs. Our findings suggest that microbial targets may have the potential to diminish insulin resistance and reduce the incidence of common metabolic and cardiovascular disorders.

Acetate Mediates a Microbiome–Brain–β Cell Axis Promoting the Metabolic Syndrome
Gerald I. Shulman, MD, PhD, Howard Hughes Medical Institute and Yale University School of Medicine

Obesity, insulin resistance, and metabolic syndrome are associated with changes to the gut microbiota; however, the mechanism by which modifications to the gut microbiota might lead to these conditions is unknown. In this lecture I will review recent studies demonstrating that increased production of acetate by an altered gut microbiota leads to activation of the parasympathetic nervous system which in turn promotes increased glucose-stimulated insulin secretion, increased ghrelin secretion, hyperphagia, obesity, and its related sequelae in rodents.

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