Upcoming Seminars and Events

Seminars and events at the Max Planck Institute for Metabolism Research and at cooperating institutes

The chameleon role of TLR4 in lipid-induced macrophage inflammation

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Talk by Prof. Mark Febbraio, Garvan Institute of Medical Research, Sydney

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Optogenetic fMRI and the Investigation of Global Brain Circuit Mechanisms

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Talk by Jin Hyung Lee, PhD, Stanford University

Understanding the functional communication across brain has been a long sought-after goal of neuroscientists. However, due to the widespread and highly interconnected nature of brain circuits, the dynamic relationship between neuronal network elements remains elusive. With the development of optogenetic functional magnetic resonance imaging (ofMRI), it is now possible to observe whole-brain level network activity that results from modulating with millisecond-timescale resolution the activity of genetically, spatially, and topologically defined cell populations. ofMRI uniquely enables mapping global patterns of brain activity that result from the selective and precise control of neuronal populations. Advances in the molecular toolbox of optogenetics, as well as improvements in imaging technology, will bring ofMRI closer to its full potential. In particular, the integration of ultra-fast data acquisition, high SNR, and combinatorial optogenetics will enable powerful systems that can modulate and visualize brain activity in real-time. ofMRI is anticipated to play an important role in the dissection and control of network-level brain circuit function and dysfunction. In this talk, the ofMRI technology will be introduced with advanced approaches to bring it to its full potential, ending with examples of dissecting whole brain circuits associated with neurological diseases utilizing ofMRI. [more]

Pharmacological approaches to restore mitochondrial function

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Talk by Riekelt Houtkooper, PhD, Academic Medical Center Amsterdam

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Post-GWAS functional analyses of variants (and proxy genes) associated with type 2 diabetes

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Talk by Amélie Bonnefond, PhD, University of Lille

Type 2 diabetes (T2D) is a complex genetic metabolic disorder which has developed into major health problem responsible for early morbidities (e.g. severe vascular complications and cancers) and mortality, with a burden increasing globally. T2D results from the progressive alteration of insulin secretion from pancreatic beta cells on a background of impaired insulin action in sensitive organs and tissues. Whilst the environment is the key risk factor for T2D at the population level, one remarkable feature is the persistence of considerable individual disease risk amongst people sharing same environment. Estimates of T2D heritability range from 40 to 70%. Genome-wide association studies (GWAS) have identified >100 loci independently contributing to T2D risk. Despite this dramatic success, there has been a considerable gap between the knowledge of the genetic contribution of these loci and the understanding of how these loci physiologically impact the disease: indeed, association does not mean causality. Therefore, translational implications for precision medicine and for the development of novel treatments have been disappointing, due to the poor knowledge of how these loci impact T2D pathophysiology. During my talk, I will present several post-GWAS functional studies which enabled the identification of causal genes and pathways involved in T2D pathophysiology. [more]

Regulation of Homeostatic Boundary Control and Rheostasis by the Melanocortin-3 Receptor

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Talk by Professor Roger Cone, University of Michigan, USA

The MC4R regulates energy homeostasis, and haploinsufficiency produces hyperphagia, hypometabolism, and early onset obesity. In contrast, homozygous deletion of the MC3R does not cause hyperphagia or hypometabolism under normal conditions, producing a mild, late-onset obesity. However, the MC3R plays a critical role in regulating energy homeostasis in response to external and internal nutritional challenges. First, the MC3R regulates energy stores in response to fasting and chronic food restriction. Additionally, there are multiple roles for MC3R in regulation of energy homeostasis in response to reproductive state. MC3R KO mice exhibit defective pregnancy-induced hyperphagia and defective control of energy stores in response to ovariectomy. Thus, MC3R deletion results in defective homeostatic boundary control and rheostasis. Additional data demonstrate a molecular mechanism by which MC3R regulates homeostatic boundary control: MC3R on AgRP neurons acts presynaptically to provide autoregulatory feedback onto MC4R PVN neurons. [more]

Immunological Mechanisms in Ischemic Stroke

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Talk by Dr. Arthur Liesz, LMU Munich

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Selection workshop for Independent Research Group Leader position

Selection Workshop for Independent Research Group Leader Position

14:00 Welcome address14:15 - 14:45 Dr. Henning Fenselau: " Synaptic transmission and plasticity in feeding circuits"14:45 - 15:15 Dr. Christophe Lamy: "Brain glucose sensing and the control of energy homeostasis and behavior" [more]

A cognitive neuroscientific approach to eating and over-eating

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Talk by Professor Paul Fletcher, Cambridge

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Engineering the mouse genome using CRISPR/Cas9 technology

Talk by Dr. Martin Pal

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Quantitative proteomics to study circadian control of metabolism

Talk by Dr. Charo Robles

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Leptin and the Neural Circuit Regulating Food Intake and Metabolism

Interaction among excitatory and inhibitory circuits in the hippocampus

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Talk by Dr. Antonia Marin-Burgin

The hippocampus is a brain area that is involved in a variety of functions. In particular, the formation of memory and the codification of space depend on the functioning of the hippocampus. Virtually all areas of the hippocampus, and of most parts of the brain, contain excitatory and inhibitory neurons that form individual microcircuits. It is in the interaction between excitatory and inhibitory circuits where appropriate functional responses arise. We study how excitation and inhibition interact to activate neurons in the dentate gyrus of the hippocampus, one of the only regions of the brain in which new neurons are formed throughout life. In this seminar I will present experiments using electrophysiology and calcium imaging aiming to understand the functional role of newborn neurons in the processing of afferent stimuli, with the focus on the synaptic mechanism that generate the unique properties they present. [more]

Endogenous formaldehyde: a stem cell genotoxin and metabolic carcinogen in mammals

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Talk by Dr. Lucas Pontel

Formaldehyde is a highly reactive chemical used as a preservative and also in many industrial processes. In our cells, this aldehyde is generated as a by-product of several essential biochemical pathways. This ‘endogenous’ formaldehyde is very reactive and can damage proteins and DNA resulting in lethal toxicity. Therefore, cells harbour two protective barriers: the formaldehyde-detoxifying enzyme alcohol dehydrogenase 5 (Adh5) and the Fanconi Anemia DNA repair pathway. The simultaneous inactivation of these two systems leads to haematopoietic stem cell attrition, kidney and liver dysfunction, and development of cancer in mice. My work aims to understand the molecular mechanisms that counteract unwanted consequences of essential metabolism. [more]

Role of Activin B as a novel hepatokine in the regulation of glucose homeostasis

Talk by Prof. Kohjiro Ueki

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Histone Mimicry by Viruses

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Talk by Prof. Alexander Tarakhovsky, Rockefeller University, New York

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The Neurobiology of Homeostasis

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Talk by Zachary Knight, PhD, University of California San Francisco

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Developmental Programming of Hypothalamic Feeding Circuits

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Talk by Sebastien Bouret, PhD, Children's Hospital, LA

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Gut microbiota and energy homeostasis

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Talk by Prof. Mirko Trajkovski

The main interests of our work are the mechanisms underlying metabolic diseases, primarily obesity and insulin resistance. Mammals have two types of fat: brown and white, with opposing functions. Main role of the brown fat is to burn lipids and sugars to produce heat. Brown fat cells also emerge in the subcutaneous adipose tissue (named beige cells) in response to cold, a process known as browning. Promotion of increased brown fat development in humans and experimental mice leads to increased energy expenditure and lean and healthy phenotype without causing dysfunction in other tissues, suggesting the manipulation of the fat stores as an important therapeutic objective. The gut microbiota co-develops with the host and its composition is influenced by several physiological changes, which affect the whole-body metabolism and energy balance. With our integrative research program we are aiming to understand the mechanisms of white adipose tissue browning and the intestinal plasticity in regulating metabolic homeostasis and development of metabolic diseases from the gut microbiota related perspective. [more]

Melanocortin-driven plasticity of hypothalamic feeding circuits

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Talk by Henning Fenselau, PhD

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Brain barriers in metabolic regulation

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Talk by Prof. Markus Schwaninger, Uni Lübeck

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5th Graduate Symposium Cologne Graduate School of Ageing Research

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5th Graduate Symposium Cologne Graduate School of Ageing Research

  • Date: Nov 10, 2016
  • Speaker: Diverse
  • Additionally, there will be talks from international guest speakers: Malene Hansen on "Cellular recycling: Role of autophagy in aging and disease", David Rubinsztein on "Autophagy and other pathways that protect against neurodegeneration", Massimo Zeviani on "New genes and mechanisms in mitochondrial biogenesis and disease"
  • Location: MPI for Biology of Ageing
  • Room: Lecture Hall
  • Host: Cologne Graduate School
  • Contact: dmorick@age.mpg.de

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Food & Decision Making in humans: what is the link?

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Talk by Prof. So Young Park

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Breast Cancer Swimming in a Sea of Lipid: On a voyage to discover the link between obesity and breast cancer

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Talk by Dr. Andrew Hoy, University of Sydney

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Insular cortex: a neuroanatomical insight into interoception, emotion, and self-awareness

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Talk by Henry Evrard, PhD

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Mechanisms guarding brown fat against metabolic stress in cold and obesity

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Talk by Dr. Alexander Bartelt

Brown adipose tissue (BAT) needs to dissipate vast amounts ofintracellular and circulating nutrients to sustain its exceptional oxidativemetabolic activity for thermogenesis, and in doing so BAT activity exertsbeneficial metabolic effects on obesity, insulin resistance andatherosclerosis. Identifying factors that protect adipocytes from metabolicstress during the adaptation to cold and obesity may hold great potentialtowards therapeutic approaches for metabolic diseases. As the dramaticmetabolic changes in BAT not only involve dissipation of energy-rich nutrientsbut also the de novo synthesis of new proteins, lipids and cellular organelles,adaptation to cold or excess nutrients might require special mechanisms forincreased quality control of these metabolic processes. While the endoplasmic reticulum (ER) is a critical organelle formetabolic homeostasis, the mechanisms that mediate adaptation of the ER inadipocytes are unclear. We will discuss novel insight into the molecularmechanisms guarding brown fat againstmetabolic stress in cold and obesity. In particular, we will focus on theunfolded protein response and ER-associated protein degradation as the mostcritical pathways by which the ER responds to increased metabolic demand anddiscuss how these are engaged in brown adipocytes. In this context, we haveidentified Nfe2l1, also known as Nrf1, as a novel regulator of ER homeostasisin BAT. Using in vitro systems and mouse models we will address thephysiological, pathological and translational relevance of Nfe2l1/Nrf1 for the adaptationof BAT to cold and obesity. [more]

Deciphering dynamics and connectivity of brain orexin cells

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Talk by Denis Burdakov, PhD

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Developing ceramide synthase inhibitors for insulin resistance and neurodegenerative disease

Talk by Anthony Don, University of New South Wales, Sydney

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Epigenetic control of neurodegeneration

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Talk by Anne Schaefer, MD, PhD

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Understanding how we get fat: Dietary regulation of adipocyte precursors

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Talk by Matthew Rodeheffer, PhD, Yale University

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Insulin action on the brain: Role in metabolism and brain function

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Talk by Prof. Ronald Kahn

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" To eat? To sleep? To run? Coordination of innate behaviors by lateral hypothalamus"

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Talk by Tatiana Korotkova, PhD, Leibniz Institut für Molekulare Pharmakologie

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Mechanisms of brown and white fat formation

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Talk by Prof. Dr. Christian Wolfrum, ETH Zürich

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Tanycytes: the Hypothalamic Hyperdrive for Metabolic Hormones

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Talk by Vincent Prevot, University of Lille, France

The survival of an organism relies on its ability to promptly, effectively and reproducibly communicate with brain networks that control food intake and energy homeostasis. To achieve this, circulating factors of hunger and satiety reflecting nutrient availability must cross the blood-brain barrier (BBB) to reach effectors neurons. A defect in this process invariably leads to uncontrolled body weight. Here I will discuss the key role played in this process by a peculiar type of glial cells named tanycytes, which have their cell bodies lining the floor of the third ventricle and their endfeet contacting the pial surface of the brain. Recent studies indeed suggest that tanycytes, besides regulating hypothalamic BBB plasticity according to nutrient status, capture metabolic signals such as leptin from the bloodstream and transport them towards their cell body for release into the cerebrospinal fluid. Blockade of this conduit for peripheral metabolic factors into the brain of obese individuals is thought to contribute to the pathophysiology of central hormonal resistance. [more]

The molecular and systems neuroscience of hunger

Editing of mouse and human genomes using CRISPR/Cas

Talk by Dr. Ralf Kühn, Max Delbrück Center, Berlin

  • Date: Jan 11, 2016
  • Time: 14:00 - 15:30
  • Speaker: Dr. Ralf Kühn
  • Dr. Kühn is a tenured scientist at the Max-Delbrück-Center for Molecular Medicine & the Berlin Institute for Health, head of the Transgenic core facility and a lecturer for genetics at the Technical University of Munich in Germany. He has a long track record in mouse genetic engineering technology, including gene targeting in one-cell embryos using zinc-finger nucleases and TALEN. His current research is focused on utilizing and improving the efficiency of CRISPR/Cas9 based mutagenesis in mouse zygotes and human iPS cells, in particular the interference with non-homologous end joining to promote homology-directed repair.
  • Location: MPI for Metabolism Resarch
  • Room: Seminar 1
  • Host: Dr. Thomas Wunderlich
  • Contact: thomas.wunderlich@sf.mpg.de

Engineering of the mouse germline to create targeted mutants is a key technology for biomedical research. We use an expedite approach for the generation of mouse mutants by microinjection of engineered, sequence-specific nucleases into one-cell embryos. Such nucleases create targeted double-strand breaks (DSBs) and stimulate DNA repair by non-homologous end joining (NHEJ) or homology directed repair (HDR). NHEJ religates the open ends, frequently leading to frameshift (knockout) mutations by the loss of nucleotides, whereas HDR enables the insertion of targeted (knockin) mutations from gene targeting vectors or oligonucleotides as repair templates. By this means mutant knockout and knockin founders are identified 7 weeks after embryo injections, enabling the fast establishment of mutant lines. Three nuclease generations, ZFNs, TALENs and the CRISPR/Cas9 system were validated in recent years for direct mutagenesis in embryos. In particular, CRISPR/Cas9 enables the generation of knockout and knockin alleles at frequencies of up to 40% and 10%, respectively, among pups derived from embryo injections. Nevertheless, the dominance of NHEJ versus HDR requires further improvement. To tackle this problem we established `traffic light´ reporter lines indicating DSB repair by NHEJ or HDR through the expression of red or green fluorescent proteins. To enhance HDR, we suppressed NHEJ key molecules by gene silencing, by the inhibitor SCR7 or by the adenoviral proteins E1B55K and E4orf6. In cell lines, SCR7 or the knockdown of KU70 and DNA Ligase IV promotes the efficiency of HDR up to 5-fold. Coexpression of the DNA Ligase IV degrading E1B55K and E4orf6 proteins improves the efficiency of HDR up to 8-fold and essentially abolishes NHEJ repair. We are presently using TLR transgenic mice to enhance HDR repair of CRISPR/Cas-induced DSBs by NHEJ suppression in early embryos and somatic cells to optimize the generation of precisely targeted alleles in vivo. [more]

Regulatory RNAs

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Regulatory RNAs

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Imaging human brain insulin sensitivity over the lifespan

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Brain Endophenotypes of Obesity

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Intestinal regulators of whole body metabolism

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NonCode 2015 - CECAD Mini-Symposium on regulatory RNAs

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NonCode 2015 - CECAD Mini-Symposium on regulatory RNAs

With the advent of modern sequencing techniques, regulatory RNA biology is gaining significant focus in myriads of avenues ranging from control of development to ageing and ageing-associated diseases. We bring together a group of young, internationally acclaimed scientists specializing in diverse aspects of RNA biology ranging from novel mechanisms of alternative splicing to single cell RNA sequencing. This will be a great opportunity to familiarize with the latest developments in regulatory RNA biology. In order to facilitate easy and convenient scientific exchange, this symposium is free and registration is not required. [more]

 
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