Seminare und andere Veranstaltung am Max-Planck-Institut für Stoffwechselforschung oder an kooperierenden Instituten

Gastgeber: Dr. Jan-Wilhelm Kornfeld

Talk by Kim Ravnskjær, PhD, University of Southern Denmark

Global Analyses of Hepatic Stellate Cell Biology

Talk by PD Dr. Michael Potente, MPI for Heart and Lung Research, Bad Nauheim Bad Nauheim

Metabolic regulation of endothelial growth and quiescence

Talk by Riekelt Houtkooper, PhD, Academic Medical Center Amsterdam

Pharmacological approaches to restore mitochondrial function

Talk by Amélie Bonnefond, PhD, University of Lille

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

Talk by Prof. Mirko Trajkovski

Gut microbiota and energy homeostasis
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. [mehr]

Talk by Dr. Alexander Bartelt

Mechanisms guarding brown fat against metabolic stress in cold and obesity
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. [mehr]

Talk by Prof. Dr. Christian Wolfrum, ETH Zürich

Mechanisms of brown and white fat formation

Talk by Vincent Prevot, University of Lille, France

Tanycytes: the Hypothalamic Hyperdrive for Metabolic Hormones
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. [mehr]

Regulatory RNAs

Regulatory RNAs
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