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The Bartelt Lab studies metabolic adaptation as a fundamental process by which cells and organisms respond to environmental challenges
- We are particularly interested in the regulation of energy balance, adipocyte health, and obesity associated comorbidities such as type 2 diabetes and cardiovascular disease.
- Our goal is to understand the molecular basis of metabolic biology and find new approaches to tackle metabolic disease clusters.
LATEST NEWS FROM THE LAB
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Brown fat thermogenesis and metabolic health
Thermogenic adipocytes are a remarkable type of metabolic cell. These UCP1-expressing cells are activated by cold and use energy-dense nutrient such as fatty acids, carbohydrates, and derived carbohydrates for producing heat to maintain body temperature homeostasis. Activation of thermogenic adipocytes has been shown to improve metabolic health in regular rodents, preclinical animal models of metabolic disease and humans. Thermogenesis is a process that depends on the environmental temperature and the physiognomy of the animal. Hence the thermogenic activity greatly varies from warmer to colder season as well as differs from mice to men. Our goal is to understand how thermogenic adipocytes adapt their metabolism to the extreme challenges of high metabolic flux, high oxidative activity, as well as synthesis of new organelles and cellular structural remodeling.
- Adipose tissue inflammation and metabolic disease
Adipocytes are key regulators of metabolic health: healthy white adipocytes are essential as in the complete absence of white adipose tissue in mice and humans systemic metabolic homeostasis is compromised. In the very different condition of obesity, excess accumulation of white adipocytes leads to the same phenotypic alterations of metabolic disease. Obesity is a chronic inflammatory disease and adipocytes are actively recruiting professional immune cells with chemokines when they are stressed. Interestingly, white adipose tissue inflammation is both required for the development of healthy fat cells but also contributes to their dysfunction in obesity. Our goal is to define molecular mechanisms of adipocyte health that direct the nature of adipose inflammation and associated systemic pathologies such as diabetes and atherosclerosis.
- Cardiomyocyte adaptation in myocardial infarction
The heart is a fascinating and dynamic organ essential for human life. However, its metabolic flexibility is compromised in many critical medical conditions such as cardiohypertrophy, heart failure and during myocardial infarction. Both physiological changes in heart rate as well as the very distinct condition of heart disease require special mechanisms of adaptation. This is even more apparent in light of the unique structural features of myocyte organelles, particularly the endoplasmic reticulum and mitochondria. Like in other conditions of metabolic disease, heart disease has s strong inflammatory component, both for healthy as well as maladaptive regeneration and tissue scarring. Our goal is to understand the molecular adaption of a trained heart versus dysfunctional heart, particularly after myocardial infarction. A detailed molecular understanding of cardiomyocyte-immune cell interaction would be transformative for designing new therapeutic strategies of myocardial infarction outcomes.
- Shivering, exercise and skeletal muscle function
Next to age and genetic predisposition, physical activity and exercise are the most important factors for maintaining a healthy metabolism throughout life. Also, even as a therapeutic life style intervention, exercise or mild physical activity have beneficial effects on cardiometabolic health. Surprisingly, we know very little about how skeletal muscle cells control the change in metabolism during the transition from sedentariness to physical activity and such knowledge would be critical for developing molecular therapies in support of life style changes or vice versa. Somewhat paradoxically, in other severe myopathies, such as muscle wasting in immobilized subjects or cancer cachexia, similar metabolic alterations take place as in beneficial exercise but the underlying mechanisms remain elusive. Our goal is to identify novel regulators of skeletal myocyte adaptation, and explore how these relate to physical activity and metabolic disease.
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Bartelt and Ries Lab
PRINCIPAL INVESTIGATOR
Alexander Bartelt, PhDPrincipal InvestigatorPOSTDOCTORAL RESEARCHERS
Henrika Jodeleit, DVMAnimal Welfare OfficerLaura Heimann, DVMDeputy Lead Animal Operation | Laboratory Animal VeterinarianVgfpgsZilvguuavimeävfsmiJoel Garcia Guerra, PhDPostdoctoral researcherQüiaä-XgpyYlgvimsävfemiImke Leonie Lemmer, PhDPostdoctoral researcherEvoisVivvipvSimtävftmiLeonardo Matta, PhDPostdoctoral researcheräiüugpmüevgbbgvimYedSnävfsmiPHD STUDENTS
Lukas BlaasPhD studentVfoYgc SSAäggcvim fuWl+vfiuyziuemiAlba Mena GomezPhD StudentFäj;geOiugvimsäv:fsYmiCarolin JethwaPhD studentygpüälaSu Yvfä:iјvimeävf miAnna JungPhD studentFuug Qfuxvim/ävf: miMin MaoPhD studentOlu OgüvimsävfsmiAnahita OfoghiPhD studentFugzlbg-Éwüxzlvimsävf-miMD STUDENTS
Jan CacaMD studentQgueHgygvim ful#v;fYiuyziusJmiChristoph GibisMD studentHzplcbüözeXljlcvims;ävftJmiUNDERGRADUATE STUDENTS
Theresa AuerM.Sc. studentKzipic,gsFfipvi:m-ädvfsmiDiamela T. PaezM.Sc. studentTECHNICIANS
Thomas PitschTechnicianMary IbrahimVeterinaryTechnician+49-(0)89-4400-43911Associated Research Lab
Bartelt Lab over the years
AlummniHenver Brunetta, former PostDoc
Maude Giroud, former PostDoc
Nazia Hilal, former PostDoc
Sajjad Khani, former PostDoc
Stefan Kotschi, former PostDoc
Nienke Willemsen, former PhD student
Batoul Bayer, former M.Sc. student
Janina Caesar, former MSc. student
Zeynep Koçberber, former M.Sc. student
Ellen Thiemann, former M.Sc. student
Hala Zahran, former M.Sc. student
Isabel Arigoni, former MD student
Yuri Kechur, former MD student
Aurora Wallney, former MD student
Alexandra Aaldijk, former research intern
Ana Bici, former Research Assistant
Julia Schluckebier, former Technician
Irmak Toksöz, former Research Assistant
Silvia Weidner, former Technician
Tugce M. Yildirim, former Technician
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We are currently looking for Postdoctoral fellows interested in our research.
If you are interested please email us with a letter of motivation/research interests, full CV and two references.
Motivated Undergrads, Bachelor and Master students who want to engage in our research, please email us with a letter of motivation and short CV.
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- Lemmer IL, Haas DT, Willemsen N, Kotschi S, Toksöz I, Gjika E, Khani S, Rohm M, Diercksen N, Nguyen BPH, Menden MP, Egu DT, Waschke J, Larsen S, Ma T, Gerhart-Hines Z, Herzig S, Dyar K, Krahmer N, Bartelt A. Nfe2l1-mediated proteasome function controls muscle energy metabolism in obesity. Biorxiv 2023
- Ofoghi, A., Kotschi, S., Lemmer, I. L., Haas, D. T., Willemsen, N., Bayer, B., Jung, A. S., Möller, S., Haberecht-Müller, S., Krüger, E., Krahmer, N., Bartelt, A. Activating the NFE2L1-ubiquitin-proteasome system by DDI2 protects from ferroptosis. Cell Death Differ. 2024
- Brunetta HS, Jung AS, Valdivieso-Rivera F, de Campos Zani SC, Guerra J, Furino VO, Francisco A, Bercot M, Moraes-Vieira PM, Keipert S, Jastroch M, Martinez LO, Sponton CH, Castilho RF, Mori MA, Bartelt A. IF1 is a cold-regulated switch of ATP synthase hydrolytic activity to support thermogenesis in brown fat. EMBO J 2024
- Giroud M, Kotschi S, Kwon Y, Le Thuc O, Hoffmann A, Gil-Lozano M, Karbiener M, Higareda-Almaraz JC, Khani S, Tews D, Fischer-Posovszky P, Sun W, Dong H, Ghosh A, Wolfrum C, Wabitsch M, Virtanen KA, Blüher M, Nielsen S, Zeigerer A, García-Cáceres C, Scheideler M, Herzig S, Bartelt A. The obesity-linked human lncRNA AATBC stimulates mitochondrial function in adipocytes. EMBO Reports 2023
- Koçberber Z, Willemsen N, Bartelt A.The role of proteasome activators PA28αβ and PA200 in brown adipocyte differentiation and function. Frontiers in Endocrinology 2023
- Willemsen N, Arigoni I, Studencka-Turski M, Krüger E, Bartelt A. Proteasome dysfunction disrupts adipogenesis and induces inflammation via ATF3. Molecular Metabolism 2022
- Kotschi S, Jung A, Willemsen N, Ofoghi A, Proneth B, Conrad M, Bartelt A. NFE2L1-mediated proteasome function protects from ferroptosis. Molecular Metabolism 2022
- Muley C, Kotschi S, Bartelt A. Role of Ubiquilins for Brown Adipocyte Proteostasis and Thermogenesis. Frontiers in Endocrinology 2021
- Giroud M, Tsokanos FF, Caratti G, Kotschi S, Khani S, Jouffe C, Vogl ES, Irmler M, Glantschnig C, Gil-Lozano M, Hass D, Khan AA, Garcia MR, Mattijssen F, Maida A, Tews D, Fischer-Posovszky P, Feuchtinger A, Virtanen KA, Beckers J, Wabitsch M, Uhlenhaut H, Blüher M, Tuckermann J, Scheideler M, Bartelt A, Herzig S. HAND2 is a novel obesity-linked adipogenic transcription factor regulated by glucocorticoid signalling. Diabetologia 2021
- Bartelt A, Widenmaier SB, Schlein C, Johann K, Goncalves RLS, Eguchi K, Fischer AW, Parlakgül G, Snyder NA, Nguyen TB, Bruns OT, Franke D, Bawendi MG, Lynes MD, Leiria LO, Tseng YH, Inouye KE, Arruda AP, Hotamisligil GS. Brown adipose tissue thermogenic adaptation requires Nrf1-mediated proteasomal activity. Nature Medicine 2018
- Lemmer IL, Haas DT, Willemsen N, Kotschi S, Toksöz I, Gjika E, Khani S, Rohm M, Diercksen N, Nguyen BPH, Menden MP, Egu DT, Waschke J, Larsen S, Ma T, Gerhart-Hines Z, Herzig S, Dyar K, Krahmer N, Bartelt A. Nfe2l1-mediated proteasome function controls muscle energy metabolism in obesity. Biorxiv 2023