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  1. AU="Jonas, Wenke"
  2. AU="Khan, Nawal"
  3. AU="Martini, Lígia A"
  4. AU="Guzzetta, Melissa" AU="Guzzetta, Melissa"
  5. AU="Reiter, Gregor S"
  6. AU="Alberghina, Daniela"
  7. AU=D'Arena Giovanni AU=D'Arena Giovanni
  8. AU="Rutland, Catrin S"
  9. AU="Gocher-Demske, Angela M"
  10. AU="Koide, S S"
  11. AU=Barnbaum Deborah R AU=Barnbaum Deborah R
  12. AU=Xiang Hongfei AU=Xiang Hongfei
  13. AU="Whitehall, Julia"
  14. AU=Silva Severino Jefferson Ribeiro da
  15. AU="Piñero-Pérez, Rocío"
  16. AU="Voss, Stephan"
  17. AU="Jović, Ines"
  18. AU="Pérez-Guerrero, Edsaúl Emilio"
  19. AU="Akiyama, Shoko"
  20. AU="Greene, Wendy R"
  21. AU="Renzetti, Paolo"
  22. AU="Knöpfle, K T"
  23. AU="Peitzsch, Mirko" AU="Peitzsch, Mirko"
  24. AU=Bonet-Sola Daniel
  25. AU="Martín-Alfonso, J.E."
  26. AU=Ramesh BA
  27. AU="Dayanandan, Selvadurai"
  28. AU="Strathmann, Eike A"
  29. AU=Hewitt Stephen M
  30. AU="Meroni, Marco"
  31. AU="Gutierrez Amezcua, Jose Manuel"
  32. AU="Pfeifer, Susanne P"
  33. AU=McGrath Eric J
  34. AU="Wang, Pengyu"
  35. AU="Becker, Joscha Nico"
  36. AU="Chillrud, Steven N"
  37. AU=Werner L P
  38. AU="Tianmin Xu"
  39. AU="Matsagkas, Miltos"
  40. AU="Cosentino, Claudia"
  41. AU="Radbruch, Lukas"
  42. AU=Edwards Justin P.
  43. AU="Morse, Dan J"
  44. AU="Priya, Vansh"
  45. AU="Chen, Eric R"
  46. AU=Behrens Kevin G.
  47. AU=Radtke Heather B
  48. AU="Erdmann, Kati"
  49. AU="Anh, Nguyen P Q"
  50. AU="Arias, Manuel"
  51. AU="Badhrees, I."

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  1. Artikel ; Konferenzbeitrag: Time-restricted feeding improves insulin secretion and prevents hyperglycemia in diabetes-prone mice despite obesity

    Jonas, Wenke / Birkenfeld, Andreas L. / Vogel, Heike / Schürmann, Annette

    Diabetologie und Stoffwechsel

    (Diabetes Kongress 2024 – 58. Jahrestagung der DDG)

    2024  Band 19, Heft S 01

    Veranstaltung/Kongress Diabetes. Umwelt. Leben. Perspektiven aus allen Blickwinkeln, CityCube Berlin, 2024-05-08
    Serientitel Diabetes Kongress 2024 – 58. Jahrestagung der DDG
    Sprache Deutsch
    Erscheinungsdatum 2024-04-01
    Verlag Georg Thieme Verlag KG
    Erscheinungsort Stuttgart ; New York
    Dokumenttyp Artikel ; Konferenzbeitrag
    ZDB-ID 2222993-0
    ISSN 1861-9010 ; 1861-9002
    ISSN (online) 1861-9010
    ISSN 1861-9002
    DOI 10.1055/s-0044-1785268
    Datenquelle Thieme Verlag

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    Verfügbar in ZB MED Köln/Königswinter

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  2. Artikel ; Online: Genetic and epigenetic factors determining NAFLD risk.

    Jonas, Wenke / Schürmann, Annette

    Molecular metabolism

    2020  Band 50, Seite(n) 101111

    Abstract: Background: Hepatic steatosis is a common chronic liver disease that can progress into more severe stages of NAFLD or promote the development of life-threatening secondary diseases for some of those affected. These include the liver itself (nonalcoholic ...

    Abstract Background: Hepatic steatosis is a common chronic liver disease that can progress into more severe stages of NAFLD or promote the development of life-threatening secondary diseases for some of those affected. These include the liver itself (nonalcoholic steatohepatitis or NASH; fibrosis and cirrhosis, and hepatocellular carcinoma) or other organs such as the vessels and the heart (cardiovascular disease) or the islets of Langerhans (type 2 diabetes). In addition to elevated caloric intake and a sedentary lifestyle, genetic and epigenetic predisposition contribute to the development of NAFLD and the secondary diseases.
    Scope of review: We present data from genome-wide association studies (GWAS) and functional studies in rodents which describe polymorphisms identified in genes relevant for the disease as well as changes caused by altered DNA methylation and gene regulation via specific miRNAs. The review also provides information on the current status of the use of genetic and epigenetic factors as risk markers.
    Major conclusion: With our overview we provide an insight into the genetic and epigenetic landscape of NAFLD and argue about the applicability of currently defined risk scores for risk stratification and conclude that further efforts are needed to make the scores more usable and meaningful.
    Mesh-Begriff(e) Animals ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; DNA Methylation ; Diabetes Mellitus, Type 2/genetics ; Disease Models, Animal ; Epigenesis, Genetic ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Liver Cirrhosis/diagnosis ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; MicroRNAs/metabolism ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/pathology ; Polymorphism, Single Nucleotide ; Risk Factors ; Severity of Illness Index
    Chemische Substanzen MicroRNAs
    Sprache Englisch
    Erscheinungsdatum 2020-11-05
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2020.101111
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Alterations of Lipid Profile in Livers with Impaired Lipophagy.

    Jonas, Wenke / Schwerbel, Kristin / Zellner, Lisa / Jähnert, Markus / Gottmann, Pascal / Schürmann, Annette

    International journal of molecular sciences

    2022  Band 23, Heft 19

    Abstract: Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Various mechanisms such as an increased uptake in fatty acids or de novo synthesis contribute to the development of steatosis and progression to more ...

    Abstract Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Various mechanisms such as an increased uptake in fatty acids or de novo synthesis contribute to the development of steatosis and progression to more severe stages. Furthermore, it has been shown that impaired lipophagy, the degradation of lipids by autophagic processes, contributes to NAFLD. Through an unbiased lipidome analysis of mouse livers in a genetic model of impaired lipophagy, we aimed to determine the resulting alterations in the lipidome. Observed changes overlap with those of the human disease. Overall, the entire lipid content and in particular the triacylglycerol concentration increased under conditions of impaired lipophagy. In addition, we detected a reduction in long-chain polyunsaturated fatty acids (PUFAs) and an increased ratio of n-6 PUFAs to n-3 PUFAs, which was due to the depletion of n-3 PUFAs. Although the abundance of major phospholipid classes was reduced, the ratio of phosphatidylcholines to phosphatidylethanolamines was not affected. In conclusion, this study demonstrates that impaired lipophagy contributes to the pathology of NAFLD and is associated with an altered lipid profile. However, the lipid pattern does not appear to be specific for lipophagic alterations, as it resembles mainly that described in relation to fatty liver disease.
    Mesh-Begriff(e) Animals ; Autophagy ; Fatty Acids/metabolism ; Fatty Acids, Omega-3/metabolism ; Humans ; Lipid Metabolism ; Liver/metabolism ; Mice ; Non-alcoholic Fatty Liver Disease/metabolism ; Phosphatidylcholines/metabolism ; Phospholipids/metabolism ; Triglycerides/metabolism
    Chemische Substanzen Fatty Acids ; Fatty Acids, Omega-3 ; Phosphatidylcholines ; Phospholipids ; Triglycerides
    Sprache Englisch
    Erscheinungsdatum 2022-10-06
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms231911863
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Mitochondrial stress-induced GFRAL signaling controls diurnal food intake and anxiety-like behavior.

    Igual Gil, Carla / Coull, Bethany M / Jonas, Wenke / Lippert, Rachel N / Klaus, Susanne / Ost, Mario

    Life science alliance

    2022  Band 5, Heft 11

    Abstract: Growth differentiation factor 15 (GDF15) is a mitochondrial stress-induced cytokine that modulates energy balance in an endocrine manner. However, the importance of its brainstem-restricted receptor GDNF family receptor alpha-like (GFRAL) to mediate ... ...

    Abstract Growth differentiation factor 15 (GDF15) is a mitochondrial stress-induced cytokine that modulates energy balance in an endocrine manner. However, the importance of its brainstem-restricted receptor GDNF family receptor alpha-like (GFRAL) to mediate endocrine GDF15 signaling to the brain upon mitochondrial dysfunction is still unknown. Using a mouse model with muscle-specific mitochondrial dysfunction, we here show that GFRAL is required for activation of systemic energy metabolism via daytime-restricted anorexia but not responsible for muscle wasting. We further find that muscle mitochondrial stress response involves a GFRAL-dependent induction of hypothalamic corticotropin-releasing hormone, without elevated corticosterone levels. Finally, we identify that GFRAL signaling governs an anxiety-like behavior in male mice with muscle mitochondrial dysfunction, with females showing a less robust GFRAL-dependent anxiety-like phenotype. Together, we here provide novel evidence of a mitochondrial stress-induced muscle-brain crosstalk via the GDF15-GFRAL axis to modulate food intake and anxiogenic behavior.
    Mesh-Begriff(e) Female ; Male ; Humans ; Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Growth Differentiation Factor 15/pharmacology ; Glial Cell Line-Derived Neurotrophic Factor Receptors/metabolism ; Obesity/metabolism ; Corticotropin-Releasing Hormone ; Corticosterone ; Glial Cell Line-Derived Neurotrophic Factor ; Eating/genetics ; Anxiety
    Chemische Substanzen Growth Differentiation Factor 15 ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Corticotropin-Releasing Hormone (9015-71-8) ; Corticosterone (W980KJ009P) ; Glial Cell Line-Derived Neurotrophic Factor
    Sprache Englisch
    Erscheinungsdatum 2022-09-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202201495
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Buch ; Online ; Dissertation / Habilitation: Untersuchung zur transkriptionellen Regulation des Angiopoietin-2 in humanen Endothelzellen

    Jonas, Wenke

    2009  

    Verfasserangabe von Wenke Jonas
    Sprache Deutsch
    Umfang Online-Ressource
    Dokumenttyp Buch ; Online ; Dissertation / Habilitation
    Dissertation / Habilitation Berlin, Humboldt-Univ., Diss., 2009
    Datenquelle Katalog der Technische Informationsbibliothek Hannover

    Volltext online

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  6. Artikel: Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival

    Chubanov, Vladimir / Ferioli, Silvia / Wisnowsky, Annika / Simmons, David G / Leitzinger, Christin / Einer, Claudia / Jonas, Wenke / Shymkiv, Yuriy / Bartsch, Harald / Braun, Attila / Akdogan, Banu / Mittermeier, Lorenz / Sytik, Ludmila / Torben, Friedrich / Jurinovic, Vindi / van der Vorst, Emiel PC / Weber, Christian / Yildirim, Önder A / Sotlar, Karl /
    Schürmann, Annette / Zierler, Susanna / Zischka, Hans / Ryazanov, Alexey G / Gudermann, Thomas

    eLife, 5:e20914

    2016  

    Abstract: Mg2+ regulates many physiological processes and signalling pathways. However, little is known about the mechanisms underlying the organismal balance of Mg2+. Capitalizing on a set of newly generated mouse models, we provide an integrated mechanistic ... ...

    Körperschaft Deutsches Institut für Ernährungsforschung Potsdam-Rehbrücke
    Abstract Mg2+ regulates many physiological processes and signalling pathways. However, little is known about the mechanisms underlying the organismal balance of Mg2+. Capitalizing on a set of newly generated mouse models, we provide an integrated mechanistic model of the regulation of organismal Mg2+ balance during prenatal development and in adult mice by the ion channel TRPM6. We show that TRPM6 activity in the placenta and yolk sac is essential for embryonic development. In adult mice, TRPM6 is required in the intestine to maintain organismal Mg2+ balance, but is dispensable in the kidney. Trpm6 inactivation in adult mice leads to a shortened lifespan, growth deficit and metabolic alterations indicative of impaired energy balance. Dietary Mg2+ supplementation not only rescues all phenotypes displayed by Trpm6-deficient adult mice, but also may extend the lifespan of wildtype mice. Hence, maintenance of organismal Mg2+ balance by TRPM6 is crucial for prenatal development and survival to adulthood.
    Schlagwörter biophysics ; human biology ; intestine ; kidney ; longevity ; magnesium ; medicine ; mouse ; placenta ; structural biology ; trophoblast stem cells
    Sprache Englisch
    Erscheinungsdatum 2016-12-19
    Dokumenttyp Artikel
    Datenquelle Fachrepositorium Lebenswissenschaften

    Volltext online

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  7. Buch ; Online ; Dissertation / Habilitation: Untersuchung zur transkriptionellen Regulation des Angiopoietin-2 in humanen Endothelzellen

    Jonas, Wenke [Verfasser]

    2009  

    Verfasserangabe von Wenke Jonas
    Schlagwörter Biowissenschaften, Biologie ; Life Science, Biology
    Thema/Rubrik (Code) sg570
    Sprache Deutsch
    Dokumenttyp Buch ; Online ; Dissertation / Habilitation
    Datenquelle Digitale Dissertationen im Internet

    Volltext online

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  8. Artikel: Obesity Hinders the Protective Effect of Selenite Supplementation on Insulin Signaling.

    Hauffe, Robert / Rath, Michaela / Agyapong, Wilson / Jonas, Wenke / Vogel, Heike / Schulz, Tim J / Schwarz, Maria / Kipp, Anna P / Blüher, Matthias / Kleinridders, André

    Antioxidants (Basel, Switzerland)

    2022  Band 11, Heft 5

    Abstract: The intake of high-fat diets (HFDs) containing large amounts of saturated long-chain fatty acids leads to obesity, oxidative stress, inflammation, and insulin resistance. The trace element selenium, as a crucial part of antioxidative selenoproteins, can ... ...

    Abstract The intake of high-fat diets (HFDs) containing large amounts of saturated long-chain fatty acids leads to obesity, oxidative stress, inflammation, and insulin resistance. The trace element selenium, as a crucial part of antioxidative selenoproteins, can protect against the development of diet-induced insulin resistance in white adipose tissue (WAT) by increasing glutathione peroxidase 3 (GPx3) and insulin receptor (IR) expression. Whether selenite (Se) can attenuate insulin resistance in established lipotoxic and obese conditions is unclear. We confirm that
    Sprache Englisch
    Erscheinungsdatum 2022-04-28
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11050862
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Identification of Novel Genes Involved in Hyperglycemia in Mice.

    Jonas, Wenke / Kluth, Oliver / Helms, Anett / Voß, Sarah / Jähnert, Markus / Gottmann, Pascal / Speckmann, Thilo / Knebel, Birgit / Chadt, Alexandra / Al-Hasani, Hadi / Schürmann, Annette / Vogel, Heike

    International journal of molecular sciences

    2022  Band 23, Heft 6

    Abstract: Current attempts to prevent and manage type 2 diabetes have been moderately effective, and a better understanding of the molecular roots of this complex disease is important to develop more successful and precise treatment options. Recently, we initiated ...

    Abstract Current attempts to prevent and manage type 2 diabetes have been moderately effective, and a better understanding of the molecular roots of this complex disease is important to develop more successful and precise treatment options. Recently, we initiated the collective diabetes cross, where four mouse inbred strains differing in their diabetes susceptibility were crossed with the obese and diabetes-prone NZO strain and identified the quantitative trait loci (QTL)
    Mesh-Begriff(e) Animals ; Diabetes Mellitus, Type 2/genetics ; Genotype ; Hyperglycemia/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Quantitative Trait Loci
    Sprache Englisch
    Erscheinungsdatum 2022-03-16
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23063205
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Gut microbiota and glucometabolic alterations in response to recurrent partial sleep deprivation in normal-weight young individuals

    Benedict, Christian / Vogel, Heike / Jonas, Wenke / Woting, Anni / Blaut, Michael / Schurmann, Annette / Cedernaes, Jonathan

    Molecular Metabolism. 2016,

    2016  

    Abstract: Changes to the microbial community in the human gut have been proposed to promote metabolic disturbances that also occur after short periods of sleep loss (including insulin resistance). However, whether sleep loss affects the gut microbiota remains ... ...

    Abstract Changes to the microbial community in the human gut have been proposed to promote metabolic disturbances that also occur after short periods of sleep loss (including insulin resistance). However, whether sleep loss affects the gut microbiota remains unknown.In a randomized within-subject crossover study utilizing a standardized in-lab protocol (with fixed meal times and exercise schedules), we studied nine normal-weight men at two occasions: after two nights of partial sleep deprivation (PSD; sleep opportunity 02:45-07:00 h), and after two nights of normal sleep (NS; sleep opportunity 22:30-07:00 h). Fecal samples were collected within 24 h before, and after two in-lab nights, of either NS or PSD. In addition, participants underwent an oral glucose tolerance test following each sleep intervention.Microbiota composition analysis (V4 16S rRNA gene sequencing) revealed that after two days of PSD vs. after two days of NS, individuals exhibited an increased Firmicutes:Bacteroidetes ratio and of the families Coriobacteriaceae and Erysipelotrichaceae, with decreases in Tenericutes (all P < 0.05) - previously all associated with metabolic perturbations in animal or human models. However, no PSD vs. NS effect on beta diversity or on fecal short-chain fatty acid concentrations was found. Fasting and postprandial insulin sensitivity decreased after PSD (all P < 0.05).Our findings demonstrate that short-term sleep loss induces subtle effects on human microbiota. To what extent changes to the microbial community contribute to metabolic consequences of sleep loss warrants further investigations in larger and more prolonged sleep studies, to also assess how sleep loss impacts the microbiota in individuals who already are metabolically compromised.
    Schlagwörter Bacteroidetes ; Firmicutes ; Insulin resistance ; Intestinal microbiome ; Short-chain fatty acid ; Sleep restriction ; d2 ; F:B ; HDL ; HOMA-IR ; LDL ; NS ; OGTT ; OTU ; PERMANOVA ; PSD ; SCFA ; T2DM
    Sprache Englisch
    Erscheinungsort Elsevier GmbH
    Dokumenttyp Artikel ; Online
    Anmerkung Pre-press version
    ZDB-ID 2708735-9
    ISSN 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2016.10.003
    Datenquelle NAL Katalog (AGRICOLA)

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