Eva Tsaousidou

ORCID: 0000-0003-2751-1911
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Adipokines, Inflammation, and Metabolic Diseases
  • Regulation of Appetite and Obesity
  • Biochemical Analysis and Sensing Techniques
  • Olfactory and Sensory Function Studies
  • Metabolism, Diabetes, and Cancer
  • Cancer, Hypoxia, and Metabolism
  • Fibroblast Growth Factor Research
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • Cancer-related Molecular Pathways
  • Pancreatic function and diabetes
  • interferon and immune responses
  • IL-33, ST2, and ILC Pathways
  • Immune Cell Function and Interaction
  • Cardiovascular Disease and Adiposity
  • RNA Research and Splicing
  • Evolutionary Game Theory and Cooperation
  • Cancer Research and Treatments

Dana-Farber Cancer Institute
2024

Max Planck Institute for Metabolism Research
2012-2017

Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2012-2017

University of Cologne
2012-2017

University Hospital Cologne
2014-2017

Max Planck Institute for Biology of Ageing
2017

German Center for Diabetes Research
2016

Sexual dimorphism in energy metabolism is now established and suggested to affect many aspects of metabolic diseases particular diabetes obesity. This strongly related sex-based differences whole-body insulin resistance. Women are more sensitive compared men, but this advantage gradually disappears after menopause or when resistance progresses hyperglycemia diabetes. In narrative review, first, we describe the pathophysiology then present epidemiological evidence as well important biological...

10.1530/joe-23-0245 article EN Journal of Endocrinology 2024-01-24

Activation of c-Jun N-terminal kinase 1 (JNK1)- and inhibitor nuclear factor kappa-B 2 (IKK2)-dependent signaling plays a crucial role in the development obesity-associated insulin leptin resistance not only peripheral tissues but also CNS. Here, we demonstrate that constitutive JNK activation agouti-related peptide (AgRP)-expressing neurons hypothalamus is sufficient to induce weight gain adiposity mice as consequence hyperphagia. increases spontaneous action potential firing AgRP cells...

10.1016/j.celrep.2014.10.045 article EN cc-by Cell Reports 2014-11-01

Rat insulin promoter (RIP)-expressing neurons in the hypothalamus control body weight and energy homeostasis. However, genetic approaches to study role of these have been limited by fact that RIP expression is predominantly found pancreatic β-cells, which impedes selective targeting neurons. To define function hypothalamic RIP-expressing neurons, we set out acutely selectively eliminate them via diphtheria toxin-mediated ablation. Therefore, toxin receptor transgene was specifically...

10.1073/pnas.1206147109 article EN Proceedings of the National Academy of Sciences 2012-10-11

Summary Chronic metabolic inflammation is a key feature of obesity, insulin resistance and diabetes, although the initiation propagation mechanisms metaflammation are not fully established, particularly in adipose tissue. Here we show that adipocytes, altered regulation Ca 2+ channel inositol triphosphate receptor (IP3Rs) key, adipocyte-intrinsic, event involved emergence inflammatory signaling resulting resistance. Inflammation, either induced by cytokine exposure vitro or obesity vivo lead...

10.1101/2020.10.28.360008 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-10-29

Riera et al. developed ways to temporarily eliminate the sense of smell in adult mice. They discovered that mice lacking could eat a high-fat diet and stay significantly thinner than littermates with normal smell. Conversely, hyperosmia gained more weight wild-type on diet. The fact smell-deficient show an increase energy expenditure suggests odor what we may play important role how body deals calories. These new findings give us interesting insights so far uninvestigated coherences but...

10.1530/ey.15.11.10 article EN Yearbook of pediatric endocrinology 2018-09-11
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