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| http://dx.doi.org/10.3389/fendo.2022.1037159 | DOI Listing |
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GalNT2-mediated O-glycosylation affects pancreas development and function in mice.
Sci Rep
November 2024
Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
GALNT2, also known as polypeptide N-acetylgalactosaminyltransferase 2, is an enzyme that catalyzes the initial step of O-linked glycosylation, a crucial posttranslational modification that affects protein folding, stability, and function. Alterations in GALNT2 activity have been implicated in various diseases, such as cancer, metabolic disorders, and cardiovascular diseases, highlighting its importance in maintaining normal physiological functions. To investigate the impact of GalNT2 overexpression in vivo for the first time, we generated a conditional transgenic mouse line in which GalNT2 was expressed specifically in the pancreas.
View Article and Find Full Text PDFSympathetic NPY Boosts Thermogenic Adipocytes.
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Center for Hypothalamic Research and Department of Internal medicine, UT Southwestern, Medical Center, 5323 Harry Hines Blvd, Dallas, Texas, 75390 USA.
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Editorial Special Issue: 2022 consortium for trans-pyrenean investigations on obesity and diabetes.
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Adipocyte and Fat Biology Laboratory (AdipoFat), Translational Research Unit, Instituto de Investigación Sanitaria (IIS)-Aragón, Zaragoza, 50009, Spain.
Article Synopsis
- The Special Issue of the Journal of Physiology and Biochemistry highlights 7 contributions from the long-running "Consortium of Trans-Pyrenean Investigations on Obesity and Diabetes" (CTPIOD), which focuses on understanding obesity, diabetes, and related diseases.
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NOX4-reactive oxygen species axis: critical regulators of bone health and metabolism.
Front Cell Dev Biol
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Laboratory of Molecular Physiology of Bone, Institute of Physiology of the Czech Academy of Sciences, Prague, Czechia.
Bone marrow stromal cells (BMSCs) play a significant role in bone metabolism as they can differentiate into osteoblasts, bone marrow adipocytes (BMAds), and chondrocytes. BMSCs chronically exposed to nutrient overload undergo adipogenic programming, resulting in bone marrow adipose tissue (BMAT) formation. BMAT is a fat depot transcriptionally, metabolically, and morphologically distinct from peripheral adipose depots.
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