Center for International Health, University of Bergen, Bergen, Norway
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Department of Microbiology, Innlandet Hospital Trust, Lillehammer, Norway
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Department of Clinical Science, University of Bergen, Bergen, Norway
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Department of Research, Innlandet Hospital Trust, Lillehammer, Norway
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participate in adipocyte differentiation and lipolysis regulation and adipocyte cytokines interact with regulation of thyrotropin ( 31 ). Unfortunately, the MBRN does not have good quality data on maternal BMI, and therefore, we could not explore the
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( 13 ) and mediating insulin desensitization in adipocytes ( 14 ). Our previous study demonstrated that serum SDF-1 levels are closely related to hyperglycemia, hypercoagulability, and inflammation in patients with T2D ( 15 ). Since chronic
Fujian Maternal-Fetal Clinical Medicine Research Center, Fuzhou, China
Fujian Key Laboratory of Prenatal Diagnosis and Birth Defect, Fuzhou, China
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Fujian Maternal-Fetal Clinical Medicine Research Center, Fuzhou, China
Fujian Key Laboratory of Prenatal Diagnosis and Birth Defect, Fuzhou, China
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implicated in various physiological processes such as insulin sensitivity, adipocyte differentiation, and vascular function, and has been shown to regulate the formation and function of MAMs ( 16 ). Taken together, mitochondria ( 17 ) and ER ( 18 ) play
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Diabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland
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insulin resistance, adipocytes proliferation and dysfunction, and alteration of intestinal microbiota. Subsequently, insulin resistance leads to lipolysis, release of adipokines such as TNF-α or IL-6, and stimulates hepatic DNL. As a consequence, the
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( 27 , 84 ), however determining the contribution of fatty acids from visceral adipose tissue to IHTAG, in humans, in vivo , is challenging. As visceral adipocytes are more lipolytically active than subcutaneous adipocytes in vitro ( 85 , 86 ) it
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with particular cognitive agency, as though neurones were clever in ways that endocrine cells are not. We can extend this argument to encompass all endocrine cells in the body. For example, the adipocytes that store our fat not only sense the
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), where it is responsible for the conversion of osteoblasts into adipocyte-like cells ( 63 , 64 ) and their differentiation ( 65 ). Different PPARγ ligands can affect bone metabolism; for example, rosiglitazone inhibits the expression of Runx2/Cba1, the
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Eye Hospital and School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
National Clinical Research Center for Ocular Diseases, Wenzhou, Zhejiang, China
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suppresses mesenteric adipocyte hypertrophy, declines damaged glucose tolerance during the oral glucose tolerance test, and mitigates insulin resistance in both metabolic syndrome and obese mouse models ( 15 , 33 ). Available evidence reports that TREH may
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Paediatric Neurosciences Research Group, Royal Hospital for Children, NHS Greater Glasgow & Clyde, Glasgow, UK
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, mesenchymal stem cells are also the precursor of marrow adipocytes, and the differentiation of these stem cells to these two cell lineages is competitive and reciprocally regulated ( 5 ). Bone marrow adiposity (BMA) itself is increasingly recognised to have a
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status, the insulin receptor, and glucose uptake in 3T3-L1 adipocytes . Archives of Biochemistry and Biophysics 2002 397 384 – 391 . 58 Konrad D Somwar R Sweeney G Yaworsky K Hayashi M Ramlal T Klip A . The antihyperglycemic drug α