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-cells and decreased peripheral insulin sensitivity by an increased systemic inflammation as 1,25-OH 2 -D is involved in the inhibition of synthesis of Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) ( 14 ). On the other hand, a stimulation of
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the mere accumulation of lipid within hepatocytes (hepatic steatosis, HS), or the inflammation of the liver (nonalcoholic steatohepatitis, NASH), liver fibrosis, or cirrhosis (2) . The evolution of HS to NASH occurs through the development of insulin
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associated with DR ( 20 ). Obesity-induced inflammation and adipose tissue dysfunction might also play a role in the pathogenesis of DR ( 20 ). However, the specific mechanism remains unknown. The definitions of overweight and obesity vary among studies
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and worsened prognosis. Neutrophil-to-lymphocyte ratio (NLR), one of the indicators of inflammation and immunology, is easily measured via peripheral blood sampling and is reportedly useful as a prognosis index of various types of cancer ( 12 , 13
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vascular inflammation and increased proinflammatory cytokines ( 35 ). In diabetes, PKC is activated by advanced glycation end (AGE) products and polyol pathway flux ( 36 ). Also, chronic hyperglycemia stimulates synthesis of DAG and activates DAG
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Department of Laboratory Medicine, University of Groningen, University Medical Center, Groningen, the Netherlands
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Department of Internal Medicine, VUMC Free University, Amsterdam, the Netherlands
Wallenberg Laboratory, Sahlgrenska Hospital, University of Gothenburg, Gothenburg, Sweden
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Horaizon BV, Delft, the Netherlands
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overproduction is induced by chronic inflammation, one of the mechanisms promoting development of type 2 diabetes ( 23 ). We found a positive correlation between duodenal L cell density and kynurenine. Proliferation of L cells may be a physiological response to
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Institute of Pharmacology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
PhD Program in Toxicology, Kaohsiung Medical University, Kaohsiung, Taiwan
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Faculty of Medicine, National Yang Ming Chiao Tung University School of Medicine, Taipei, Taiwan
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effects through various mechanisms, including DNA and protein adduction, disruption of mitochondria and endoplasmic reticulum, cell membrane damage, oxidative stress, and inflammation and immune dysfunction ( 8 ). Due to an abundance of polyunsaturated
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Betty and Guy Beatty Center for Integrated Research, Inova Health System, Falls Church, Virginia, USA
Inova Medicine, Inova Health System, Falls Church, Virginia, USA
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(NASH), which is histologic evidence of hepatic steatosis, lobular inflammation, hepatocyte ballooning with or without pericellular fibrosis, and/or Mallory-Denk bodies. NASH is considered the potentially progressive form of NAFLD that can progress to
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Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Steno Diabetes Center Copenhagen, Gentofte, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Gentofte, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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) ( 26 ). The presented gluco-metabolic results represent a sub-study of an investigation of hepatic inflammation (unpublished). Therefore, the sample size was calculated to detect a minimal difference of 15% in the inflammation marker CD163
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associated with a higher mortality and were strongly correlated with markers of inflammation (including hs-CRP and IL6). There was an increase in hazard ratio for mortality with every 100 mg/dL increase in plasma glucose level. Patients admitted with plasma