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Journal of Lipid Research
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    • Buxton, Orfeu M1
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    • diet and dietary lipids2
    • diacylglycerol acyltransferase 11
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    • diseases1
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    • Patient-Oriented and Epidemiological Research
      Open Access

      Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety

      Journal of Lipid Research
      Vol. 60Issue 11p1935–1945Published online: September 4, 2019
      • Kelly M. Ness
      • Stephen M. Strayer
      • Nicole G. Nahmod
      • Margeaux M. Schade
      • Anne-Marie Chang
      • Gregory C. Shearer
      • and others
      Cited in Scopus: 9
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        Chronic sleep restriction, or inadequate sleep, is associated with increased risk of cardiometabolic disease. Laboratory studies demonstrate that sleep restriction causes impaired whole-body insulin sensitivity and glucose disposal. Evidence suggests that inadequate sleep also impairs adipose tissue insulin sensitivity and the NEFA rebound during intravenous glucose tolerance tests, yet no studies have examined the effects of sleep restriction on high-fat meal lipemia. We assessed the effect of 5 h time in bed (TIB) per night for four consecutive nights on postprandial lipemia following a standardized high-fat dinner (HFD).
        Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety
      • Patient-Oriented and Epidemiological Research
        Open Access

        DGAT2 partially compensates for lipid-induced ER stress in human DGAT1-deficient intestinal stem cells

        Journal of Lipid Research
        Vol. 60Issue 10p1787–1800Published online: July 17, 2019
        • Jorik M. van Rijn
        • Marliek van Hoesel
        • Cecilia de Heus
        • AnkeH.M. van Vugt
        • Judith Klumperman
        • EdwardE.S. Nieuwenhuis
        • and others
        Cited in Scopus: 9
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          Dietary lipids are taken up as FAs by the intestinal epithelium and converted by diacylglycerol acyltransferase (DGAT) enzymes into triglycerides, which are packaged in chylomicrons or stored in cytoplasmic lipid droplets (LDs). DGAT1-deficient patients suffer from vomiting, diarrhea, and protein losing enteropathy, illustrating the importance of this process to intestinal homeostasis. Previously, we have shown that DGAT1 deficiency causes decreased LD formation and resistance to unsaturated FA lipotoxicity in patient-derived intestinal organoids.
          DGAT2 partially compensates for lipid-induced ER stress in human DGAT1-deficient intestinal stem cells[S]
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