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Author
- Bunn, Janice Y1
- Buxton, Orfeu M1
- Chang, Anne-Marie1
- Crain, Karen I1
- de Heus, Cecilia1
- Ebenstein, David B1
- Fukagawa, Naomi K1
- Houwen, RoderickHJ1
- Kien, CLawrence1
- Klumperman, Judith1
- Koves, Timothy R1
- Matthews, Dwight E1
- Middendorp, Sabine1
- Muoio, Deborah M1
- Nahmod, Nicole G1
- Ness, Kelly M1
- Nieuwenhuis, EdwardES1
- Poynter, Matthew E1
- Schade, Margeaux M1
- Shearer, Gregory C1
- Stevens, Robert D1
- Strayer, Stephen M1
- Tarleton, Emily K1
- van Hoesel, Marliek1
- van Rijn, Jorik M1
Keyword
- inflammation2
- nutrition2
- triglycerides2
- cytokines1
- dehydrogenases1
- diacylglycerol acyltransferase 11
- diacylglycerol acyltransferase 21
- diseases1
- fatty acid/oxidation1
- glucose1
- hormones1
- incomplete β-oxidation of fatty acids1
- innate immunity1
- insulin resistance1
- intestine1
- lipid droplets1
- lipids/oxidation1
- lipolysis and fatty acid metabolism1
- lipotoxicity1
- macrophages/monocytes1
- mass spectrometry1
- oleic acid1
- palmitic acid1
JLR Patient-Oriented and Epidemiological Research
3 Results
- Patient-Oriented and Epidemiological ResearchOpen Access
Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety
Journal of Lipid ResearchVol. 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: 9Chronic 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). - Patient-Oriented and Epidemiological ResearchOpen Access
DGAT2 partially compensates for lipid-induced ER stress in human DGAT1-deficient intestinal stem cells
Journal of Lipid ResearchVol. 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: 9Dietary 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. - Patient-Oriented and Epidemiological ResearchOpen Access
Increased palmitate intake: higher acylcarnitine concentrations without impaired progression of β-oxidation
Journal of Lipid ResearchVol. 56Issue 9p1795–1807Published online: July 8, 2015- C.Lawrence Kien
- Dwight E. Matthews
- Matthew E. Poynter
- Janice Y. Bunn
- Naomi K. Fukagawa
- Karen I. Crain
- and others
Cited in Scopus: 5Palmitic acid (PA) is associated with higher blood concentrations of medium-chain acylcarnitines (MCACs), and we hypothesized that PA may inhibit progression of FA β-oxidation. Using a cross-over design, 17 adults were fed high PA (HPA) and low PA/high oleic acid (HOA) diets, each for 3 weeks. The [1-13C]PA and [13-13C]PA tracers were administered with food in random order with each diet, and we assessed PA oxidation (PA OX) and serum AC concentration to determine whether a higher PA intake promoted incomplete PA OX.