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Author
- Bunn, Janice Y1
- Buxton, Orfeu M1
- Cederholm, Tommy1
- Chang, Anne-Marie1
- Crain, Karen I1
- Ebenstein, David B1
- Eriksdotter, Maria1
- Freund-Levi, Yvonne1
- Fukagawa, Naomi K1
- Hjorth, Erik1
- Kien, CLawrence1
- Koves, Timothy R1
- Matthews, Dwight E1
- Muoio, Deborah M1
- Nahmod, Nicole G1
- Ness, Kelly M1
- Palmblad, Jan1
- Poynter, Matthew E1
- Schade, Margeaux M1
- Schultzberg, Marianne1
- Shearer, Gregory C1
- Stevens, Robert D1
- Strayer, Stephen M1
- Tarleton, Emily K1
- Vedin, Inger1
Keyword
- inflammation3
- diet and dietary lipids2
- Alzheimer's disease1
- amyloid β1
- clinical trials1
- cytokines1
- dehydrogenases1
- docosahexaenoic acid1
- fatty acid/oxidation1
- fish oil1
- glucose1
- hormones1
- incomplete β-oxidation of fatty acids1
- innate immunity1
- insulin resistance1
- lipids/oxidation1
- lipolysis and fatty acid metabolism1
- lipoxin1
- macrophages/monocytes1
- mass spectrometry1
- oleic acid1
- palmitic acid1
- peripheral blood mononuclear cell1
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
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. - Patient-Oriented and Epidemiological ResearchOpen Access
Effects of n-3 FA supplementation on the release of proresolving lipid mediators by blood mononuclear cells: the OmegAD study
Journal of Lipid ResearchVol. 56Issue 3p674–681Published online: January 23, 2015- Xiuzhe Wang
- Erik Hjorth
- Inger Vedin
- Maria Eriksdotter
- Yvonne Freund-Levi
- Lars-Olof Wahlund
- and others
Cited in Scopus: 59Specialized proresolving mediators (SPMs) induce resolution of inflammation. SPMs are derivatives of n-3 and n-6 PUFAs and may mediate their beneficial effects. It is unknown whether supplementation with PUFAs influences the production of SPMs. Alzheimer's disease (AD) is associated with brain inflammation and reduced levels of SPMs. The OmegAD study is a randomized, double-blind, and placebo-controlled clinical trial on AD patients, in which placebo or a supplement of 1.7 g DHA and 0.6 g EPA was taken daily for 6 months.