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Sökning: WFRF:(Plomgaard Peter)

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1.
  • Dullaart, Robin P. F., et al. (författare)
  • Plasma apolipoprotein M is reduced in metabolic syndrome but does not predict intima media thickness
  • 2009
  • Ingår i: Clinica Chimica Acta. - : Elsevier BV. - 0009-8981. ; 406:1-2, s. 129-133
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Apolipoprotein (apo) M may exert anti-atherogenic properties in experimental studies. Its hepatic gene expression may be linked to glucose and lipid metabolism. Plasma apoM is decreased in obese mouse models. We hypothesized that plasma apoM is lower in metabolic syndrome (MetS) subjects, and determined whether intima media thickness (IMT) is associated with apoM. Methods: In 19 non-diabetic subjects with and 60 non-diabetic subjects without MetS (NCEP, ATP III criteria), the relationships of plasma apoM with obesity, glucose, insulin, lipids and adipokines, as well as with IMT were determined. Results: Plasma apoM was on average 15% lower in subjects with MetS compared to subjects without MetS (p=0.036). ApoM correlated inversely with body mass index and waist circumference (p<0.001), and positively with total cholesterol, LDL cholesterol and apoA-I (p<0.05). ApoM was not significantly correlated with glucose, insulin, leptin, adiponectin or resistin (p>0.20). Age- and sex adjusted IMT was lower in subjects with MetS (p<0.05), but was unrelated to apoM (p=0.68). In a multiple linear regression model that included the presence of both MetS and apoM, IMT was only related to MetS (p=0.05). Conclusions: Plasma apoM is reduced in MetS. In this study, apoM did not predict subclinical atherosclerosis. (C) 2009 Elsevier B.V. All rights reserved.
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2.
  • Elsoe, Sara, et al. (författare)
  • Apolipoprotein M binds oxidized phospholipids and increases the antioxidant effect of HDL
  • 2012
  • Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 221:1, s. 91-97
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Oxidation of LDL plays a key role in the development of atherosclerosis. HDL may, in part, protect against atherosclerosis by inhibiting LDL oxidation. Overexpression of HDL-associated apolipoprotein M (apoM) protects mice against atherosclerosis through a not yet clarified mechanism. Being a lipocalin, apoM contains a binding pocket for small lipophilic molecules. Here, we report that apoM likely serves as an antioxidant in HDL by binding oxidized phospholipids, thus enhancing the antioxidant potential of HDL. Methods and results: HDL was isolated from wild type mice, apoM-deficient mice, and two lines of apoM-Tg mice with similar to 2-fold and similar to 10-fold increased plasma apoM, respectively. Increasing amounts of HDL-associated apoM were associated with an increase in the resistance of HDL to oxidation with Cu2+ or 2,2'-azobis 2-methyl-propanimidamide, dihydrochloride (AAPH) and to an increased ability of HDL to protect human LDL against oxidation. Oxidized phospholipids, but not native phospholipids, quenched the intrinsic fluorescence of recombinant human apoM and the quenching could be competed with myristic acid suggesting selective binding of oxidized phospholipid in the lipocalin-binding pocket of apoM. Conclusions: The results suggest that apoM can bind oxidized phospholipids and that it increases the antioxidant effect of HDL. This new mechanism may explain at least part of the antiatherogenic potential of apoM. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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3.
  • Gejl, Kasper D., et al. (författare)
  • Changes in metabolism but not myocellular signaling by training with CHO-restriction in endurance athletes
  • 2018
  • Ingår i: Physiological Reports. - : Wiley. - 2051-817X. ; 6:17
  • Tidskriftsartikel (refereegranskat)abstract
    • Carbohydrate (CHO) restricted training has been shown to increase the acute training response, whereas less is known about the acute effects after repeated CHO restricted training. On two occasions, the acute responses to CHO restriction were examined in endurance athletes. Study 1 examined cellular signaling and metabolic responses after seven training-days including CHO manipulation (n = 16). The protocol consisted of 1 h high-intensity cycling, followed by 7 h recovery, and 2 h of moderate-intensity exercise (120SS). Athletes were randomly assigned to low (LCHO: 80 g) or high (HCHO: 415 g) CHO during recovery and the 120SS. Study 2 examined unaccustomed exposure to the same training protocol (n = 12). In Study 1, muscle biopsies were obtained at rest and 1 h after 120SS, and blood samples drawn during the 120SS. In Study 2, substrate oxidation and plasma glucagon were determined. In Study 1, plasma insulin and proinsulin C-peptide were higher during the 120SS in HCHO compared to LCHO (insulin: 0 min: +37%; 60 min: +135%; 120 min: +357%, P = 0.05; proinsulin C-peptide: 0 min: +32%; 60 min: +52%; 120 min: +79%, P = 0.02), whereas plasma cholesterol was higher in LCHO (+15-17%, P = 0.03). Myocellular signaling did not differ between groups. p-AMPK and p-ACC were increased after 120SS (+35%, P = 0.03; +59%, P = 0.0004, respectively), with no alterations in p-p38, p-53, or p-CREB. In Study 2, glucagon and fat oxidation were higher in LCHO compared to HCHO during the 120SS (+26-40%, P = 0.03; +44-76%, P = 0.01 respectively). In conclusion, the clear respiratory and hematological effects of CHO restricted training were not translated into superior myocellular signaling after accustomization to CHO restriction.
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4.
  • Gejl, Kasper D., et al. (författare)
  • Local depletion of glycogen with supra-maximal exercise in human skeletal muscle fibres
  • 2017
  • Ingår i: Journal of Physiology. - 0022-3751 .- 1469-7793. ; 595:9, s. 2809-2821
  • Tidskriftsartikel (refereegranskat)abstract
    • Skeletal muscle glycogen is heterogeneous distributed in three separated compartments (intramyofibrillar, intermyofibrillar and subsarcolemmal). Although only constituting 4-15% of the total glycogen volume, the availability of intramyofibrillar glycogen has been shown to be of particular importance to muscle function. The present study was designed to investigate the depletion of these three sub-cellular glycogen compartments during repeated supra-maximal exercise in elite athletes. Ten elite cross-country skiers (age: 25 +/- 4 yrs., VO2 max : 65 +/- 4 ml kg-1 min-1 , mean +/- SD) performed four approximately 4-minute supra-maximal sprint time trials (STT 1-4) with 45 min recovery. The sub-cellular glycogen volumes in m. triceps brachii were quantified from electron microscopy images before and after both STT 1 and STT 4. During STT 1, the depletion of intramyofibrillar glycogen was higher in type I fibres (-52% [-89:-15%]) than type 2 fibres (-15% [-52:22%]) (P = 0.02), while the depletion of intermyofibrillar glycogen (main effect: -19% [-33:0], P = 0.006) and subsarcolemmal glycogen (main effect: -35% [-66:0%], P = 0.03) was similar between fibre types. In contrast, only intermyofibrillar glycogen volume was significantly reduced during STT 4, in both fibre types (main effect: -31% [-50:-11%], P = 0.002). Furthermore, for each of the sub-cellular compartments, the depletion of glycogen during STT 1 was associated with the volumes of glycogen before STT 1. In conclusion, the depletion of spatially distinct glycogen compartments differs during supra-maximal exercise. Furthermore, the depletion changes with repeated exercise and is fibre type-dependent. 
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5.
  • Gejl, Kasper Degn, et al. (författare)
  • No Superior Adaptations to Carbohydrate Periodization in Elite Endurance Athletes
  • 2017
  • Ingår i: Medicine & Science in Sports & Exercise. - 0195-9131 .- 1530-0315. ; 49:12, s. 2486-2497
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose The present study investigated the effects of periodic carbohydrate (CHO) restriction on endurance performance and metabolic markers in elite endurance athletes. Methods Twenty-six male elite endurance athletes (maximal oxygen consumption (VO2max), 65.0 mL O(2)kg(-1)min(-1)) completed 4 wk of regular endurance training while being matched and randomized into two groups training with (low) or without (high) CHO manipulation 3 dwk(-1). The CHO manipulation days consisted of a 1-h high-intensity bike session in the morning, recovery for 7 h while consuming isocaloric diets containing either high CHO (414 2.4 g) or low CHO (79.5 1.0 g), and a 2-h moderate bike session in the afternoon with or without CHO. VO2max, maximal fat oxidation, and power output during a 30-min time trial (TT) were determined before and after the training period. The TT was undertaken after 90 min of intermittent exercise with CHO provision before the training period and both CHO and placebo after the training period. Muscle biopsies were analyzed for glycogen, citrate synthase (CS) and -hydroxyacyl-coenzyme A dehydrogenase (HAD) activity, carnitine palmitoyltransferase (CPT1b), and phosphorylated acetyl-CoA carboxylase (pACC). Results The training effects were similar in both groups for all parameters. On average, VO2max and power output during the 30-min TT increased by 5% +/- 1% (P < 0.05) and TT performance was similar after CHO and placebo during the preload phase. Training promoted overall increases in glycogen content (18% +/- 5%), CS activity (11% +/- 5%), and pACC (38% +/- 19%; P < 0.05) with no differences between groups. HAD activity and CPT1b protein content remained unchanged. Conclusions Superimposing periodic CHO restriction to 4 wk of regular endurance training had no superior effects on performance and muscle adaptations in elite endurance athletes.
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6.
  • Ooi, Esther M. M., et al. (författare)
  • Association of apolipoprotein M with high-density lipoprotein kinetics in overweight-obese men
  • 2010
  • Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 210:1, s. 326-330
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The aim of this study was to investigate associations between plasma apoM concentration and HDL apoA-I and apoA-II kinetics in 60 overweight-obese, insulin resistant men. Methods: Plasma apoM concentration was determined using a sandwich ELISA with two monoclonal antibodies (CV < 5%). The kinetics of HDL apoA-I and apoA-II were measured using intravenous administration of D-3-leucine, gas chromatography-mass spectrometry and multi-compartmental modeling. Results: Plasma apoM was inversely associated with body mass index and positively associated with plasma total cholesterol, LDL cholesterol and HDL cholesterol (p < 0.05). There were no associations between plasma apoM and plasma triglyceride, NEFA, insulin, glucose, HOMA score or adiponectin concentrations. Plasma apoM was positively associated with both apoA-I and apoA-II concentrations (r = 0.406, p < 0.01 and r = 0.510, p < 0.01, respectively) and negatively associated with HDL apoA-I and apoA-II fractional catabolic rate (FCR) (r = -0.291, p = 0.03 and r = -0.291, p = 0.026, respectively). No significant associations were observed between plasma apoM and HDL apoA-I and apoA-II production rate. In multivariate regression models, both plasma apoM and triglycerides were significant, independent predictors of HDL apoA-I FCR (adjusted R-2 = 16%, p < 0.01) and HDL apoA-II FCR (adjusted R-2 = 14%, p < 0.01). Conclusion: ApoM may be a significant, independent predictor of HDL apoA-I and apoA-II catabolism in overweight-obese, insulin resistant men. Crown Copyright (C) 2009 Published by Elsevier Ireland Ltd. All rights reserved.
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