Patrick Schrauwen

Maastricht Universitair Medisch Centrum, Maestricht, Limburg, Netherlands

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Publications (237)1372.71 Total impact

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    ABSTRACT: Offspring of obese mothers have a greater risk of developing obesity, cardiovascular disease and metabolic syndrome later in life due to a phenomenon termed maternal imprinting.
    11/2015; 10(3):110-111. DOI:10.1007/s12467-012-0051-x
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    ABSTRACT: Obesity is associated with increased lipid supply to skeletal muscle. However, high intramyocellular lipid (IMCL) levels do not necessarily result in impaired insulin signaling. Lipid droplet coat proteins modulate IMCL metabolism.
    11/2015; 10(3):117-117. DOI:10.1007/s12467-012-0063-6
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    ABSTRACT: Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme of triglyceride hydrolysis and is mainly expressed in adipocytes and myocytes, thus ATGL-KO mice show abnormal triglyceride accumulation in those tissues. Intramyocellular lipids (IMCL) are often used as biomarker of insulin resistance and type 2 diabetes, potentially reflecting lipotoxic effects on mitochondrial function. Whether IMCL accumulation per se has adverse effects on mitochondria is unclear. Therefore, we assessed IMCL levels and mitochondrial oxidative capacity of ATGL-KO mice in vivo with 1HMRS and gated-dynamic-31PMRS of contracting calf-muscles.
    11/2015; 9(3):138-139. DOI:10.1007/s12467-011-0096-2
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    ABSTRACT: Intramuscular fat accumulation, skeletal muscle mitochondrial dysfunction and oxidative stress have all been implicated in the development of human insulin resistance and type 2 diabetes mellitus (T2DM).
    11/2015; 10(3):130-130. DOI:10.1007/s12467-012-0080-5
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    ABSTRACT: Proton Magnetic Resonance Spectroscopy (1H-MRS) is the gold standard to non-invasively measure intrahepatic lipid (IHL). Although 1H-MRS is an accurate method with a high intra-individual reproducibility, it is time-consuming. In-Phase/Opposed-Phase Magnetic Resonance Imaging (IP/OP MRI) is a fat-selective MRI method that can measure IHL within one breath hold and could be a more efficient alternative. Moreover, while MRS determines IHL in a voxel of typically 10-30 cm3, the whole liver volume can be quantified when using IP/OP MRI. Recently, it was shown in a large group of type 2 diabetic subjects that IP/OP MRI correlates with 1H-MRS. However, it is still unclear whether IP/OP MRI can be used as an alternative for 1H-MRS in small intervention studies.
    11/2015; 9(3):104-104. DOI:10.1007/s12467-011-0046-z
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    ABSTRACT: Physical exercise training is perhaps the single most effective intervention to both prevent and treat insulin resistance and type 2 diabetes. Accumulating evidence now suggests that the liver plays an important role in determining the overall health benefits of exercise training.
    11/2015; 10(3):108-109. DOI:10.1007/s12467-012-0048-5
  • 11/2015; 11(4):159-160. DOI:10.1007/s12467-013-0103-x
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    ABSTRACT: Fat storage at so-called “ectopic” sites (liver, skeletal muscle, heart) is associated with insulin resistance and comprised organ function. Regarding liver fat content, it was shown in mice that exposure to a high fat (HF) diet during early development increased the susceptibility to high-fat diet induced hepatic steatosis and decreased markers of hepatic mitochondrial function (Bruce et al, Hepatology, 2009).
    11/2015; 10(3):115-116. DOI:10.1007/s12467-012-0060-9
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    ABSTRACT: Increased skeletal muscle lipid (IMCL) storage is associated with both insulin resistant and sensitive conditions as seen in muscle biopsies taken from either type II diabetes patients (T2D) or endurance trained athletes respectively. The mechanism behind this so called ‘athlete’s paradox’ is still unknown. In the present study, we propose that the C5L2 receptor might be a regulating factor in IMCL accumulation. C5L2 has been shown to stimulate fatty acid uptake and storage in adipose tissue. Interestingly, this receptor is expressed in muscle, yet its function and relative expression has not been investigated. In the present study, we investigated the role of C5L2 in both human and animal models of insulin resistance.
    11/2015; 9(3):138-138. DOI:10.1007/s12467-011-0095-3
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    ABSTRACT: Exercise is known to be a powerful way to prevent and treat type 2 diabetes mellitus. Skeletal muscle is the predominant organ impacted by exercise but many of the metabolic changes induced by exercise seem to be a result of changes in the liver. An important question is how exercise- or better skeletal muscle contraction - can alter hepatic function and insulin action. It is hypothesized that myokines play an important role in the cross-talk between skeletal muscle and liver.
    11/2015; 9(3):117-117. DOI:10.1007/s12467-011-0063-y
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    ABSTRACT: Disturbances in fatty acid metabolism may result in lipid accumulation in skeletal muscle (IMCL) and is associated with skeletal muscle insulin resistance (IR) and type 2 diabetes (T2D). Paradoxically, IMCL is increased in highly insulin sensitive endurance-trained athletes (ETAs), suggesting IMCL are not causative in IR. ETAs have a high capacity to oxidize IMCL, suggesting high IMCL turnover protects against IR. We investigated whether markers of IMCL turnover are elevated in ETAs.
    11/2015; 9(3):118-119. DOI:10.1007/s12467-011-0065-9
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    ABSTRACT: A high hepatic lipid content (IntraHepatic Lipid, IHL) markedly increases the risk of metabolic complications, including insulin resistance and cardiovascular events. Exercise training has been shown to lower IHL, however it is unknown if acute exercise has the same effect. Performing exercise while fasted induces elevation of plasma fatty acid (FA) concentrations, which lead to increased lipid accumulation in the heart and in non-active skeletal muscle.
    11/2015; 9(3):116-117. DOI:10.1007/s12467-011-0062-z
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    ABSTRACT: The obesity pandemic has spurred a need for novel therapies to prevent and treat metabolic complications. The recent rediscovery of brown adipose tissue (BAT) in humans made this tissue a possible therapeutic target, due to its potentially substantial contributions to energy homeostasis. Fibroblast growth factor 21 (FGF21) has been identified as a facilitator of cold-induced thermogenesis in humans. Furthermore, pre-clinical studies revealed that FGF21 administration leads to improvement in the metabolic consequences of obesity, such as dyslipidemia and type 2 diabetes. Here we studied plasma FGF21 levels in two cohorts of human subjects, in whom BAT activity was determined using an individualized cooling protocol by [ 18 F]FDG-PET/CT scan. Importantly, we found that circulating FGF21 levels correlated with BAT activity during acute cold exposure in male subjects. In addition, FGF21 levels were related to the change in core temperature upon acute cold exposure, indicating a role for FGF21 in maintaining normothermia, possibly via activation of BAT. Furthermore, cold acclimation increased BAT activity in parallel with increased FGF21 levels. In conclusion, our results demonstrate that FGF21 levels in humans are related to BAT activity, suggesting that FGF21 may represent a novel mechanism via which BAT activity in humans may be enhanced. The obesity pandemic is associated with major metabolic disturbances, including type 2 diabetes, non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease. Lifestyle interventions aimed at increasing physical activity and decreasing food intake can be effective in treating these disorders. However, due to poor adherence such interventions are not easily translated to the general population. As such, there is an ongoing need for novel therapies that may alleviate obesity-induced metabolic complications, especially as currently available therapies offer only modest efficacy. Fibroblast growth factor-21 (FGF21) was originally discovered in 2000 as a new member of the FGF superfamily
    Scientific Reports 05/2015; 5(10275). DOI:10.1038/srep10275 · 5.58 Impact Factor
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    ABSTRACT: The recent recognition that humans possess active depots of brown adipose tissue has boosted the interest in this tissue as a potential target for the prevention and treatment of obesity and related metabolic disorders. Furthermore, it was also revealed that brown adipose tissue (BAT) in humans may consist of so-called beige or brite adipocytes. So far, cold exposure is recognised as the strongest activator of BAT in humans, but there is much ongoing research focused on finding alternative activators of BAT. The consequences of long-term BAT activation and/or cold exposure on metabolic health are still unknown, and this represents an area of intensive research. This is one of a series of commentaries under the banner '50 years forward', giving personal opinions on future perspectives in diabetes, to celebrate the 50th anniversary of Diabetologia (1965-2015).
    Diabetologia 05/2015; DOI:10.1007/s00125-015-3611-y · 6.88 Impact Factor
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    ABSTRACT: Elevated hepatic lipid content (IntraHepatic Lipid, IHL) increases the risk of metabolic complications. Although prolonged exercise training lowers IHL, it is unknown if acute exercise has the same effect. Furthermore, hepatic ATP content may be related to insulin resistance and IHL. We aimed to investigate if acute exercise leads to changes in IHL and whether this is accompanied by changes in hepatic ATP. Twenty-one men (age 54.8 ± 7.2 years, BMI 29.7 ± 2.2 kg/m(2)) performed a 2 h cycling protocol, once while staying fasted and once while ingesting glucose. IHL was determined at baseline, 30 min post-exercise and 4 h post-exercise. Additionally ATP/Total P ratio was measured at baseline and 4 h post-exercise. Compared with baseline values we did not observe any statistically significant changes in IHL within 30 min post-exercise in neither the fasted nor the glucose-supplemented condition. However, IHL was elevated 4 h post-exercise compared with baseline in the fasted condition (from 8.3 ± 1.8 to 8.7 ± 1.8%, p = 0.010), an effect that was blunted by glucose supplementation (from 8.3 ± 1.9 to 8.3 ± 1.9%, p = 0.789). Acute exercise does not decrease liver fat in overweight middle-aged men. Moreover, IHL increased 4 h post-exercise in the fasted condition, an increase that was absent in the glucose-supplemented condition. These data suggest that a single bout of exercise may not be able to lower IHL.
    Scientific Reports 04/2015; 5:9709. DOI:10.1038/srep09709 · 5.58 Impact Factor
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    ABSTRACT: An early hallmark in the development of type 2 diabetes is the resistance to the effect of insulin in skeletal muscle and in the heart. Since mitochondrial function was found to be diminished in patients with type 2 diabetes, it was suggested that this defect might be involved in the etiology of insulin resistance. Although several hypotheses were suggested, yet unclear is the mechanistic link between these two phenomena. Recent advances: Herein, we review the evidence for disturbances in mitochondrial function in skeletal muscle and the heart in the diabetic state. Also the mechanisms involved in improving mitochondrial function are considered and, whenever possible, human data is cited. Reported evidence shows that interventions that improve skeletal muscle mitochondrial function also improve insulin sensitivity in humans. In the heart, available data from animal studies suggests that enhancement of mitochondrial function can reverse aging-induced changes in heart function, and can be protective against cardiomyopathy and heart failure. Mitochondria and their functions can be targeted with the aim of improving skeletal muscle insulin sensitivity and cardiac function. However, human clinical intervention studies are needed to fully substantiate the potential of mitochondria as a target to prevent cardiometabolic disease.
    Antioxidants & Redox Signaling 03/2015; DOI:10.1089/ars.2015.6291 · 7.67 Impact Factor
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    ABSTRACT: Accumulation of fat in muscle tissue as intramyocellular lipids (IMCLs) is closely related to the development of insulin resistance and subsequent type 2 diabetes. Most IMCLs organize into lipid droplets (LDs), the fates of which are regulated by lipid droplet coat proteins. Perilipin 5 (PLIN5) is an LD coating protein, which is strongly linked to lipid storage in muscle tissue. Here we employ a tandem in vitro / ex vivo approach and use chemical imaging by label-free, hyperspectral coherent Raman microscopy to quantify compositional changes in individual LDs upon PLIN5 overexpression. Our results directly show that PLIN5 overexpression in muscle, alters individual LD composition and physiology, resulting in larger LDs with higher esterified acyl chain concentration, increased methylene content, and more saturated lipid species. These results suggest that lipotoxic protection afforded by natural PLIN5 upregulation in muscle involves molecular changes in lipid composition within LDs.
    Integrative Biology 03/2015; 7(4). DOI:10.1039/C4IB00271G · 4.00 Impact Factor
  • Jason R B Dyck, Patrick Schrauwen
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 02/2015; 1852(6). DOI:10.1016/j.bbadis.2015.02.002 · 5.09 Impact Factor
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    ABSTRACT: Fat accumulation in nonadipose tissue is linked to insulin resistance and metabolic diseases. Earlier studies have shown that hepatic lipid accumulation can occur after 4 d of a high-fat diet in humans, and this fat accumulation can be blunted by the ingestion of additional proteins. In this study, we explored whether a single high-fat meal increased the lipid content in liver and skeletal muscle as measured by using in vivo proton magnetic resonance spectroscopy ((1)H-MRS) and whether the addition of protein can modulate the postprandial ectopic lipid storage. Intrahepatic lipid (IHL) and intramyocellular lipid (IMCL) concentrations were determined by using (1)H-MRS before and 3 and 5 h after a high-fat with added protein meal (61.5% of energy from fat) or a high-fat without added protein meal (mean ± SEM: 51.1 ± 7.9 g of protein; 191.9 ± 9.9 kcal added) in a randomized crossover study. IHL and IMCL concentrations were converted to absolute concentrations (g/kg wet weight) by using water as an internal reference. Nine lean, healthy subjects [6 men and 3 women; mean (±SD) age: 22.7 ± 3.0 y; mean body mass index (in kg/m(2)): 21.8 ± 1.8] were included in this study. IHL concentrations increased ∼20% (P < 0.01) at 3 h after the meal and did not further increase after 5 h. In contrast, IMCL concentrations were not altered during the postprandial period (P = 0.74). The addition of protein to a single high-fat meal did not change the postprandial accumulation of fat in the liver (P = 0.93) or skeletal muscle (P = 0.84). In this study, we showed that a single energy-dense, high-fat meal induced net lipid accumulation in the liver, which was detected by using in vivo (1)H-MRS. This noninvasive approach might bring new opportunities to study postprandial hepatic lipid dynamics. The addition of protein did not change the ectopic lipid retention after a single high-fat meal. This trial was registered at as NCT01709643. © 2015 American Society for Nutrition.
    American Journal of Clinical Nutrition 01/2015; 101(1):65-71. DOI:10.3945/ajcn.114.094730 · 6.92 Impact Factor
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    ABSTRACT: Aims/hypothesis Human brown adipose tissue (BAT) has recently emerged as a potential target in the treatment of type 2 diabetes, owing to its capacity to actively clear glucose from the circulation—at least upon cold exposure. The effects of insulin resistance on the capacity of human BAT to take up glucose are unknown. Prolonged fasting is known to induce insulin resistance in peripheral tissues in order to spare glucose for the brain. Methods We studied the effect of fasting-induced insulin resistance on the capacity of BAT to take up glucose during cold exposure as well as on cold-stimulated thermogenesis. BAT glucose uptake was assessed by means of cold-stimulated dynamic 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography/computed tomography ([18F]FDG-PET/CT) imaging. Results We show that a 54 h fasting period markedly decreases both cold-induced BAT glucose uptake and nonshivering thermogenesis (NST) during cold stimulation. In vivo molecular imaging and modelling revealed that the reduction of glucose uptake in BAT was due to impaired cellular glucose uptake and not due to decreased supply. Interestingly, decreased BAT glucose uptake upon fasting was related to a decrease in core temperature during cold exposure, pointing towards a role for BAT in maintaining normothermia in humans. Conclusions/interpretation Cold-stimulated glucose uptake in BAT is strongly reduced upon prolonged fasting. When cold-stimulated glucose uptake in BAT is also reduced under other insulin-resistant states, such as diabetes, cold-induced activation of BAT may not be a valid way to improve glucose clearance by BAT under such conditions. Trial registration: NTR3523 Funding: This work was supported by the EU FP7 project DIABAT (HEALTH-F2-2011-278373 to WDvML) and by the Netherlands Organization for Scientific Research (TOP 91209037 to WDvML).
    Diabetologia 12/2014; 58(3). DOI:10.1007/s00125-014-3465-8 · 6.88 Impact Factor

Publication Stats

8k Citations
1,372.71 Total Impact Points


  • 2009–2015
    • Maastricht Universitair Medisch Centrum
      • Central Diagnostic Laboratory
      Maestricht, Limburg, Netherlands
  • 1997–2015
    • Maastricht University
      • • Humane Biologie
      • • Bewegingswetenschappen
      Maestricht, Limburg, Netherlands
  • 2011
    • Leiden University Medical Centre
      • Department of Human Genetics
      Leiden, South Holland, Netherlands
  • 2006
    • Technische Universiteit Eindhoven
      Eindhoven, North Brabant, Netherlands
  • 1999
    • National Institutes of Health
      • National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
      Maryland, United States