TY - GEN
A1 - Engel, Tilman
A1 - Schraplau, Anne
A1 - Wochatz, Monique
A1 - Kopinski, Stephan
A1 - Sonnenburg, Dominik
A1 - Schomöller, Anne
A1 - Risch, Lucie
A1 - Kaplick, Hannes
A1 - Mayer, Frank
T1 - Feasability of An Eccentric Isokinetic Protocol to Induce Trunk Muscle Damage: A Pilot Study
T2 - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe
N2 - Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn’s post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.
T3 - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe - 773
KW - exercise
KW - eccentric
KW - muscle fatigue
KW - trunk muscles
KW - isokinetics
KW - repeated bout effect
KW - inflammation
KW - exercise induced muscle damage
KW - interleukin-6
KW - internleukin-10
KW - tumor necrosis factor-α
Y1 - 2022
U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-557409
SN - 1866-8364
SP - E9
EP - E17
PB - Universitätsverlag Potsdam
CY - Potsdam
ER -
TY - JOUR
A1 - Engel, Tilman
A1 - Schraplau, Anne
A1 - Wochatz, Monique
A1 - Kopinski, Stephan
A1 - Sonnenburg, Dominik
A1 - Schomöller, Anne
A1 - Risch, Lucie
A1 - Kaplick, Hannes
A1 - Mayer, Frank
T1 - Feasability of An Eccentric Isokinetic Protocol to Induce Trunk Muscle Damage: A Pilot Study
JF - Sports Medicine International Open
N2 - Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn’s post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.
KW - exercise
KW - eccentric
KW - muscle fatigue
KW - trunk muscles
KW - isokinetics
KW - repeated bout effect
KW - inflammation
KW - exercise induced muscle damage
KW - interleukin-6
KW - internleukin-10
KW - tumor necrosis factor-α
Y1 - 2021
U6 - https://doi.org/10.1055/a-1757-6724
SN - 2367-1890
VL - 6
SP - E9
EP - E17
PB - Thieme
CY - Stuttgart
ET - 1
ER -
TY - JOUR
A1 - Henkel, Janin
A1 - Coleman, Charles Dominic
A1 - Schraplau, Anne
A1 - Joehrens, Korinna
A1 - Weiss, Thomas Siegfried
A1 - Jonas, Wenke
A1 - Schürmann, Annette
A1 - Püschel, Gerhard Paul
T1 - Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model
JF - Scientific reports
N2 - In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.
Y1 - 2018
U6 - https://doi.org/10.1038/s41598-018-34633-y
SN - 2045-2322
VL - 8
PB - Nature Publ. Group
CY - London
ER -
TY - JOUR
A1 - Henkel, Janin
A1 - Coleman, Charles Dominic
A1 - Schraplau, Anne
A1 - Jöhrens, Korinna
A1 - Weber, Daniela
A1 - Castro, Jose Pedro
A1 - Hugo, Martin
A1 - Schulz, Tim Julius
A1 - Krämer, Stephanie
A1 - Schürmann, Annette
A1 - Püschel, Gerhard Paul
T1 - Induction of Steatohepatitis (NASH) with Insulin Resistance in Wild-type B6 Mice by a Western-type Diet Containing Soybean Oil and Cholesterol
JF - Molecular medicine
N2 - Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are hepatic manifestations of the metabolic syndrome. Many currently used animal models of NAFLD/NASH lack clinical features of either NASH or metabolic syndrome such as hepatic inflammation and fibrosis (e.g., high-fat diets) or overweight and insulin resistance (e.g., methionine-choline-deficient diets), or they are based on monogenetic defects (e.g., ob/ob mice). In the current study, a Western-type diet containing soybean oil with high n-6-PUFA and 0.75% cholesterol (SOD + Cho) induced steatosis, inflammation and fibrosis accompanied by hepatic lipid peroxidation and oxidative stress in livers of C57BL/6-mice, which in addition showed increased weight gain and insulin resistance, thus displaying a phenotype closely resembling all clinical features of NASH in patients with metabolic syndrome. In striking contrast, a soybean oil-containing Western-type diet without cholesterol (SOD) induced only mild steatosis but not hepatic inflammation, fibrosis, weight gain or insulin resistance. Another high-fat diet, mainly consisting of lard and supplemented with fructose in drinking water (LAD + Fru), resulted in more prominent weight gain, insulin resistance and hepatic steatosis than SOD + Cho, but livers were devoid of inflammation and fibrosis. Although both LAD + Fru-and SOD + Cho-fed animals had high plasma cholesterol, liver cholesterol was elevated only in SOD + Cho animals. Cholesterol induced expression of chemotactic and inflammatory cytokines in cultured Kupffer cells and rendered hepatocytes more susceptible to apoptosis. In summary, dietary cholesterol in the SOD + Cho diet may trigger hepatic inflammation and fibrosis. SOD + Cho-fed animals may be a useful disease model displaying many clinical features of patients with the metabolic syndrome and NASH.
KW - Nonalcoholic Steatohepatitis (NASH)
KW - Typical Western Diet
KW - Nonalcoholic Fatty Liver Disease (NAFLD)
KW - Dietary Cholesterol
KW - Kupffer Cells
Y1 - 2017
U6 - https://doi.org/10.2119/molmed.2016.00203
SN - 1076-1551
SN - 1528-3658
VL - 23
SP - 70
EP - 82
PB - Feinstein Inst. for Medical Research
CY - Manhasset
ER -
TY - GEN
A1 - Henkel, Janin
A1 - Coleman Mac Gregor of Inneregny, Charles Dominic
A1 - Schraplau, Anne
A1 - Jöhrens, Korinna
A1 - Weiss, Thomas Siegfried
A1 - Jonas, Wenke
A1 - Schürmann, Annette
A1 - Püschel, Gerhard Paul
T1 - Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model
T2 - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe
N2 - In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.
T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 483
KW - suppress VLDL secretion
KW - mice lacking
KW - nonalcoholic steatohepatthis
KW - insulin-resistance
KW - rat hepatocytes
KW - kupffer cells
KW - E-2
KW - disease
KW - expression
KW - accumulation
Y1 - 2018
U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-420879
SN - 1866-8372
IS - 483
ER -
TY - JOUR
A1 - Henkel, Janin
A1 - Coleman Mac Gregor of Inneregny, Charles Dominic
A1 - Schraplau, Anne
A1 - Jöhrens, Korinna
A1 - Weiss, Thomas Siegfried
A1 - Jonas, Wenke
A1 - Schürmann, Annette
A1 - Püschel, Gerhard Paul
T1 - Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model
JF - Scientific Reports
N2 - In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.
KW - suppress VLDL secretion
KW - mice lacking
KW - nonalcoholic steatohepatthis
KW - insulin-resistance
KW - rat hepatocytes
KW - kupffer cells
KW - E-2
KW - disease
KW - expression
KW - accumulation
Y1 - 2018
U6 - https://doi.org/10.1038/s41598-018-34633-y
SN - 2045-2322
IS - 8
SP - 1
EP - 11
PB - Nature Research
CY - London
ER -
TY - JOUR
A1 - Neuschaefer-Rube, Frank
A1 - Schraplau, Anne
A1 - Schewe, Bettina
A1 - Lieske, Stefanie
A1 - Kruetzfeldt, Julia-Mignon
A1 - Ringel, Sebastian
A1 - Henkela, Janin
A1 - Birkenfeld, Andreas L.
A1 - Püschel, Gerhard Paul
T1 - Arylhydrocarbon receptor-dependent mIndy (SIc13a5) induction as possible contributor to benzo[a]pyrene-induced lipid accumulation in hepatocytes
JF - Toxicology
N2 - Non-alcoholic fatty liver disease is a growing problem in industrialized and developing countries. Hepatic lipid accumulation is the result of an imbalance between fatty acid uptake, fatty acid de novo synthesis, beta-oxidation and secretion of triglyceride-rich lipoproteins from the hepatocyte. A central regulator of hepatic lipid metabolism is cytosolic citrate that can either be derived from the mitochondrium or be taken up from the blood via the plasma membrane sodium citrate transporter NaCT, the product of the mammalian INDY gene (SLC13A5). mINDY ablation protects against diet-induced steatosis whereas mINDY expression is increased in patients with hepatic steatosis. Diet-induced hepatic steatosis is also enhanced by activation of the arylhyrocarbon receptor (AhR) both in humans and animal models. Therefore, the hypothesis was tested whether the mINDY gene might be a target of the AhR. In accordance with such a hypothesis, the AhR activator benzo[a]pyrene induced the mINDY expression in primary cultures of rat hepatocytes in an AhR-dependent manner. This induction resulted in an increased citrate uptake and citrate incorporation into lipids which probably was further enhanced by the benzo[a]pyrene-dependent induction of key enzymes of fatty acid synthesis. A potential AhR binding site was identified in the mINDY promoter that appears to be conserved in the human promoter. Elimination or mutation of this site largely abolished the activation of the mINDY promoter by benzo[a]pyrene. This study thus identified the mINDY as an AhR target gene. AhR-dependent induction of the mINDY gene might contribute to the development of hepatic steatosis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
KW - SLC13A5
KW - Non-alcoholic fatty liver disease
KW - NAFLD
Y1 - 2015
U6 - https://doi.org/10.1016/j.tox.2015.08.007
SN - 0300-483X
VL - 337
SP - 1
EP - 9
PB - Elsevier
CY - Clare
ER -
TY - GEN
A1 - Schomöller, Anne
A1 - Risch, Lucie
A1 - Kaplick, Hannes
A1 - Schraplau, Anne
A1 - Wochatz, Monique
A1 - Engel, Tilman
A1 - Sonnenburg, Dominik
A1 - Mayer, Frank
T1 - Changes in paraspinal muscle T2 times and creatine kinase after a bout of eccentric exercise
T2 - Medicine and science in sports and exercise : official journal of the American College of Sports Medicine
N2 - Eccentric (ECC) exercises might cause muscle damage, characterized by delayed-onset muscle soreness, elevated creatine kinase (CK) levels and local muscle oedema, shown by elevated T2 times in magnet resonance imaging (MRI) scans. Previous research suggests a high inter-individual difference regarding these systemic and local responses to eccentric workload. PURPOSE: To analyze ECC exercise-induced muscle damage in lumbar paraspinal muscles assessed via MRI. METHODS: Ten participants (3f/7m; 33±6y; 174±8cm; 71±12kg) were included in the study. Quantitative paraspinal muscle constitution of M. erector spinae and M. multifidius were assessed in supine position before and 72h after an intense eccentric trunk exercise bout in a mobile 1.5 tesla MRI device. MRI scans were recorded on spinal level L3 (T2-weighted TSE echo sequences, 11 slices, 2mm slice thickness, 3mm gap, echo times: 20, 40, 60, 80, 100ms, TR time: 2500ms). Muscle T2 times were calculated for manually traced regions of interest of the respective muscles with an imaging software. The exercise protocol was performed in an isokinetic device and consisted of 120sec alternating ECC trunk flexion-extension with maximal effort. Venous blood samples were taken before and 72h after the ECC exercise. Descriptive statistics (mean±SD) and t-testing for pre-post ECC exercises were performed. RESULTS: T2 times increased from pre- to post-ECC MRI measurements from 55±3ms to 79±28ms in M. erector spinae and from 62±5ms to 78±24ms in M. multifidius (p<0.001). CK increased from 126±97 U/L to 1447±20579 U/L. High SDs of T2 time and CK in post-ECC measures could be due to inter-individual reactions to ECC exercises. 3 participants showed high local and systemic reactions (HR) with T2 time increases of 120±24% (M. erector spinae) and 73±50% (M. multifidius). In comparison, the remaining 7 participants showed increases of 11±12% (M. erector spinae) and 7±9% (M. multifidius) in T2 time. Mean CK increased 9.5-fold in the 3 HR subjects compared with the remaining 7 subjects. CONCLUSIONS: The 120sec maximal ECC trunk flexion-extension protocol induced high amounts of muscle damage in 3 participants. Moderate to low responses were found in the remaining 7 subjects, assuming that inter-individual predictors play a role regarding physiological responses to ECC workload.
Y1 - 2020
U6 - https://doi.org/10.1249/01.mss.0000685648.68626.f1
SN - 0195-9131
SN - 1530-0315
SN - 0025-7990
VL - 52
IS - 17
SP - 929
EP - 929
PB - Lippincott Williams & Wilkins
CY - Philadelphia
ER -
TY - JOUR
A1 - Schomöller, Anne
A1 - Risch, Lucie
A1 - Kaplick, Hannes
A1 - Wochatz, Monique
A1 - Engel, Tilman
A1 - Schraplau, Anne
A1 - Sonnenburg, Dominik
A1 - Huppertz, Alexander
A1 - Mayer, Frank
T1 - Inter-rater and inter-session reliability of lumbar paraspinal muscle composition in a mobile MRI device
JF - BJR : an international journal of radiology, radiation oncology and all related sciences / British Institute of Radiology
N2 - Objective: To assess the reliability of measurements of paraspinal muscle transverse relaxation times (T2 times) between two observers and within one observer on different time points.
Methods: 14 participants (9f/5m, 33 +/- 5 years, 176 +/- 10 cm, 73 +/- 12 kg) underwent 2 consecutive MRI scans (M1,M2) on the same day, followed by 1 MRI scan 13-14 days later (M3) in a mobile 1.5 Tesla MRI. T2 times were calculated in T-2 weighted turbo spin- echo-sequences at the spinal level of the third lumbar vertebrae (11 slices, 2 mm slice thickness, 1 mm interslice gap, echo times: 20, 40, 60, 80, 100 ms) for M. erector spinae (ES) and M. multifidius (MF). The following reliability parameter were calculated for the agreement of T2 times between two different investigators (OBS1 & OBS2) on the same MRI (inter rater reliability, IR) and by one investigator between different MRI of the same participant (intersession variability, IS): Test-Retest Variability (TRV, Differences/Mean*100); Coefficient of Variation (CV, Standard deviation/Mean*100); Bland-Altman Analysis (systematic bias = Mean of the Differences; Upper/Lower Limits of Agreement = Bias+/-1.96*SD); Intraclass Correlation Coefficient 3.1 (ICC) with absolute agreement, as well as its 95% confidence interval.
Results: Mean TRV for IR was 2.6% for ES and 4.2% for MF. Mean TRV for IS was 3.5% (ES) and 5.1% (MF). Mean CV for IR was 1.9 (ES) and 3.0 (MF). Mean CV for IS was 2.5% (ES) and 3.6% (MF). A systematic bias of 1.3 ms (ES) and 2.1 ms (MF) were detected for IR and a systematic bias of 0.4 ms (ES) and 0.07 ms (MF) for IS. ICC for IR was 0.94 (ES) and 0.87 (MF). ICC for IS was 0.88 (ES) and 0.82 (MF).
Conclusion: Reliable assessment of paraspinal muscle T2 time justifies its use for scientific purposes. The applied technique could be recommended to use for future studies that aim to assess changes of T2 times, e.g. after an intense bout of eccentric exercises.
Y1 - 2021
U6 - https://doi.org/10.1259/bjr.20210141
SN - 0007-1285
SN - 1748-880X
VL - 94
IS - 1127
PB - Wiley
CY - Bognor Regis
ER -
TY - THES
A1 - Schraplau, Anne
T1 - Regulation der Expression von Xenobiotika-metabolisierenden Enzymen und Deiodasen durch die Xenobiotika-abhängige wechselseitige Induktion von Xenosensor-Transkriptionsfaktoren und Prostaglandin E2
BT - Auswirkung auf die Aktivierung und Inaktivierung von Schilddrüsenhormonen
Y1 - 2017
ER -