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| 1 | Effects of resveratrol in experimental and clinical non-alcoholic fatty liver disease显示文摘The prevalence of obesity and related conditions like non-alcoholic fatty liver disease(NAFLD) is increasing worldwide and therapeutic options are limited.Alternative treatment options are therefore intensively sought after.An interesting candidate is the natural polyphenol resveratrol(RSV) that activates adenosinmonophosphate-activated protein kinase(AMPK) and silent information regulation-2 homolog 1(SIRT1).In addition,RSV has known anti-oxidant and anti-inflammatory effects.Here,we review the current evidence for RSVmediated effects on NAFLD and address the different aspects of NAFLD and non-alcoholic steatohepatitis(NASH) pathogenesis with respect to free fatty acid(FFA) flux from adipose tissue,hepatic de novo lipogenesis,inadequate FFA β-oxidation and additional intra- and extrahepatic inflammatory and oxidant hits.We review the in vivo evidence from animal studies and clinical trials.The abundance of animal studies reports a decrease in hepatic triglyceride accumulation,liver weight and a general improvement in histological fatty liver changes,along with a reduction in circulating insulin,glucose and lipid levels.Some studies document AMPK or SIRT1 activation,and modulation of relevant markers of hepatic lipogenesis,inflammation and oxidation status.However,AMPK/SIRT1-independent actions are also likely.Clinical trials are scarce and have primarily been performed with a focus on overweight/obese participants without a focus on NAFLD/NASH and histological liver changes.Future clinical studies with appropriate design are needed to clarify the true impact of RSV treatment in NAFLD/NASH patients. | Sara Heebll Karen Louise Thomsen Steen B Pedersen Hendrik Vilstrup Jacob George Henning Grnbk | 2014 | World Journal of Hepatology2014，6，4： | 11 |
| 2 | Vasopres- sin induces phosphorylation of the thiazide-sensitive sodium chlo- ride cotransporter in the distal convoluted tubule显示文摘 | Pedersen NB Hofmeister MV Rosenbaek LL | 2010 | Kidney Int2010，78，2： | 1 |
| 3 | Porcine glucagon-like peptide-2:structure,signaling,metabolism and effects显示文摘 | Pedersen NB Hjollund KR Johnsen AH | | 0，，1： | 1 |
| 4 | Porcine Glucagon-like peptide-2:Structure,signaling,metabolism and ef-fects显示文摘 | Pedersen NB Hjollund KR Johnsen AH | 2008 | Regul Pept2008，146，13： | 1 |
| 5 | Comparison of atorvas- tatin 80 mg/day versus simvastatin 20 to 40 mg/day on frequency of cardiovascular events late (five years) after acute myocardial in- farction (from the Incremental Decrease in End Points through Ag- gressive Lipid Lowering trial 显示文摘 | Pedersen TR Cater NB Faergeman O | 2010 | Am J Cardiol2010，106，3： | 1 |
| 6 | Comparison of atorvastatin 80 mg/day versus simvastatin 20 Lo 40 mg/day on frequency of cardiovascular events late (five years) after acute myocardial infarction (from the Incremental Decrease in End Points through Aggressive Lipid Lowering trial) 显示文摘 | Pedersen TR Cater NB Faergeman O Kastelein JJ Olsson AG Tikkanen M J Holme I Larsen ML Lindahl C Szarek M | 2010 | Am J Cardiol2010，106，3： | 1 |
| 7 | Comparison of atorvastatin 80 mg/day versus simvastatin 20 to 40 mg/day on frequency of cardiovascular events late(five years)after acute myocardial infarction(from the Incremental Decrease in End Points through Aggressive Lipid Lowering trial显示文摘 | Pedersen TR Cater NB Faergeman O | 2010 | Am J Cardiol2010，106，3： | 1 |
| 8 | Comparison of atorvas- tatin 80 mg/day versus simvastatin 20 to 40 rag/day on frequency of cardiovascular events late(five years) after acute myocardial infarction (from the Incremental Decrease in End Points through Aggressive Lipid Lowering trial显示文摘 | Pedersen TR Cater NB Faergeman O | 2010 | Am J Cardiol2010，106，3： | 1 |
| 9 | Comparison of atorvastatin 80mg/day versus simvastatin 20 to 40mg/day on frequency of cardiovascular events late (five years) after acute myocardial infarction (from the Incremental Decrease in End Points through Aggressive Lipid Lowering trial)显示文摘 | Pedersen TR Cater NB Faergeman O | 2010 | Am J Cardiol2010，106，3： | 1 |
| 10 | Genetic ablation of aquaporin-2 in the mouse connecting tubules results in defective renal water handling显示文摘 | Kortenoeven ML Pedersen NB Miller RL | 2013 | J Physiology2013，591，8： | 1 |
| 11 | Porcine glucagonlike peptide-2 : structure, signaling, metabolism and effects 显示文摘 | Pedersen NB Hjollund KR Johnsen AH | 2008 | Regul Pept2008，146，13： | 1 |
| 12 | The incidence and prevalence of pervasive developmental disorders: a Dan ish population-based study显示文摘 | Lauritsen MB Pedersen CB Mortensen NB | 2004 | Psychological Medicine2004，34，7： | 1 |
| 13 | Comparison of atorvasta- tin 80mg,/day versus simvastatin 20 to 40 mg/day on frequency of cardiovascular events late ( five years) after acute myocardial infarc- tion( from the incremental Decrease in End Points through Aggressive Lipid Lowering thai) 显示文摘 | Pedersen TR Cater NB Faergeman O | 2010 | Am J Cardiol2010，106，3： | 1 |
| 14 | Characteriza- tion of a novel phosphorylation site in the sodium - chloride co- transporter, NCC 显示文摘 | Rosenbaek LL Assentoft M Pedersen NB | 2012 | J Physiol2012，590，23： | 1 |
| 15 | Comparison of atorvastatin 80 mg/day versus simvastatin 20 to 40 mg/day on frequency of cardiovascular events late (five years)after acute myocardial infarction (from the Incremental Decrease in End Points through Aggressive Lipid Lowering[IDEAL] trial)显示文摘 | Pedersen TR Cater NB Faergeman O | | 0，，03： | 1 |
| 16 | Comparison of atorvas-tatin 80 mg/day versus simvastatin 20 to 40 mg/day on frequencyof cardiovascular events late(five years)after acute myocardialinfarction(from the Incremental Decrease in End Points throughAggressive Lipid Loweringtrial显示文摘 | Pedersen TR Cater NB Faergeman O | 2010 | Am J Cardiol2010，106，3： | 1 |
| 17 | Comparison of atorvastatin 80 mg/day versus simvastatin 20 to 40 mg/day on frequency of cardiovascular events late (five years) after acute myocardial infarction (from the Incremental Decrease in End Points through Aggressive Lipid Lowering[IDEAL] trial)显示文摘 | Pedersen TR Cater NB Faergeman O | | 0，，： | 1 |
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