Difference between revisions of "Van den Broek 2010 FASEB J"
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{{Publication | {{Publication | ||
|title=van den Broek NM, Ciapaite J, De Feyter HM, Houten SM, Wanders | |title=van den Broek NM, Ciapaite J, De Feyter HM, Houten SM, Wanders RJA, Jeneson JA, Nicolay K, Prompers JJ (2010) Increased mitochondrial content rescues ''in vivo'' muscle oxidative capacity in long-term high-fat-diet-fed rats. FASEB J 24:1354-64. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20040520 PMID:20040520] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/20040520 PMID: 20040520 Open Access] | ||
|authors=van den Broek NM, Ciapaite J, De Feyter HM, Houten SM, Wanders | |authors=van den Broek NM, Ciapaite J, De Feyter HM, Houten SM, Wanders RJA, Jeneson JA, Nicolay K, Prompers JJ | ||
|year=2010 | |year=2010 | ||
|journal=FASEB J | |journal=FASEB J | ||
|abstract=Mitochondria are thought to play a crucial role in the etiology of muscle insulin resistance (IR). The aim of this study was to gain more insight into the timing and nature of mitochondrial adaptations during the development of high-fat-diet (HFD)-induced IR. Adult Wistar rats were fed HFD or normal chow for 2.5 and 25 wk. Intramyocellular lipids (IMCLs) were quantified in vivo using (1)H magnetic resonance spectroscopy (MRS). Muscle oxidative capacity was assessed in vivo using (31)P MRS and in vitro by measuring mitochondrial DNA copy number and oxygen consumption in isolated mitochondria. MRS in tibialis anterior muscle revealed 3.3-fold higher IMCL content and 1.2-fold increased oxidative capacity after 2.5 wk of HFD feeding. The latter result could be fully accounted for by increased mitochondrial content. After 25 wk of HFD, maximal ADP-stimulated oxygen consumption in isolated mitochondria oxidizing pyruvate plus malate remained unaffected, while IMCL and mitochondrial content had further increased compared to controls (5.1-fold and 1.4-fold, respectively). Interestingly, in vivo oxidative capacity at this time point was identical to controls. These results show that skeletal muscle in HFD-induced IR accompanied by IMCL accumulation requires a progressively larger mitochondrial pool size to maintain normal oxidative capacity in vivo. | |abstract=Mitochondria are thought to play a crucial role in the etiology of muscle insulin resistance (IR). The aim of this study was to gain more insight into the timing and nature of mitochondrial adaptations during the development of high-fat-diet (HFD)-induced IR. Adult Wistar rats were fed HFD or normal chow for 2.5 and 25 wk. Intramyocellular lipids (IMCLs) were quantified ''in vivo'' using (1)H magnetic resonance spectroscopy (MRS). Muscle oxidative capacity was assessed ''in vivo'' using (31)P MRS and ''in vitro'' by measuring mitochondrial DNA copy number and oxygen consumption in isolated mitochondria. MRS in tibialis anterior muscle revealed 3.3-fold higher IMCL content and 1.2-fold increased oxidative capacity after 2.5 wk of HFD feeding. The latter result could be fully accounted for by increased mitochondrial content. After 25 wk of HFD, maximal ADP-stimulated oxygen consumption in isolated mitochondria oxidizing pyruvate plus malate remained unaffected, while IMCL and mitochondrial content had further increased compared to controls (5.1-fold and 1.4-fold, respectively). Interestingly, ''in vivo'' oxidative capacity at this time point was identical to controls. These results show that skeletal muscle in HFD-induced IR accompanied by IMCL accumulation requires a progressively larger mitochondrial pool size to maintain normal oxidative capacity ''in vivo''. | ||
|keywords= | |keywords=Diabetes, Insulin resistance, Magnetic resonance spectroscopy, Intramyocellular lipid, Mitochondrial function | ||
|mipnetlab=NL Eindhoven Nicolay K | |mipnetlab=NL Eindhoven Nicolay K | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |||
|tissues=Skeletal muscle | |||
|preparations=Isolated mitochondria | |||
|diseases=Parkinson's | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Latest revision as of 13:31, 24 June 2019
van den Broek NM, Ciapaite J, De Feyter HM, Houten SM, Wanders RJA, Jeneson JA, Nicolay K, Prompers JJ (2010) Increased mitochondrial content rescues in vivo muscle oxidative capacity in long-term high-fat-diet-fed rats. FASEB J 24:1354-64. |
van den Broek NM, Ciapaite J, De Feyter HM, Houten SM, Wanders RJA, Jeneson JA, Nicolay K, Prompers JJ (2010) FASEB J
Abstract: Mitochondria are thought to play a crucial role in the etiology of muscle insulin resistance (IR). The aim of this study was to gain more insight into the timing and nature of mitochondrial adaptations during the development of high-fat-diet (HFD)-induced IR. Adult Wistar rats were fed HFD or normal chow for 2.5 and 25 wk. Intramyocellular lipids (IMCLs) were quantified in vivo using (1)H magnetic resonance spectroscopy (MRS). Muscle oxidative capacity was assessed in vivo using (31)P MRS and in vitro by measuring mitochondrial DNA copy number and oxygen consumption in isolated mitochondria. MRS in tibialis anterior muscle revealed 3.3-fold higher IMCL content and 1.2-fold increased oxidative capacity after 2.5 wk of HFD feeding. The latter result could be fully accounted for by increased mitochondrial content. After 25 wk of HFD, maximal ADP-stimulated oxygen consumption in isolated mitochondria oxidizing pyruvate plus malate remained unaffected, while IMCL and mitochondrial content had further increased compared to controls (5.1-fold and 1.4-fold, respectively). Interestingly, in vivo oxidative capacity at this time point was identical to controls. These results show that skeletal muscle in HFD-induced IR accompanied by IMCL accumulation requires a progressively larger mitochondrial pool size to maintain normal oxidative capacity in vivo. β’ Keywords: Diabetes, Insulin resistance, Magnetic resonance spectroscopy, Intramyocellular lipid, Mitochondrial function
β’ O2k-Network Lab: NL Eindhoven Nicolay K
Labels:
Pathology: Parkinson's
Organism: Rat Tissue;cell: Skeletal muscle Preparation: Isolated mitochondria
HRR: Oxygraph-2k