Difference between revisions of "Wijers 2008 PLoS One"
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{{Publication | {{Publication | ||
|title=Wijers SL, Schrauwen P, Saris WH, van Marken Lichtenbelt WD (2008) Human skeletal muscle mitochondrial uncoupling is associated with cold induced adaptive thermogenesis. PLoS | |title=Wijers SL, Schrauwen P, Saris WH, van Marken Lichtenbelt WD (2008) Human skeletal muscle mitochondrial uncoupling is associated with cold induced adaptive thermogenesis. PLoS One 3:e1777. | ||
|authors=Wijers SL, Schrauwen P, Saris WH, van Marken Lichtenbelt WD | |info=[http://www.ncbi.nlm.nih.gov/pubmed?term=Human%20skeletal%20muscle%20mitochondrial%20uncoupling%20is%20associated%20with%20cold%20induced%20adaptive%20thermogenesis PMID: 18335051 Open Access] | ||
|authors=Wijers SL, Schrauwen P, Saris WH, van Marken Lichtenbelt WD | |||
|year=2008 | |year=2008 | ||
|journal= PLoS | |journal=PLoS One | ||
| | |abstract='''BACKGROUND:''' Mild cold exposure and overfeeding are known to elevate energy expenditure in mammals, including humans. This process is called adaptive thermogenesis. In small animals, adaptive thermogenesis is mainly caused by mitochondrial uncoupling in brown adipose tissue and regulated via the sympathetic nervous system. In humans, skeletal muscle is a candidate tissue, known to account for a large part of the epinephrine-induced increase in energy expenditure. However, mitochondrial uncoupling in skeletal muscle has not extensively been studied in relation to adaptive thermogenesis in humans. Therefore we hypothesized that cold-induced adaptive thermogenesis in humans is accompanied by an increase in mitochondrial uncoupling in skeletal muscle. | ||
'''METHODOLOGY/PRINCIPAL FINDINGS:''' The metabolic response to mild cold exposure in 11 lean, male subjects was measured in a respiration chamber at baseline and mild cold exposure. Skeletal muscle mitochondrial uncoupling (state 4) was measured in muscle biopsies taken at the end of the respiration chamber stays. Mild cold exposure caused a significant increase in 24h energy expenditure of 2.8% (0.32 MJ/day, range of -0.21 to 1.66 MJ/day, ''p''<0.05). The individual increases in energy expenditure correlated to state 4 respiration (''p''<0.02, ''R''(2) = 0.50). | |||
'''CONCLUSIONS/SIGNIFICANCE:''' This study for the first time shows that in humans, skeletal muscle has the intrinsic capacity for cold induced adaptive thermogenesis via mitochondrial uncoupling under physiological conditions. This opens possibilities for mitochondrial uncoupling as an alternative therapeutic target in the treatment of obesity. | |||
|keywords=Cold induced adaptive thermogenesis, mitochondrial uncoupling, obesity | |||
|mipnetlab=NL Maastricht Schrauwen P | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
| | |organism=Human | ||
|tissues=Skeletal muscle | |||
|preparations=Permeabilized tissue | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 14:13, 27 March 2015
| Wijers SL, Schrauwen P, Saris WH, van Marken Lichtenbelt WD (2008) Human skeletal muscle mitochondrial uncoupling is associated with cold induced adaptive thermogenesis. PLoS One 3:e1777. |
Wijers SL, Schrauwen P, Saris WH, van Marken Lichtenbelt WD (2008) PLoS One
Abstract: BACKGROUND: Mild cold exposure and overfeeding are known to elevate energy expenditure in mammals, including humans. This process is called adaptive thermogenesis. In small animals, adaptive thermogenesis is mainly caused by mitochondrial uncoupling in brown adipose tissue and regulated via the sympathetic nervous system. In humans, skeletal muscle is a candidate tissue, known to account for a large part of the epinephrine-induced increase in energy expenditure. However, mitochondrial uncoupling in skeletal muscle has not extensively been studied in relation to adaptive thermogenesis in humans. Therefore we hypothesized that cold-induced adaptive thermogenesis in humans is accompanied by an increase in mitochondrial uncoupling in skeletal muscle.
METHODOLOGY/PRINCIPAL FINDINGS: The metabolic response to mild cold exposure in 11 lean, male subjects was measured in a respiration chamber at baseline and mild cold exposure. Skeletal muscle mitochondrial uncoupling (state 4) was measured in muscle biopsies taken at the end of the respiration chamber stays. Mild cold exposure caused a significant increase in 24h energy expenditure of 2.8% (0.32 MJ/day, range of -0.21 to 1.66 MJ/day, p<0.05). The individual increases in energy expenditure correlated to state 4 respiration (p<0.02, R(2) = 0.50).
CONCLUSIONS/SIGNIFICANCE: This study for the first time shows that in humans, skeletal muscle has the intrinsic capacity for cold induced adaptive thermogenesis via mitochondrial uncoupling under physiological conditions. This opens possibilities for mitochondrial uncoupling as an alternative therapeutic target in the treatment of obesity. • Keywords: Cold induced adaptive thermogenesis, mitochondrial uncoupling, obesity
• O2k-Network Lab: NL Maastricht Schrauwen P
Labels:
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Coupling state: OXPHOS
HRR: Oxygraph-2k
