Difference between revisions of "Goodpaster 2014 Diabetes"
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{{Publication | {{Publication | ||
|title=Goodpaster BH, Coen PM (2014) Improved mitochondrial function is linked with improved insulin sensitivity through reductions in FFA. Diabetes 63:2611-2. | |title=Goodpaster BH, Coen PM (2014) Improved mitochondrial function is linked with improved insulin sensitivity through reductions in FFA. Diabetes 63:2611-2. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/?term=Improved+Mitochondrial+Function+Is+Linked+With+Improved+Insulin+Sensitivity+Through+Reductions+in+FFA PMID:25060892] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/?term=Improved+Mitochondrial+Function+Is+Linked+With+Improved+Insulin+Sensitivity+Through+Reductions+in+FFA PMID:25060892] | ||
|authors=Goodpaster BH, Coen PM | |authors=Goodpaster BH, Coen PM | ||
|year=2014 | |year=2014 | ||
|journal=Diabetes | |journal=Diabetes | ||
|mipnetlab=US FL Orlando Goodpaster BH, | |abstract=Skeletal muscle insulin resistance (IR) is inextricably | ||
linked with the etiology of type 2 diabetes (T2D) and is | |||
a key target for prevention and treatment strategies. IR | |||
likely has many mechanistic origins, but the primary | |||
causes remain elusive, particularly in humans. Of the many | |||
possible mediators of IR, a considerable body of work has | |||
debated the potential roles of mitochondria (1–3), lipid | |||
oversupply (i.e., “lipotoxicity”) (4,5), and the association | |||
between mitochondria, fatty acid metabolism, and intramyocellular | |||
lipid accumulation—the subject of this article. | |||
Indeed, substantial evidence exists to both support and | |||
refute a role for mitochondria in skeletal muscle insulin | |||
resistance (6,7). | |||
... | |||
|mipnetlab=US FL Orlando Goodpaster BH, | |||
}} | |||
{{Labeling | |||
|area=Respiration | |||
|diseases=Diabetes, Obesity | |||
|additional=Commentary | |||
}} | }} | ||
Latest revision as of 12:12, 14 December 2015
Goodpaster BH, Coen PM (2014) Improved mitochondrial function is linked with improved insulin sensitivity through reductions in FFA. Diabetes 63:2611-2. |
Goodpaster BH, Coen PM (2014) Diabetes
Abstract: Skeletal muscle insulin resistance (IR) is inextricably linked with the etiology of type 2 diabetes (T2D) and is a key target for prevention and treatment strategies. IR likely has many mechanistic origins, but the primary causes remain elusive, particularly in humans. Of the many possible mediators of IR, a considerable body of work has debated the potential roles of mitochondria (1–3), lipid oversupply (i.e., “lipotoxicity”) (4,5), and the association between mitochondria, fatty acid metabolism, and intramyocellular lipid accumulation—the subject of this article. Indeed, substantial evidence exists to both support and refute a role for mitochondria in skeletal muscle insulin resistance (6,7).
...
• O2k-Network Lab: US FL Orlando Goodpaster BH
Labels: MiParea: Respiration
Pathology: Diabetes, Obesity
Commentary