Difference between revisions of "Williams 2015 J Biol Chem"
Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Williams AS, Kang L, Zheng J, Grueter CA, Bracy DP, James FD, Pozzi A, Wasserman DH (2015) Integrin α1-null mice exhibit improved fatty liver when fed a high fat diet despite severe hepatic insulin resistance. J Biol Chem | |title=Williams AS, Kang L, Zheng J, Grueter CA, Bracy DP, James FD, Pozzi A, Wasserman DH (2015) Integrin α1-null mice exhibit improved fatty liver when fed a high fat diet despite severe hepatic insulin resistance. J Biol Chem 290:6546-57. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25593319 PMID:25593319] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/25593319 PMID:25593319] | ||
|authors=Williams AS, Kang L, Zheng J, Grueter CA, Bracy DP, James FD, Pozzi A, Wasserman DH | |authors=Williams AS, Kang L, Zheng J, Grueter CA, Bracy DP, James FD, Pozzi A, Wasserman DH | ||
Line 22: | Line 22: | ||
|substratestates=CI, Other combinations | |substratestates=CI, Other combinations | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels | |additional=Labels | ||
}} | }} |
Revision as of 12:29, 21 December 2015
Williams AS, Kang L, Zheng J, Grueter CA, Bracy DP, James FD, Pozzi A, Wasserman DH (2015) Integrin α1-null mice exhibit improved fatty liver when fed a high fat diet despite severe hepatic insulin resistance. J Biol Chem 290:6546-57. |
Williams AS, Kang L, Zheng J, Grueter CA, Bracy DP, James FD, Pozzi A, Wasserman DH (2015) J Biol Chem
Abstract: Hepatic insulin resistance is associated with increased collagen. Integrin α1β1 is a collagen binding receptor expressed on hepatocytes. Here we show that expression of the α1 subunit is increased in hepatocytes isolated from high fat fed (HF-fed) mice. To determine whether the integrin α1 subunit protects against impairments in hepatic glucose metabolism, we analyzed glucose tolerance and insulin sensitivity in HF-fed integrin α1-null (itgα1-/-) and wild-type littermates (itgα1+/+). Using the insulin clamp, we found that insulin-stimulated hepatic glucose production was suppressed by ~50% in HF-fed itgα1+/+ mice. In contrast, it was not suppressed in HF-fed itgα1-/- mice indicating severe hepatic insulin resistance. This was associated with decreased hepatic insulin signaling in HF-fed itgα1-/- mice. Interestingly, hepatic triglyceride and diglyceride content were normalized to chow-fed levels in HF-fed itgα1-/- mice. This indicates that hepatic steatosis is dissociated from insulin resistance in HF-fed itgα1-/- mice. The decrease in hepatic lipid accumulation in HF-fed itgα1-/- mice was associated with altered free fatty acid metabolism. These studies establish a role for integrin signaling in facilitating hepatic insulin action, while promoting lipid accumulation in mice challenged with a HF diet.
Copyright © 2015, The American Society for Biochemistry and Molecular Biology. • Keywords: Extracellular matrix, Insulin resistance, Integrin lipid metabolism Liver metabolism
• O2k-Network Lab: US TN Nashville Wasserman DH
Labels: MiParea: Exercise physiology;nutrition;life style
Pathology: Diabetes
Organism: Mouse Tissue;cell: Liver Preparation: Permeabilized tissue
Regulation: Cyt c Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
Labels