PMID- 20885388
OWN - NLM
STAT- MEDLINE
DCOM- 20120504
LR  - 20211020
IS  - 1930-739X (Electronic)
IS  - 1930-7381 (Print)
IS  - 1930-7381 (Linking)
VI  - 19
IP  - 5
DP  - 2011 May
TI  - Increased mitochondrial oxidative phosphorylation in the liver is associated with 
      obesity and insulin resistance.
PG  - 917-24
LID - 10.1038/oby.2010.214 [doi]
AB  - Obesity is the result of excess energy intake relative to expenditure, however 
      little is known about why some individuals are more prone to weight gain than 
      others. Inbred strains of mice also vary in their susceptibility to obesity and 
      therefore represent a valuable model to study the genetics and physiology of 
      weight gain and its co-morbidities such as type 2 diabetes. C57BL/6J mice are 
      susceptible to obesity and insulin resistance when fed an obesogenic diet, 
      whereas A/J mice are resistant despite increased caloric intake. Analysis of B6- 
      and A/J-derived chromosome substitution strains and congenic strains revealed a 
      complex genetic and physiological basis for this phenotype. To improve our 
      understanding of the molecular mechanisms underlying susceptibility to metabolic 
      disease we analyzed global gene expression patterns in 6C1 and 6C2 congenic 
      strains. 6C1 is susceptible whereas 6C2 is resistant to diet-induced obesity. In 
      addition, we demonstrate that 6C1 is glucose intolerant and insulin resistant 
      relative to 6C2. Pathway analysis of global gene expression patterns in muscle, 
      adipose, and liver identified expression level differences between 6C1 and 6C2 in 
      pathways related to basal transcription factors, endocytosis, and mitochondrial 
      oxidative phosphorylation (OxPhos). The OxPhos expression differences were subtle 
      but evident in each complex of the electron transport chain and were associated 
      with a marked increase in mitochondrial oxidative capacity in the livers of the 
      obese strain 6C1 relative to the obesity-resistant strain 6C2. These data 
      suggests the importance of hepatic mitochondrial function in the development of 
      obesity and insulin resistance.
FAU - Buchner, David A
AU  - Buchner DA
AD  - Department of Genetics, Case Western Reserve University School of Medicine, 
      Cleveland, Ohio, USA. david.buchner@case.edu
FAU - Yazbek, Soha N
AU  - Yazbek SN
FAU - Solinas, Paola
AU  - Solinas P
FAU - Burrage, Lindsay C
AU  - Burrage LC
FAU - Morgan, Michael G
AU  - Morgan MG
FAU - Hoppel, Charles L
AU  - Hoppel CL
FAU - Nadeau, Joseph H
AU  - Nadeau JH
LA  - eng
GR  - U54 CA116867/CA/NCI NIH HHS/United States
GR  - P40 RR012305/RR/NCRR NIH HHS/United States
GR  - RR12305/RR/NCRR NIH HHS/United States
GR  - P30 CA43703/CA/NCI NIH HHS/United States
GR  - P30 CA043703/CA/NCI NIH HHS/United States
GR  - F32 HL082213/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20100930
PL  - United States
TA  - Obesity (Silver Spring)
JT  - Obesity (Silver Spring, Md.)
JID - 101264860
SB  - IM
EIN - Obesity (Silver Spring). 2011 Nov;19(11):2286
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Diabetes Mellitus, Type 2/genetics/*metabolism
MH  - Gene Expression Regulation
MH  - Genetic Predisposition to Disease
MH  - *Insulin Resistance
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mitochondria, Liver/genetics/*metabolism
MH  - Muscle, Skeletal/metabolism
MH  - Obesity/genetics/*metabolism
MH  - *Oxidative Phosphorylation
MH  - Polymerase Chain Reaction
PMC - PMC3749733
MID - NIHMS495276
EDAT- 2010/10/05 06:00
MHDA- 2012/05/05 06:00
PMCR- 2013/08/22
CRDT- 2010/10/02 06:00
PHST- 2010/10/02 06:00 [entrez]
PHST- 2010/10/05 06:00 [pubmed]
PHST- 2012/05/05 06:00 [medline]
PHST- 2013/08/22 00:00 [pmc-release]
AID - oby2010214 [pii]
AID - 10.1038/oby.2010.214 [doi]
PST - ppublish
SO  - Obesity (Silver Spring). 2011 May;19(5):917-24. doi: 10.1038/oby.2010.214. Epub 
      2010 Sep 30.