PMID- 23913731
OWN - NLM
STAT- MEDLINE
DCOM- 20140228
LR  - 20141120
IS  - 1930-739X (Electronic)
IS  - 1930-7381 (Linking)
VI  - 21
IP  - 6
DP  - 2013 Jun
TI  - Adipocyte size is associated with NAFLD independent of obesity, fat distribution, 
      and PNPLA3 genotype.
PG  - 1174-9
LID - 10.1002/oby.20114 [doi]
AB  - OBJECTIVE: Adipocyte hypertrophy has been suggested to be causally linked with 
      inflammation and systemic insulin resistance. The aim of the study was to 
      determine whether increased adipocyte size is associated with increased liver fat 
      content due to nonalcoholic fatty liver disease (NAFLD) in humans independent of 
      obesity, fat distribution and genetic variation in the patatin-like phospholipase 
      domain-containing 3 gene (PNPLA3; adiponutrin) at rs738409. DESIGN AND METHODS: 
      One hundred nineteen non-diabetic subjects in a cross-sectional study with a 
      median age of 39 years, mean +/- SD BMI of 30.0 +/- 5.7 kg m(-2) were studied. 
      Abdominal subcutaneous (SC) adipocyte size, liver fat [proton magnetic resonance 
      spectroscopy ((1) H-MRS)], intra-abdominal (IA), and abdominal SC adipose tissue 
      volumes [magnetic resonance imaging (MRI)] and the PNPLA3 genotype at rs738409 
      were determined. Univariate and multiple linear regression analysis were used to 
      identify independent predictors of liver fat content. RESULTS: In multiple linear 
      regression analysis, age, gender, BMI, the IA/SC ratio, and PNPLA3 genotype 
      explained 42% of variation in liver fat content. Addition of adipocyte size (P < 
      0.0001) to the model increased the percent of explanation to 53%. Thus, 21% of 
      known variation in liver fat could be explained by adipocyte size alone. 
      CONCLUSIONS: Increased adipocyte size highly significantly contributes to liver 
      fat accumulation independent of other causes.
CI  - Copyright (c) 2012 The Obesity Society.
FAU - Petaja, Elina M
AU  - Petaja EM
AD  - Minerva Foundation Institute for Medical Research, Helsinki, Finland. 
      elina.petaja@helsinki.fi
FAU - Sevastianova, Ksenia
AU  - Sevastianova K
FAU - Hakkarainen, Antti
AU  - Hakkarainen A
FAU - Orho-Melander, Marju
AU  - Orho-Melander M
FAU - Lundbom, Nina
AU  - Lundbom N
FAU - Yki-Jarvinen, Hannele
AU  - Yki-Jarvinen H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Obesity (Silver Spring)
JT  - Obesity (Silver Spring, Md.)
JID - 101264860
RN  - 0 (Membrane Proteins)
RN  - EC 3.1.1.3 (Lipase)
RN  - EC 3.1.1.3 (adiponutrin, human)
SB  - IM
MH  - Adipocytes/*cytology
MH  - Adult
MH  - Body Composition
MH  - *Body Fat Distribution
MH  - Cross-Sectional Studies
MH  - Fatty Liver/*genetics/physiopathology
MH  - Female
MH  - Genotype
MH  - Humans
MH  - Insulin Resistance
MH  - Lipase/*genetics/metabolism
MH  - Liver/metabolism
MH  - Male
MH  - Membrane Proteins/*genetics/metabolism
MH  - Middle Aged
MH  - Non-alcoholic Fatty Liver Disease
MH  - Obesity/*physiopathology
MH  - Organ Size
MH  - Subcutaneous Fat, Abdominal/physiopathology
EDAT- 2013/08/06 06:00
MHDA- 2014/03/01 06:00
CRDT- 2013/08/06 06:00
PHST- 2013/08/06 06:00 [entrez]
PHST- 2013/08/06 06:00 [pubmed]
PHST- 2014/03/01 06:00 [medline]
AID - 10.1002/oby.20114 [doi]
PST - ppublish
SO  - Obesity (Silver Spring). 2013 Jun;21(6):1174-9. doi: 10.1002/oby.20114.