Inflammation in subcutaneous adipose tissue: relationship to adipose cell size.
OBJECTIVE
Inflammation is associated with increased body mass and purportedly with increased size of adipose cells. We sought to determine whether increased size of adipose cells is associated with localised inflammation in weight-stable, moderately obese humans.


METHODS
We recruited 49 healthy, moderately obese individuals for quantification of insulin resistance (modified insulin suppression test) and subcutaneous abdominal adipose tissue biopsy. Cell size distribution was analysed with a multisizer device and inflammatory gene expression with real-time PCR. Correlations between inflammatory gene expression and cell size variables, with adjustment for sex and insulin resistance, were calculated.


RESULTS
Adipose cells were bimodally distributed, with 47% in a 'large' cell population and the remainder in a 'small' cell population. The median diameter of the large adipose cells was not associated with expression of inflammatory genes. Rather, the fraction of small adipose cells was consistently associated with inflammatory gene expression, independently of sex, insulin resistance and BMI. This association was more pronounced in insulin-resistant than insulin-sensitive individuals. Insulin resistance also independently predicted expression of inflammatory genes.


CONCLUSIONS
This study demonstrates that among moderately obese, weight-stable individuals an increased proportion of small adipose cells is associated with inflammation in subcutaneous adipose tissue, whereas size of mature adipose cells is not. The observed association between small adipose cells and inflammation may reflect impaired adipogenesis and/or terminal differentiation. However, it is unclear whether this is a cause or consequence of inflammation. This question and whether small vs large adipose cells contribute differently to inflammation in adipose tissue are topics for future research.


BACKGROUND
ClinicalTrials.gov NCT00285844.
McLaughlin
T
T
Division of Endocrinology, Stanford University School of Medicine, 300 Pasteur Drive, Rm S025, Stanford, CA 94305-5103, USA. tmclaugh@stanford.edu
Deng
A
A
Yee
G
G
Lamendola
C
C
Reaven
G
G
Tsao
P S
PS
Cushman
S W
SW
Sherman
A
A
D017667:Adipocytes / Q000166:cytology* / Q000473:pathology; D000273:Adipose Tissue / Q000166:cytology* / Q000473:pathology; D000328:Adult; D000368:Aged; D015992:Body Mass Index; D001835:Body Weight; D048429:Cell Size; D005260:Female; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000473:pathology*; D007333:Insulin Resistance / Q000502:physiology*; D017493:Leukocyte Common Antigens / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D018579:Patient Selection; D016133:Polymerase Chain Reaction; D012313:RNA / Q000235:genetics / Q000302:isolation & purification; D012337:RNA, Ribosomal, 18S / Q000235:genetics; D012867:Skin / Q000503:physiopathology; D055105:Waist Circumference
D018950:Lipopolysaccharide Receptors; D012337:RNA, Ribosomal, 18S; D012313:RNA; D017493:Leukocyte Common Antigens