Article

Inflammation in subcutaneous adipose tissue: relationship to adipose cell size.

Division of Endocrinology, Stanford University School of Medicine, 300 Pasteur Drive, Rm S025, Stanford, CA 94305-5103, USA.
Diabetologia (Impact Factor: 6.88). 10/2009; 53(2):369-77. DOI: 10.1007/s00125-009-1496-3
Source: PubMed

ABSTRACT 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.
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.
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.
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. Trial registration: ClinicalTrials.gov NCT00285844.

0 Followers
 · 
115 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Introduction Adipocyte size and body fat distribution are strongly linked to the metabolic complications of obesity. The aim of the present study was to test the plasticity of white adipose tissue in response to insulin deprivation and replacement. We have characterized the changes of adipose cell size repartition and gene expressions in type 1 diabetes Sprague-Dawley rats and type 1 diabetic supplemented with insulin. Methods Using streptozotocin (STZ)-induced diabetes, we induced rapid changes in rat adipose tissue weights to study the changes in the distribution of adipose cell sizes in retroperitoneal (rWAT), epididymal (eWAT) and subcutaneous adipose tissues (scWAT). Adipose tissue weights of type 1 diabetic rats were then rapidly restored by insulin supplementation. Cell size distributions were analyzed using multisizer IV (Beckman Coulter). Cell size changes were correlated to transcriptional regulation of genes coding for proteins involved in lipid and glucose metabolisms and adipocytokines. Results The initial body weight of the rats was 465±5.2 g. Insulin privation was stopped when rats lost 100 g which induced reductions in fat mass of 68% for rWAT, 42% for eWAT and 59% for scWAT corresponding to decreased mode cell diameters by 31.1%, 20%, 25.3%, respectively. The most affected size distribution by insulin deprivation was observed in rWAT. The bimodal distribution of adipose cell sizes disappeared in response to insulin deprivation in rWAT and scWAT. The most important observation is that cell size distribution returned close to control values in response to insulin treatment. mRNAs coding for adiponectin, leptin and apelin were more stimulated in scWAT compared to other depots in diabetic plus insulin group. Conclusion Fat depots have specific responses to insulin deprivation and supplementation. The results show that insulin is a major determinant of bimodal cell repartition in adipose tissues.
    PLoS ONE 08/2014; 9(8):e106214. DOI:10.1371/journal.pone.0106214 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The ability of adipose tissue to adapt to a changing nutrient environment is critical to the maintenance of metabolic control. Nutrient excess and deficiency alter the shape of adipose tissue drastically and trigger many events that are collectively known as adipose tissue remodeling. Remodeling of adipose tissue involves more than adipocytes and is controlled by an extensive network of stromal cells and extracellular matrix proteins. Prominent players in this process are adipose tissue macrophages, which are a specialized leukocyte present in lean and obese states that contributes to adipose tissue inflammation. The interest in adipose tissue remodeling has been accelerated by the current epidemic of obesity and the chronic generation of signals that lead to expansion of adipose tissue. It is clear that evidence of dysfunctional remodeling events is a hallmark of obesity associated with metabolic disease. This review summarizes and highlights the recent work in this area and provides a framework in which to consider how adipose tissue macrophages contribute to the remodeling events in lean and obese states. Advancing our understanding of the involvement of macrophages in adipose tissue remodeling will promote one aspect of the new field of "immunometabolism," which connects control systems developed for regulation of immunity with those that control metabolism. It will also provide insight into how physiologic and pathophysiologic remodeling differs in adipose tissue and identify potential nodes for intervention to break the link between obesity and disease. Expected final online publication date for the Annual Review of Nutrition Volume 34 is July 17, 2014. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
    Annual Review of Nutrition 09/2012; DOI:10.1146/annurev-nutr-071812-161113 · 10.46 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Adipose tissue and adipocytes play a central role in the pathogenesis of metabolic diseases related to obesity. Size of fat cells depends on the balance of synthesis and mobilization of lipids and can undergo important variations throughout the life of the organism. These variations usually occur when storing and releasing lipids according to energy demand. In particular when confronted to severe food restriction, adipocyte releases its lipid content via a process called lipolysis. We propose a mathematical model that combines cell diameter distribution and lipolytic response to show that lipid release is a surface (radius squared) limited mechanism. Since this size-dependent rate affects the cell's shrinkage speed, we are able to predict the cell size distribution evolution when lipolysis is the only factor at work: such as during an important food restriction. Performing recurrent surgical biopsies on rats, we measured the evolution of adipose cell size distribution for the same individual throughout the duration of the food restriction protocol. We show that our microscopic model of size dependent lipid release can predict macroscopic size distribution evolution.
    Journal of Theoretical Biology 09/2014; 364. DOI:10.1016/j.jtbi.2014.08.046 · 2.30 Impact Factor

Preview

Download
1 Download
Available from