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Release of inflammatory mediators by human adipose tissue is enhanced in obesity and primarily by the nonfat cells: a review.

Fain JN - Mediators Inflamm. (2010)

Bottom Line: Inflammatory adipokines [IL-6, IL-10, ACE, TGFbeta1, TNFalpha, IL-1beta, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue.In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue.The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA. jfain@uthsc.edu

ABSTRACT
This paper considers the role of putative adipokines that might be involved in the enhanced inflammatory response of human adipose tissue seen in obesity. Inflammatory adipokines [IL-6, IL-10, ACE, TGFbeta1, TNFalpha, IL-1beta, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue. In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue. The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed. The conclusion is that the release of many inflammatory adipokines by adipose tissue is enhanced in obese humans.

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The correlation between releases of 30 adipokines over 48 hours incubation by fat cells isolated from human adipose tissue as compared to gene expression of these adipokines at the start of the incubation. The release data are from Table 1 and expressed as release by fat cells as % of that by fat cells plus nonfat cells over 48 hours. The data for mRNA are derived from those shown in Table 2 except that they are plotted as the ΔCp for the difference between mRNA in fat cells and nonfat cells instead of the ratios, which are derived from the ΔCp values.   Data are not included for resistin, CRP and IL-18 since release by fat cells was below the sensitivity of the assays and mRNA was not measured for MIF, HGF, VEGF, and VCAM-1.
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fig1: The correlation between releases of 30 adipokines over 48 hours incubation by fat cells isolated from human adipose tissue as compared to gene expression of these adipokines at the start of the incubation. The release data are from Table 1 and expressed as release by fat cells as % of that by fat cells plus nonfat cells over 48 hours. The data for mRNA are derived from those shown in Table 2 except that they are plotted as the ΔCp for the difference between mRNA in fat cells and nonfat cells instead of the ratios, which are derived from the ΔCp values. Data are not included for resistin, CRP and IL-18 since release by fat cells was below the sensitivity of the assays and mRNA was not measured for MIF, HGF, VEGF, and VCAM-1.

Mentions: The circulating levels of zinc-α2-glycoprotein (ZAG) have been reported to be unaltered in obesity [17], but the level of ZAG gene expression in human adipose tissue is reduced in obesity [69, 70]. This illustrates the problem that changes in circulating levels of adipokines do not necessarily reflect changes in their release by or correlate with their mRNA levels in adipose tissue. Most of the adipokines are also cytokines and are released primarily by cells other than fat cells in human adipose tissue (Figure 1). Furthermore, circulating levels of all adipokines are also regulated by their release from other tissues as well as their degradation. For others such as interleukin 1β (IL-1β), no reports have been published indicating that IL-1β is elevated in the circulation of obese humans. However, IL-1β is an important regulator of the inflammatory response in human adipose tissue. It may well be a paracrine regulator that acts locally and never reaches the blood in mild inflammatory conditions such as obesity. The same may apply to PGE2, which is the primary product of the cyclooxygenase-2 (COX-2) enzyme.


Release of inflammatory mediators by human adipose tissue is enhanced in obesity and primarily by the nonfat cells: a review.

Fain JN - Mediators Inflamm. (2010)

The correlation between releases of 30 adipokines over 48 hours incubation by fat cells isolated from human adipose tissue as compared to gene expression of these adipokines at the start of the incubation. The release data are from Table 1 and expressed as release by fat cells as % of that by fat cells plus nonfat cells over 48 hours. The data for mRNA are derived from those shown in Table 2 except that they are plotted as the ΔCp for the difference between mRNA in fat cells and nonfat cells instead of the ratios, which are derived from the ΔCp values.   Data are not included for resistin, CRP and IL-18 since release by fat cells was below the sensitivity of the assays and mRNA was not measured for MIF, HGF, VEGF, and VCAM-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2874930&req=5

fig1: The correlation between releases of 30 adipokines over 48 hours incubation by fat cells isolated from human adipose tissue as compared to gene expression of these adipokines at the start of the incubation. The release data are from Table 1 and expressed as release by fat cells as % of that by fat cells plus nonfat cells over 48 hours. The data for mRNA are derived from those shown in Table 2 except that they are plotted as the ΔCp for the difference between mRNA in fat cells and nonfat cells instead of the ratios, which are derived from the ΔCp values. Data are not included for resistin, CRP and IL-18 since release by fat cells was below the sensitivity of the assays and mRNA was not measured for MIF, HGF, VEGF, and VCAM-1.
Mentions: The circulating levels of zinc-α2-glycoprotein (ZAG) have been reported to be unaltered in obesity [17], but the level of ZAG gene expression in human adipose tissue is reduced in obesity [69, 70]. This illustrates the problem that changes in circulating levels of adipokines do not necessarily reflect changes in their release by or correlate with their mRNA levels in adipose tissue. Most of the adipokines are also cytokines and are released primarily by cells other than fat cells in human adipose tissue (Figure 1). Furthermore, circulating levels of all adipokines are also regulated by their release from other tissues as well as their degradation. For others such as interleukin 1β (IL-1β), no reports have been published indicating that IL-1β is elevated in the circulation of obese humans. However, IL-1β is an important regulator of the inflammatory response in human adipose tissue. It may well be a paracrine regulator that acts locally and never reaches the blood in mild inflammatory conditions such as obesity. The same may apply to PGE2, which is the primary product of the cyclooxygenase-2 (COX-2) enzyme.

Bottom Line: Inflammatory adipokines [IL-6, IL-10, ACE, TGFbeta1, TNFalpha, IL-1beta, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue.In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue.The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA. jfain@uthsc.edu

ABSTRACT
This paper considers the role of putative adipokines that might be involved in the enhanced inflammatory response of human adipose tissue seen in obesity. Inflammatory adipokines [IL-6, IL-10, ACE, TGFbeta1, TNFalpha, IL-1beta, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue. In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue. The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed. The conclusion is that the release of many inflammatory adipokines by adipose tissue is enhanced in obese humans.

Show MeSH
Related in: MedlinePlus