In situ profiling of adipokines in subcutaneous microdialysates from lean and obese individuals.
Adipose tissue (AT) had emerged as an endocrine organ and a key regulator of the metabolically triggered inflammation. The aims of this study were 1) to investigate the usefulness of a multiplexed bioassay in characterizing a panel of adipokines in subcutaneous (sc) microdialysate samples and 2) to determine whether lean and obese individuals differ in their interstitial adipokines levels following microdialysis (MD) probe insertion. Ultrafiltrating MD membranes were inserted in opposite sites of the sc abdominal AT of six lean (L) and six obese (OB) males at the beginning (M1) and during the last 120 min (M2) of the study. Interstitial and serum concentrations of adipokines were quantified using the Luminex technique and ELISA at 60-min intervals for 5 h. In comparison with L subjects, OB subjects exhibited elevated interstitial leptin (P < 0.001), IL-8 (P < 0.05), and IL-18 levels (P = 0.05), as well as higher serum concentrations of leptin (P < 0.0001), IL-6 (P < 0.0001), tumor necrosis factor-alpha (P < 0.001), IL-8 (P = 0.01) and interferon-gamma-inducible protein 10 (P < 0.05). In samples from the M1 membranes, leptin decreased and IL-1alpha, IL-18, and RANTES (regulated on activation, normal T-cell expressed and secreted) remained relatively stable, whereas IL-6, IL-8, and monocyte chemoattractant protein-1 significantly increased after the first hour (P < 0.0001 vs. baseline). Notably, either the magnitude of increase from the initial values or the time pattern of all the adipokines in M1 and M2 dialysates were similar between the groups. In conclusion, the current work provides valuable information on the optimal time frame to collect in situ AT microdialysate samples. Further studies are needed, however, to unravel the intricate interplay of cytokines in AT interstitial fluid.
Murdolo
Giuseppe
G
The Lundberg Laboratory for Diabetes Research, Center of Excellence for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, The Shalgrenska Academy at Göteborg University, Göteborg, Sweden. TUgiuseppe.murdolo@medic.gu.seUT
Herder
Christian
C
Wang
Zhaohui
Z
Rose
Bettina
B
Schmelz
Martin
M
Jansson
Per-Anders
PA
D054392:Adipokines / Q000097:blood / Q000378:metabolism*; D000328:Adult; D018932:Chemokine CCL2 / Q000097:blood / Q000378:metabolism; D018946:Chemokine CCL5 / Q000378:metabolism; D054357:Chemokine CXCL10 / Q000097:blood; D002940:Circadian Rhythm / Q000502:physiology; D006801:Humans; D020382:Interleukin-18 / Q000097:blood / Q000378:metabolism; D053582:Interleukin-1alpha / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D016209:Interleukin-8 / Q000097:blood / Q000378:metabolism; D020738:Leptin / Q000097:blood / Q000378:metabolism; D008297:Male; D008567:Membranes, Artificial; D017551:Microdialysis / Q000295:instrumentation / Q000379:methods*; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D050151:Subcutaneous Fat / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D054392:Adipokines; C483024:CCL5 protein, human; C114753:CXCL10 protein, human; D018932:Chemokine CCL2; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D020382:Interleukin-18; D053582:Interleukin-1alpha; D015850:Interleukin-6; D016209:Interleukin-8; D020738:Leptin; D008567:Membranes, Artificial; D014409:Tumor Necrosis Factor-alpha