Table 1.
Characteristics of female subjects (n = 260).
Table 2.
Frequencies for IL-1α genotypes according to BMI in females (n = 260).
Table 3.
Plasma IL-1α and CRP concentrations in the four BMI subgroups.
Figure 1.
Effect of IL-1α CC or TT at position –889 on luciferase reporter activity.
(A) Schematic representation of the 5′-flanking region of the IL-1α gene showing the major transcription start site and the putative transcription factor binding sites. NF-κB = nuclear factor-κB; AP = activator protein; GRE = glucocorticoid response element. (B) The reporter plasmids containing a fragment of 1,432 bp covering the IL-1α 5′-flanking (nucleotide −1351 to +81) was transfected into 3T3-L1 cells and measured after 48 h. For an assessment of the transfection efficiency, cells were co-transfected with pSV-β-gal, and the luciferase activity was expressed relative to the pGL3-Basic vector and normalized to the β-galactosidase activity. Data are the mean ± SE of the results from three or more experiments conducted in triplicate.
Figure 2.
Levels of serum IL-1α in high-fat diet-induced obese mouse model.
IL-1α levels were determined by ELISA method. Experiments were performed in duplicate, and values represent means ± S.E.M. (n = 10).
Figure 3.
Effect of IL-1α administration on lipids levels.
(A–C) Serum total cholesterol (TC), triglyceride (TG), and LDL levels in IL-1α administered mice. IL-1α (10 µg/kg body weight) or vehicle (normal saline) was administered IP respectively. At 0, 4, 12, and 24 hours after IL-1α or vehicle injection, blood samples were collected and levels of TC, TG, LDL cholesterol were determined using the colorimetric enzymatic method and an autoanalyzer. (D) Liver triglyceride content in IL-1α administered mice. IL-1α (10 µg/kg body weight) or vehicle (normal saline) was administered IP respectively. At 0, 4, 12, and 24 hours after IL-1α or vehicle injection, livers were collected and lipids were extracted from the livers. Levels of triglyceride were determined using the colorimetric enzymatic method and an autoanalyzer. Values represent means ± S.E.M. (n = 6). *P<0.05 as compared to the vehicle injection group.
Figure 4.
Expression of IL-1α and IL-1Ra in adipose tissue from high-fat diet-induced obese mouse models.
Levels of IL-1α mRNA (A and B) and IL-1 Ra mRNA (C and D) were determined by quantitative real-time PCR. Experiments were performed in triplicate and values represent means ± S.E.M. (n = 3). IL-1α and IL-1Ra expression levels were normalized to HPRT levels. EWAT: Epididymal White Adipose Tissue; SWAT: Subcutaneous White Adipose Tissue; BAT: Brown Adipose Tissue.
Figure 5.
IL-1α inhibits differentiation of preadipocytes.
(A) The differentiating 3T3-L1 cells were treated with IL-1α at various concentrations for 8 days. Intracellular lipids accumulation was monitored by Oil Red O staining. After staining, dishes were photographed and quantified. (B) To estimate the extent of adipose conversion, isopropanol was added to the plate. Optical density was measured at 500 nm using an automated microplate ELISA reader. Values are mean ± S.E.M. of three independent experiments. *P<0.05 compared with untreated and differentiated cells. Ins: Insulin; Dex: Dexamethasone; Ibmx: 3-isobutyl-1-methylxanthine.
Figure 6.
IL-1α inhibits PPAR-γ and adiponectin (but not IL-6) in 3T3-L1 cells.
The differentiating 3T3-L1 cells were cultured in the absence or 1 ng/ml, 10 ng/ml, and 100 ng/ml of IL-1α for 8 days. (A) Levels of PPAR-γ mRNA were determined by quantitative real-time PCR. PPAR-γ expression levels were normalized to HPRT levels. Experiments were performed in triplicate, and values represent means ± S.E.M. (B) The protein expression of PPAR-γ was examined by western blot analysis. Protein levels were quantified by densitometry. Values are mean ± S.E.M. of three independent experiments and are expressed as a percentage relative to the control (100%). (C) Adiponectin and (D) IL-6 productions were examined by ELISA method. Experiments were performed in duplicate and values are mean ± S.E.M. of three independent experiments. *P<0.05 compared with untreated and differentiated cells. Ins: Insulin; Dex: Dexamethasone; Ibmx: 3-isobutyl-1-methylxanthine.