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  • br The current study showed also positive correlation

    2020-03-24


    The current study showed also positive correlation between serum FABP-4 & serum TC, TAG, LDL-C & negative correlation with serum HDL-C. This agreed with Kralisch S et al. (2013) who stated
    Table 4
    Correlations between Serum FABP-4 and serum VEGF among Group II, III & IV pa-tients (n ΒΌ 60).
    Correlations
    Serum TNF-a
    r P-value
    *P value was considered significant at <0.05.
    that total FABP-4 promotes insulin resistance, hyper-triacylglycerolaemia and atherosclerosis [34].
    The present study revealed significant elevation in serum TNF-a level in breast cancer subjects with type 2 diabetes compared with breast cancer, diabetic & normal subjects. Moreover, it was signif-icantly elevated in breast cancer subjects compared with diabetic & normal subjects. Additionally, it was significantly elevated in dia-betic subjects in comparison with normal subjects.
    Also the present study confirmed positive correlation between serum FABP-4 & TNF-a levels. This agreed with Niu G et al. (2016) who reported that chronic inflammation is considered to be asso-ciated with obesity and insulin resistance [2]. FABP-4 participates in regulating the production of inflammatory cytokines [5]. Terra X et al. found that FABP-4 was positively correlated with inflamma-tory cytokines in obese subjects with newly diagnosed type 2 diabetes. Also, positive association of serum FABP-4 with inflam-matory factor TNF-a, has been observed in morbidly obese women [32].
    Moreover, dendritic N,N-Dimethylsphingosine that are FABP4-deficient produce lower levels of cytokines including TNF-a, and have reduced ca-pacity to activate T cells [35]. Confirmatively, fat cells may also promote inflammation linked cancer through tumor growth regu-lators and tumor necrotic factors. Adipose tissue secretes TNF-a leading to inflammation promoting cancer [36].
    Consistently, it is also well established that ROS is a common denominator in the pathogenesis of diabetic complications. This study found significant elevation of serum 8-HdOG level and sig-nificant decrease in TrxR activity in breast cancer subjects with type 2 diabetes compared with breast cancer, diabetic & normal sub-jects. Moreover, these significant changes occurred in breast cancer subjects compared with diabetic & normal subjects. Additionally in diabetic subjects in comparison with normal subjects. This con-firms the negative correlation between serum 8-HdOG & TrxR activity.
    Increased ROS activity can result from increased oxidant pro-duction and/or decreased antioxidant function. 8-OHdG levels are increased in diabetes patients and involved in the pathology of diabetes [37]. There was an increased level of 8-OHdG in the DNA of early-stage cancer tissue which suggests that ROS may play an important role in the early phases of carcinogenesis [11].
    From another point of view, high glucose in diabetic subjects diminished TrxR activity. Restoration of TrxR activity may be a potentially beneficial therapeutic strategy for the prevention of diabetes-induced vascular complications [38]. Additionally, it was found a novel chemopreventive mechanism in cancer therapy is proposed involving Se catalysis of reversible cysteine/disulfide transformations that occur in a number of redox-regulated pro-teins, including TrxR [39].
    Moreover, this study also revealed significant elevation of serum VEGF level in breast cancer subjects with type 2 diabetes compared with breast cancer, diabetic & normal subjects. Moreover, it was significantly elevated in breast cancer subjects compared with diabetic & normal subjects. Additionally, it was significantly elevated in diabetic subjects in comparison with normal subjects. One of the primary factors in the development of diabetic com-plications is pathological release of VEGF [40]. Increased VEGF release results in pathological angiogenesis that is irregularly distributed and features poorly constructed vessels that are prone to leak, leading to increased vascular leakage which is a serious risk factor for diabetic complications [41].
    VEGFA may induce the production of matrix metalloproteinases (MMPs), such as MMP-2 and MMP-9, in breast cancer [42]. VEGF has been implicated in breast cancer susceptibility and aggres-siveness. High VEGF expression was correlated with the presence of axillary nodal metastasis and lower overall survival rates [43]. 
    Furthermore, this study showed positive correlation between FABP-4 & VEGF. It was reported that treatment of endothelial cells with VEGF via VEGF-receptor-2 or basic fibroblast growth factor induced FABP-4 expression. Also, FABP-4 in endothelial cells has also been reported to promote angiogenesis [44]. Consistently, the serum VEGF increments assessed herein may be influenced by expression of other cytokines (as TNF-a) regulating vascular permeability related to angiogenesis and this aligned with Pluda JM et al., 1997 [45]. Thus the current result confirmed positive corre-lation between VEGF & TNF-a.