Comparison of adipose tissue derived genes in endogenous Cushing’s syndrome versus diet-induced obesity

Abstract

Introduction: Dysregulation of adipokine secretion and action is a characteristic feature of obesity and a key clinical feature of Cushing's syndrome (CS). We have investigated whether endogenous glucocorticoid excess influences adipose tissue-derived gene expression. Material and methods: mRNA expression of adipokines; adiponectin, resistin, tumour necrosis factor-a, interleukin-6 (IL-6), angiotensinogen (AGT), plasminogen activator inhibitor type 1, retinol binding protein 4, visfatin, and cystatin C was assessed by quantitative real-time RT-PCR in visceral adipose tissue removed during abdominal surgery of eight patients with CS, and six control patients. Results: We did not find any significant difference in the investigated genes; however, the almost significant overexpression of AGT and underexpression of IL-6 might be noteworthy (p = 0.06 in both cases). Conclusions: No significant differences were found in the expression of the investigated genes known as cardiometabolic risk factors. This indicates that there are no major differences between endogenous hypercortisolism or diet-induced obesity regarding the expression of adipokines involved in cardiometabolic disorders. However, the difference in AGT and IL-6 expression might be included in pathways affecting fat distribution in CS.

Selected adipose tissue hormones in the blood of patients with ischaemic cerebral stroke

“…Resistin is one of the best-known adipocytokines. Over the years its blood concentrations have been tested, and its role in the pathogenesis of obesity, arterial hypertension, cardiovascular diseases, and stroke has been studied [16,17]. Qian et al [18] showed a higher concentration of this adipocytokine in the blood of obese mice.…”

Expression of selected angiogenesis-related small microRNAs in patients with abnormally increased secretion of glucocorticoids

“…Patients with endogenous CS are typically exposed to high cortisol levels for longer period of time than the usual duration of laboratory experiments and interventional studies in humans, which suggests that CS could be an appropriate disease model in vivo that permits analysis of the influence of an excessive amount of GCs on the cardiovascular system and may potentially link it with GC-induced cardio-metabolic complications; thus, they could be adequately investigated. Moreover, it was reported that there were no major differences between endogenous hypercortisolism in Cushing's syndrome or diet-induced cardiometabolic disorders in terms of genetic cardiometabolic risk factors and regarding the pathogenesis of their complications [25]. We found that important "angioMIRs", both miRNA-126-3p and miRNA-126-5p, were significantly downregulated in PBNC circulating in CS patients, which, according to the literature, may indicate defective angiogenesis and reduced neovascularisation as miRNA-126 stimulates angiogenesis via VEGF signalling [26].…”