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Serum IL-15 and IL-15Rα levels are decreased in lean and obese physically active humans

Posted by D. Valadés, J. Bujan, C.V Martínez, et al. on 2017-11-08 17:33:39


Circulating IL-15 presence is required to stimulate anti-adipogenic effects of the IL-15/IL-15Ra axis in adipose tissue. Although exercise increases blood IL-15 expression post-exercise, it remains inconclusive whether physical activity can alter the baseline concentrations of this cytokine. The aim of this study was to determine whether physical activity regulates circulating IL-15 and IL-15Ra in lean and obese individuals. Two hundred and seventy-six participants were divided into five groups according to physical activity (PA), body mass and type 2 diabetes mellitus (T2DM) diagnosis: (a) lean PA (N = 25); (b) lean non-PA (N = 28); (c) obese PA (N = 64); (d) obese non-PA (N = 79); and (e) obese non-PA with T2DM (N = 80). Serum IL-15 and IL-15Ra, blood glucose/lipid profile and body composition were measured. Serum IL-15 and IL-15Ra decreased in PA participants compared to non-PA (P < .05), while IL-15 and IL-15Ra increased in obese with T2DM compared to obese without T2DM (P < .05). No differences were observed between lean non-PA and obese PA. Serum IL-15Ra was associated with fasting glucose (R2 = .063), insulin (R2 = .082), HbA1c (R2 = .108), and HOMA (R2 = .057) in obese participants. Circulating IL-15 and IL-15Ra are reduced in lean and obese participants who perform physical activity regularly (≥180 min/week), suggesting a regulative role of physical activity on the circulating concentrations of IL-15 and IL-15Ra at baseline. Moreover, the relationship observed between IL-15Ra and glucose profile may indicate a role of the alpha receptor in glucose metabolism.

ANGPTL8 (betatrophin) role in diabetes and metabolic diseases

Posted by M Abu-Farha, J Abubaker, J Tuomilehto. on 2017-11-01 19:38:03


Diabetes is a major disease worldwide that is reaching epidemic levels. Its increased prevalence as well as its association with a high number of complications such as cardiovascular diseases, nephropathy, and retinopathy makes it an important disease for investigation. ANGPTL8 is a recently identified hormone that has been associated with two functionally important processes in the development of type 2 diabetes, insulin resistance as well as lipid metabolism. Initial work has shown that ANGPTL8 was expressed in liver, white adipose, and brown adipose tissues. ANGPTL8 regulates the activity of lipoprotein lipase, which is a key enzyme in lipoprotein lipolysis pathway through its direct interaction with ANGPTL3. It has been also reported that it regulates the replication of beta-cells in response to insulin resistance. As a result, many recent studies have focused on the association of ANGPTL8 with diabetes and obesity as well as its association with various metabolic markers in order to better understand its physiological role in glucose homeostasis and lipid metabolism. In this review, we will highlight some of the key clinical findings, mainly from human studies, that investigated the role of ANGPTL8 in metabolic diseases such as diabetes, obesity, and the metabolic syndrome.


Amikacin (AMIK) is an aminoglycoside antibiotic that possesses considerable nephrotoxic adverse effects. This study examined the protective effects of vitamin E (VIT. E) or rosuvastatin (ROSU) against AMIK-induced nephrotoxicity. For this purpose, eight groups of rats were used. Two control groups received saline and vehicle, AMIK group (1.2 g/kg, i.p.), VIT. E group (1000 mg/kg; p.o.), ROSU group (10 mg/kg; p.o.), AMIK + VIT. E group, AMIK + ROSU group, and combination group. The results showed that AMIK significantly increased serum levels of urea and creatinine. Meanwhile, serum levels of total protein and albumin were decreased. The kidney content of malondialdehyde was increased, whereas glutathione content and catalase activity were decreased. Tumor necrosis factor-α and nuclear transcriptional factor levels were increased. Conversely, administration of VIT. E and/or ROSU with AMIK ameliorated such damage and reduced DNA fragmentation, apoptosis, and necrosis. In conclusion, co-administration of VIT. E, ROSU, or their combination alleviated AMIK-induced nephrotoxicity.


IL-17 Exerts Anti-Apoptotic Effect via miR-155-5p Downregulation in Experimental Autoimmune Encephalomyelitis

Posted by D Ksiazek-Winiarek, P Szpakowski, M Turniak, et al. on 2017-10-27 00:41:18


Multiple sclerosis is an autoimmune, neurodegenerative disease, affecting mostly young adults and resulting in progressive disability. It is a multifactorial disorder, with important involvement of both cellular and epigenetic components. Among the epigenetic factors, microRNAs are currently intensively investigated in the context of multiple sclerosis. It has been shown that their biogenesis and function may be regulated by various cytokines. IL-17, a hallmark cytokine of Th17 cells, has been thought to function predominantly as a pro-inflammatory factor, leading to increased disease symptoms. However, there are several studies indicating its protective role during inflammatory process. In this work, we have assessed the impact of high-dose IL-17 administration on microRNAs’ expression profile during the preclinical stage of EAE. For selected microRNA, we have performed computational analysis of its potential target mRNAs and cellular pathways. Based on results obtained from in silico analysis, we have chosen genes from neurotrophin signaling pathway for further experiments—BDNF, HRAS, and BCL2. Results obtained in this study suggested that high dose of IL-17 exerts protective activity via miR-155-5p downregulation. Increased expression of all studied genes, especially BCL2, indicated a potential anti-apoptotic function of IL-17 during the preclinical phase of EAE.

Effect of cardamonin on hepatic ischemia reperfusion induced in rats: Role of nitric oxide

Posted by Y Atef, H M.Ei-Fayoumi, M F.Mahmoud, et al. on 2017-10-19 18:51:41


Ischemia reperfusion (I/R) injury is a cellular damage in a hypoxic organ following the restoration of oxygen delivery. It may occur during organ transplantation, trauma and hepatectomies. Nitric oxide (NO) effects during hepatic I/R are complicated. The iNOS-derived NO has a deleterious effect, whereas eNOS-derived NO has a protective effect in liver I/R. Cardamonin (CDN) is an anti-inflammatory molecule and a novel iNOS inhibitor, and Nω-Nitro-L-arginine (L-NNA) is a NOS inhibitor. L-Arginine is a precursor of NOS. This study was designed to investigate the possible protective effects of CDN on hepatic I/R and the role of NO. Wistar rats were randomly divided into 5 groups (Sham, I/R, CDN, L-NNA and L-arginine). Liver ischemia was induced for 45 min then reperfusion was allowed for 1 h. L-Arginine and CDN ameliorated the deleterious effects of I/R through reducing the oxidative stress and hepatocyte degeneration. Both molecules decreased the elevated inflammatory cytokines and increased the antiapoptotic marker, Bcl2. Both agents increased NO and eNOS expression and decreased iNOS expression. In conclusion, increased NO/eNOS and suppression of iNOS expression have protective effects on I/R injury. While inhibition of eNOS and reduction of NO have deleterious effects on I/R injury. For the first time, we demonstrated that cardamonin improved functional and structural abnormalities of the liver following I/R by improving oxidative stress and inflammation and increasing the availability of NO produced by eNOS. Treatment with cardamonin could be a promising strategy in patients with hepatic I/R injury in different clinical situations.

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