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      Interleukin-18 and testosterone levels in men with metabolic syndrome

      1 , 1 , 2 , 3 , 4

      The Aging Male

      Informa UK Limited

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          Most cited references 55

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          The metabolic syndrome—a new worldwide definition

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            Cloning of a new cytokine that induces IFN-gamma production by T cells.

            The mechanism underlying the differentiation of CD4+ T cells into functionally distinct subsets (Th1 and Th2) is incompletely understood, and hitherto unidentified cytokines may be required for the functional maturation of these cells. Here we report the cloning of a recently identified IFN-gamma-inducing factor (IGIF) that augments natural killer (NK) activity in spleen cells. The gene encodes a precursor protein of 192 amino acids and a mature protein of 157 amino acids, which have no obvious similarities to any peptide in the databases. Messenger RNAs for IGIF and interleukin-12 (IL-12) are readily detected in Kupffer cells and activated macrophages. Recombinant IGIF induces IFN-gamma more potently than does IL-12, apparently through a separate pathway. Administration of anti-IGIF antibodies prevents liver damage in mice inoculated with Propionibacterium acnes and challenged with lipopolysaccharide, which induces toxic shock. IGIF may be involved in the development of Th1 cells and also in mechanisms of tissue injury in inflammatory reactions.
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              Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress.

              Circulating levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) are elevated in diabetic patients. We assessed the role of glucose in the regulation of circulating levels of IL-6, TNF-alpha, and interleukin-18 (IL-18) in subjects with normal or impaired glucose tolerance (IGT), as well as the effect of the antioxidant glutathione. Plasma glucose levels were acutely raised in 20 control and 15 IGT subjects and maintained at 15 mmol/L for 5 hours while endogenous insulin secretion was blocked with octreotide. In control subjects, plasma IL-6, TNF-alpha, and IL-18 levels rose (P<0.01) within 2 hours of the clamp and returned to basal values at 3 hours. In another study, the same subjects received 3 consecutive pulses of intravenous glucose (0.33 g/kg) separated by a 2-hour interval. Plasma cytokine levels obtained at 3, 4, and 5 hours were higher (P<0.05) than the corresponding values obtained during the clamp. The IGT subjects had fasting plasma IL-6 and TNF-alpha levels higher (P<0.05) than those of control subjects. The increase in plasma cytokine levels during the clamping lasted longer (4 hours versus 2 hours, P<0.01) in the IGT subjects than in the control subjects, and the cytokine peaks of IGT subjects after the first glucose pulse were higher (P<0.05) than those of control subjects. On another occasion, 10 control and 8 IGT subjects received the same glucose pulses as above during an infusion of glutathione; plasma cytokine levels did not show any significant change from baseline after the 3 glucose pulses. Hyperglycemia acutely increases circulating cytokine concentrations by an oxidative mechanism, and this effect is more pronounced in subjects with IGT. This suggests a causal role for hyperglycemia in the immune activation of diabetes.
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                Author and article information

                Journal
                The Aging Male
                The Aging Male
                Informa UK Limited
                1368-5538
                1473-0790
                November 07 2017
                November 23 2017
                April 03 2018
                : 21
                : 2
                : 130-137
                Affiliations
                [1 ] Clinic of Endocrinology, Alexandrovska University Hospital, Medical University-Sofia, Sofia, Bulgaria;
                [2 ] Central Clinical Laboratory, Alexandrovska University Hospital, Medical University-Sofia, Sofia, Bulgaria;
                [3 ] Laboratory of Tumor Immunology and Immunotherapy, Hyogo College of Medicine, Hyogo, Japan;
                [4 ] Laboratory of Host Defense, Hyogo College of Medicine, Hyogo, Japan
                Article
                10.1080/13685538.2017.1401993
                © 2018

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