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      Carnosine Supplementation Improves Serum Resistin Concentrations in Overweight or Obese Otherwise Healthy Adults: A Pilot Randomized Trial

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          Abstract

          Adipokines play an important role in the regulation of glucose metabolism. We have previously shown that carnosine supplementation in overweight or obese non-diabetic individuals improves glucose metabolism but does not change adiponectin concentrations. However, its effect on other adipokines has not been investigated. Herein we further determined the effect of carnosine supplementation on serum adipsin, resistin and leptin. Twenty-two overweight or obese otherwise healthy adults were randomly assigned to receive either 2 g of carnosine ( n = 13) or identically looking placebo ( n = 9) for 12 weeks. Serum adipsin, leptin and resistin were analyzed using a bead-based multiplex assay. Carnosine supplementation decreased serum resistin concentrations compared to placebo (mean change from baseline: −35 ± 83 carnosine vs. 35 ± 55 ng/mL placebo, p = 0.04). There was a trend for a reduction in serum leptin concentrations after carnosine supplementation (−76 ± 165 ng/mL carnosine vs. 20 ± 28 ng/mL placebo, p = 0.06). The changes in leptin and resistin concentrations were inversely related to the change in concentration for urinary carnosine ( r = −0.72, p = 0.0002; r = −0.67, p = 0.0009, respectively), carnosine-propanal ( r = −0.56, p = 0.005; r = −0.63, p = 0.001, respectively) and carnosine-propanol ( r = −0.61, p = 0.002; r = −0.60, p = 0.002, respectively). There were no differences between groups in change in adipsin concentrations. Our findings show carnosine supplementation may normalize some, but not all, of the serum adipokine concentrations involved in glucose metabolism, in overweight and obese individuals. Further clinical trials with larger samples are needed to confirm these results.

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          Brain regulation of appetite and satiety.

          Interest in the control of feeding has increased as a result of the obesity epidemic and rising incidence of metabolic diseases. The brain detects alterations in energy stores and triggers metabolic and behavioral responses designed to maintain energy balance. Energy homeostasis is controlled mainly by neuronal circuits in the hypothalamus and brainstem, whereas reward and motivation aspects of eating behavior are controlled by neurons in limbic regions and the cerebral cortex. This article provides an integrated perspective on how metabolic signals emanating from the gastrointestinal tract, adipose tissue, and other peripheral organs target the brain to regulate feeding, energy expenditure, and hormones. The pathogenesis and treatment of obesity and abnormalities of glucose and lipid metabolism are discussed.
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            Adiponectin as a Biomarker of the Metabolic Syndrome

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              Histidine and carnosine delay diabetic deterioration in mice and protect human low density lipoprotein against oxidation and glycation.

              In vivo effects of histidine and carnosine against diabetic deterioration in diabetic Balb/cA mice were studied. Histidine and carnosine at 0.5, 1 g/l were added into drinking water. After 4 weeks intake of these agents, the content of histidine and carnosine in plasma, heart and liver significantly elevated (P < 0.05). The intake of these agents significantly decreased plasma glucose and fibronectin levels (P < 0.05); however, only 1 g/l histidine and carnosine treatments significantly increased insulin level (P < 0.05) in diabetic mice. Triglyceride level in heart and liver was dose-dependently reduced by histidine or carnosine treatments (P < 0.05); however, only 1 g/l histidine and carnosine treatments significantly reduced cholesterol level in heart and liver (P < 0.05). The administration of histidine or carnosine significantly enhanced catalase activity and decreased lipid oxidation levels in kidney and liver (P < 0.05); however, only 1 g/l histidine and carnosine treatments significantly increased glutathione peroxidase activity (P < 0.05). The increased interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in diabetic mice were significantly suppressed by the intake of histidine or carnosine (P < 0.05). In human low density lipoprotein, histidine or carnosine showed dose-dependently suppressive effect in glucose-induced oxidation and glycation (P < 0.05). These data suggest that histidine and carnosine are potential multiple-protective agents for diabetic complications prevention or therapy.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                07 September 2018
                September 2018
                : 10
                : 9
                : 1258
                Affiliations
                [1 ]Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria 3168, Australia; estifanos.baye@ 123456monash.edu (E.B.); aya.mousa@ 123456monash.edu (A.M.); josphin.johnson@ 123456monash.edu (J.J.)
                [2 ]Institute of Experimental Endocrinology, Biomedical Research Centre, Slovak Academy of Sciences, 84236 Bratislava, Slovakia; jozef.ukropec@ 123456gmail.com (J.U.); timea.kurdiova@ 123456savba.sk (T.K.); barbara.ukropcova@ 123456gmail.com (B.U.)
                [3 ]Centre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, Victoria 3800, Australia; Maximilian.deCourten@ 123456vu.edu.au
                [4 ]Department of Immunology and Pathology, Monash University, Melbourne, Victoria 3168, Australia; kirsty.wilson@ 123456monash.edu (K.W.); magdalena.plebanski@ 123456monash.edu (M.P.)
                [5 ]School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3001, Australia
                [6 ]Department of Pharmaceutical Sciences, Università degli Studi di Milano, 20133 Milan, Italy; giancarlo.aldini@ 123456unimi.it
                [7 ]Institute of Pathological Physiology, Faculty of Medicine, Comenius University, 84215 Bratislava, Slovakia
                Author notes
                [* ]Correspondence: barbora.decourten@ 123456monash.edu ; Tel.: +61-3-8572-2651
                Author information
                https://orcid.org/0000-0002-7356-4523
                Article
                nutrients-10-01258
                10.3390/nu10091258
                6165206
                30205427
                08a6bcc3-9f63-45bc-9a39-abf9f2a50d45
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 20 August 2018
                : 04 September 2018
                Categories
                Article

                Nutrition & Dietetics
                carnosine,adipokines,obesity,type 2 diabetes,cardiovascular disease
                Nutrition & Dietetics
                carnosine, adipokines, obesity, type 2 diabetes, cardiovascular disease

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