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      Plasma glutamine and glutamic acid are potential biomarkers for predicting diabetic retinopathy

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          Abstract

          Introduction

          Diabetic patients with a long disease duration usually accompanied complication such as diabetic retinopathy, but in some patients had no complication.

          Objectives

          We analyzed differences in plasma metabolites according to the presence or absence of diabetic retinopathy (DR) in type 2 diabetic (T2D) patients with disease duration ≥ 15 years.

          Methods

          A cohort of 183 T2D patients was established. Their biospecimens and clinical information were collected in accordance with the guidelines of the National Biobank of Korea, and the Korean Diabetes Association. DR phenotypes of the subjects were verified by ophthalmologic specialists. Plasma metabolites were analyzed using gas chromatography time-of-flight mass spectrometry and ultra-performance liquid chromatography–quadrupole time-of-flight mass spectrometry. And these results were analyzed using multivariate statistics.

          Results

          For metabolomic study, propensity score matched case and control subjects were chosen. Mean age of the subjects was 66.4 years and mean T2D duration was 22.2 years. Metabolomic identification revealed various carbohydrates, amino acids, and organic compounds that distinguished between age- and sex-matched non-diabetic controls and T2D subjects. Among these, glutamine and glutamic acid were suggested as the most distinctive metabolites for the presence of DR. Receiver operating characteristics curves showed an excellent diagnostic value of combined (AUC = 0.739) and the ratio (AUC = 0.742) of glutamine and glutamic acid for DR. And these results were consistent in validation analyses.

          Conclusion

          Our results imply that plasma glutamine, glutamic acid, and their ratio may be valuable as novel biomarkers for anticipating DR in T2D subjects.

          Electronic supplementary material

          The online version of this article (10.1007/s11306-018-1383-3) contains supplementary material, which is available to authorized users.

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          Most cited references18

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          Glutamine and glutamate--their central role in cell metabolism and function.

          Glucose is widely accepted as the primary nutrient for maintenance and promotion of cell function. However, we propose that the 5-carbon amino acids, glutamine and glutamate, should be considered to be equally important for maintenance and promotion of cell function. The functions of glutamine are many and include: substrate for protein synthesis, anabolic precursor for muscle growth, acid-base balance in the kidney, substrate for ureogenesis in the liver, substrate for hepatic and renal gluconeogenesis, an oxidative fuel for intestine and cells of the immune system, inter-organ nitrogen transport, precursor for neurotransmitter synthesis, precursor for nucleotide and nucleic acid synthesis and precursor for glutathione production. Many of these functions are connected to the formation of glutamate from glutamine. We propose that the unique properties regarding concentration and routes of metabolism of these amino acids allow them to be used for a diverse array of processes related to the specialized function of each of the glutamine utilizing cells. In this review we highlight the specialized aspects of glutamine/glutamate metabolism of different glutamine-utilizing cells and in each case relate key aspects of metabolism to cell function. Copyright 2002 John Wiley & Sons, Ltd.
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            Oral glutamine increases circulating glucagon-like peptide 1, glucagon, and insulin concentrations in lean, obese, and type 2 diabetic subjects.

            Incretin hormones, such as glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in meal-related insulin secretion. We previously demonstrated that glutamine is a potent stimulus of GLP-1 secretion in vitro. Our objective was to determine whether glutamine increases circulating GLP-1 and GIP concentrations in vivo and, if so, whether this is associated with an increase in plasma insulin. We recruited 8 healthy normal-weight volunteers (LEAN), 8 obese individuals with type 2 diabetes or impaired glucose tolerance (OB-DIAB) and 8 obese nondiabetic control subjects (OB-CON). Oral glucose (75 g), glutamine (30 g), and water were administered on 3 separate days in random order, and plasma concentrations of GLP-1, GIP, insulin, glucagon, and glucose were measured over 120 min. Oral glucose led to increases in circulating GLP-1 concentrations, which peaked at 30 min in LEAN (31.9 +/- 5.7 pmol/L) and OB-CON (24.3 +/- 2.1 pmol/L) subjects and at 45 min in OB-DIAB subjects (19.5 +/- 1.8 pmol/L). Circulating GLP-1 concentrations increased in all study groups after glutamine ingestion, with peak concentrations at 30 min of 22.5 +/- 3.4, 17.9 +/- 1.1, and 17.3 +/- 3.4 pmol/L in LEAN, OB-CON, and OB-DIAB subjects, respectively. Glutamine also increased plasma GIP concentrations but less effectively than glucose. Consistent with the increases in GLP-1 and GIP, glutamine significantly increased circulating plasma insulin concentrations. Glutamine stimulated glucagon secretion in all 3 study groups. Glutamine effectively increases circulating GLP-1, GIP, and insulin concentrations in vivo and may represent a novel therapeutic approach to stimulating insulin secretion in obesity and type 2 diabetes.
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              Consumption of sweetened beverages and intakes of fructose and glucose predict type 2 diabetes occurrence.

              The role of intakes of different sugars in the development of type 2 diabetes was studied in a cohort of 4,304 men and women aged 40-60 y and initially free of diabetes at baseline in 1967-1972. Food consumption data were collected using a dietary history interview covering the habitual diet during the previous year. The intakes of different sugars were calculated and divided in quartiles. During a 12-y follow-up, 177 incidents of type 2 diabetes cases were identified from a nationwide register. Combined intake of fructose and glucose was associated with the risk of type 2 diabetes but no significant association was observed for intakes of sucrose, lactose, or maltose. The relative risk between the highest and lowest quartiles of combined fructose and glucose intake was 1.87 (95% [CI] = 1.19, 2.93; P = 0.003). The corresponding relative risks between the extreme quartiles of consumption of food items contributing to sugar intakes were 1.69 (95% [CI] = 1.17, 2.43; P < 0.001) for sweetened berry juice and 1.67 (95% [CI] = 0.98, 2.87; P = 0.01) for soft drinks. Our findings support the view that higher intake of fructose and glucose and sweetened beverages may increase type 2 diabetes risk.
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                Author and article information

                Contributors
                jtwoomd@khmc.or.kr
                chlee123@konkuk.ac.kr
                Journal
                Metabolomics
                Metabolomics
                Metabolomics
                Springer US (New York )
                1573-3882
                1573-3890
                21 June 2018
                21 June 2018
                2018
                : 14
                : 7
                : 89
                Affiliations
                [1 ]ISNI 0000 0001 2171 7818, GRID grid.289247.2, Department of Endocrinology and Metabolism, , Kyung Hee University School of Medicine, ; 23 Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447 Republic of Korea
                [2 ]ISNI 0000 0004 0532 8339, GRID grid.258676.8, Department of Systems Biotechnology, , Konkuk University, ; 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029 Republic of Korea
                [3 ]ISNI 0000 0001 0357 1464, GRID grid.411231.4, Statistics Support Department, , Kyung Hee University Medical Center Medical Science Research Institute, ; Seoul, Republic of Korea
                [4 ]ISNI 0000 0001 2171 7818, GRID grid.289247.2, Department of Ophthalmology, , Kyung Hee University School of Medicine, ; Seoul, Republic of Korea
                Author information
                http://orcid.org/0000-0001-9201-0713
                Article
                1383
                10.1007/s11306-018-1383-3
                6013531
                29950956
                f3c92820-cd6b-4457-be21-9f004c476aa7
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 19 February 2018
                : 6 June 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100003625, Ministry of Health and Welfare;
                Award ID: HD14B1246
                Award ID: HC15C3364
                Award Recipient :
                Categories
                Original Article
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2018

                Molecular biology
                diabetes mellitus, type 2,diabetes complications,diabetic retinopathy,metabolomics,glutamine,glutamic acid

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