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      Antidiabetic and Beta Cell-Protection Activities of Purple Corn Anthocyanins

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          Abstract

          Antidiabetic and beta cell-protection activities of purple corn anthocyanins (PCA) were examined in pancreatic beta cell culture and db/db mice. Only PCA among several plant anthocyanins and polyphenols showed insulin secretion activity in culture of HIT-T15 cells. PCA had excellent antihyperglycemic activity (in terms of blood glucose level and OGTT) and HbA1c-decreasing activity when compared with glimepiride, a sulfonylurea in db/db mice. In addition, PCA showed efficient protection activity of pancreatic beta cell from cell death in HIT-T15 cell culture and db/db mice. The result showed that PCA had antidiabetic and beta cell-protection activities in pancreatic beta cell culture and db/db mice.

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          Dietary cyanidin 3-O-beta-D-glucoside-rich purple corn color prevents obesity and ameliorates hyperglycemia in mice.

          Takanori Tsuda, Fumihiko Horio, Koji Uchida … (2003)
          Anthocyanins, which are used as a food coloring, are widely distributed in human diets, suggesting that we ingest large amounts of anthocyanins from plant-based foods. Mice were fed control, cyanidin 3-glucoside-rich purple corn color (PCC), high fat (HF) or HF + PCC diet for 12 wk. Dietary PCC significantly suppressed the HF diet-induced increase in body weight gain, and white and brown adipose tissue weights. Feeding the HF diet markedly induced hypertrophy of the adipocytes in the epididymal white adipose tissue compared with the control group. In contrast, the induction did not occur in the HF + PCC group. The HF diet induced hyperglycemia, hyperinsulinemia and hyperleptinemia. These perturbations were completely normalized in rats fed HF + PCC. An increase in the tumor necrosis factor (TNF)-alpha mRNA level occurred in the HF group and was normalized by dietary PCC. These results suggest that dietary PCC may ameliorate HF diet-induced insulin resistance in mice. PCC suppressed the mRNA levels of enzymes involved in fatty acid and triacylglycerol synthesis and lowered the sterol regulatory element binding protein-1 mRNA level in white adipose tissue. These down-regulations may contribute to triacylglycerol accumulation in white adipose tissue. Our findings provide a biochemical and nutritional basis for the use of PCC or anthocyanins as a functional food factor that may have benefits for the prevention of obesity and diabetes.
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            Insulin secretion by bioactive anthocyanins and anthocyanidins present in fruits.

            Bolleddula Jayaprakasam, Shaiju Vareed, L. Olson … (2005)
            Anthocyanins are responsible for a variety of bright colors including red, blue, and purple in fruits, vegetables, and flowers and are consumed as dietary polyphenols. Anthocyanin-containing fruits are implicated in a decrease in coronary heart disease and are used in antidiabetic preparations. In the present study, we have determined the ability of anthocyanins, cyanidin-3-glucoside (1), delphinidin-3-glucoside (2), cyanidin-3-galactoside (3), and pelargonidin-3-galactoside (4), and anthocyanidins, cyanidin (5), delphinidin (6), pelargonidin (7), malvidin (8), and petunidin (9), to stimulate insulin secretion from rodent pancreatic beta-cells (INS-1 832/13) in vitro. The compounds were tested in the presence of 4 and 10 mM glucose concentrations. Our results indicated that 1 and 2 were the most effective insulin secretagogues among the anthocyanins and anthocyanidins tested at 4 and 10 mM glucose concentrations. Pelargonidin-3-galactoside is one of the major anthocyanins, and its aglycone, pelargonidin, caused a 1.4-fold increase in insulin secretion at 4 mM glucose concentration. The rest of the anthocyanins and anthocyanidins tested in our assay had only marginal effects on insulin at 4 and 10 mM glucose concentrations.
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              Sulfonylurea induced beta-cell apoptosis in cultured human islets.

              Kathrin Maedler, Richard Carr, Domenico Bosco … (2005)
              Loss of beta-cell mass and function raises a concern regarding the application of sulfonylureas for the treatment of type 2 diabetes because previous studies have shown that agents that cause closure of inwardly rectifying K(+) sulfonylurea receptor subtype of ATP-sensitive potassium channels, such as tolbutamide and glibenclamide, induce apoptosis in beta-cell lines and rodent islets. Therefore, we investigated the effect of the new insulin secretagogues, repaglinide and nateglinide, and the sulfonylurea, glibenclamide, on beta-cell apoptosis in human islets. Human islets from six organ donors were cultured onto extracellular matrix-coated plates and exposed to glibenclamide, repaglinide, or nateglinide. The doses of the three compounds were chosen according to detected maximal effects, i.e. efficacy. Exposure of human islets for 4 h to 0.1 and 10 microm glibenclamide induced a 2.09- and 2.46-fold increase in beta-cell apoptosis, respectively, whereas repaglinide (0.01 and 1 microm) did not change the number of apoptotic beta-cells. At low concentration (10 microm), nateglinide did not induce beta-cell apoptosis. However, at high concentration of 1000 microm, it induced a 1.49-fold increase in the number of apoptotic beta-cells. Prolonged exposure for 4 d of the islets to the secretagogues induced beta-cell apoptosis. The increase was of 3.71- and 4.4-fold at 0.1 and 10 microm glibenclamide, 2.37- and 3.8-fold at 0.01 and 1 microm repaglinide, and of 3.2- and 4.6-fold at 10 and 1000 microm nateglinide, respectively. Glibenclamide at 0.1-10 nm (doses that were less efficient on insulin secretion) did not induce beta-cell apoptosis after 4 h incubation as well as 0.1 nm after 4 d incubation. However, 1 and 10 nm glibenclamide for 4 d induced a 2.24- and 2.53-fold increase in beta-cell apoptosis, respectively. Taken together, closure of the inwardly rectifying K(+) sulfonylurea receptor subtype of ATP-sensitive potassium channels induces beta-cell apoptosis in human islets and may precipitate the decrease in beta-cell mass observed in patients with type 2 diabetes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomol Ther (Seoul)
                Journal ID (iso-abbrev): Biomol Ther (Seoul)
                Journal ID (publisher-id): ksp
                Title: Biomolecules & Therapeutics
                Publisher: The Korean Society of Applied Pharmacology
                ISSN (Print): 1976-9148
                ISSN (Electronic): 2005-4483
                Publication date (Print): 30 July 2013
                Volume: 21
                Issue: 4
                Pages: 284-289
                Affiliations
                [1 ]Department of Biochemistry, College of Medicine, Hallym University
                [2 ]Institute of Natural Medicine, College of Medicine, Hallym University
                [3 ]FrontBio Inc., Chuncheon 200-702,
                [4 ]S&D Co., Ltd, Sejong 339-820
                [5 ]Department of Agricultural, Food and Nutritional Science, University of Alberta, Canada T6G 2P5
                [6 ]Department of Fruit, Vegetable and Cereal Technology, Wroclaw University of Environmental and Life Sciences, Wroclaw 51-630, Poland
                [7 ]Department of Internal Medicine, Chuncheon Sacred Heart Hospital/Hallym University Medical Center, Chuncheon 200-704
                [8 ]Department of Food and Nutrition, College of Natural Sciences, Hallym University, Chuncheon 200-702, Republic of Korea
                [9 ]Department of Pharmacology, College of Medicine, Hallym University, Chuncheon 200-702, Republic of Korea
                [10 ]Institute of Cell Differentiation and Aging, College of Medicine, Hallym University, Chuncheon 200-702, Republic of Korea
                Author notes
                [* ]Corresponding Author E-mail: jyolee@ 123456hallym.ac.kr Tel: +82-33-248-2540, Fax: +82-33-244-8425
                The first two authors contributed equally to this work.
                Article
                Publisher ID: ooomb4-21-284
                DOI: 10.4062/biomolther.2013.016
                PMC ID: 3819901
                PubMed ID: 24244813
                SO-VID: 5f2a1ed3-275f-46c8-9d00-8b51b535ca1c
                Copyright © Copyright ©2013, The Korean Society of Applied Pharmacology
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 07 February 2013
                Date revision received : 15 May 2013
                Date accepted : 18 June 2013
                Categories
                Subject: Articles

                Keywords: antidiabetes,purple corn anthocyanins,beta cell-protection,antihyperglycemic activity,pancreatic beta cell,db/db mice
                Data availability:
                Keywords: antidiabetes, purple corn anthocyanins, beta cell-protection, antihyperglycemic activity, pancreatic beta cell, db/db mice

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