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      Systematic review and meta-analysis of anti-hyperglycaemic effects of Pu-erh tea

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          Most cited references18

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          Primary, Secondary, and Meta-Analysis of Research

          G. GLASS (1976)
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            Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model.

            Sprague-Dawley rats fed a fructose-rich diet exhibit insulin resistance and hypertension, a pathologic status resembling human type II diabetes mellitus, and are an excellent laboratory animal model for research on insulin action and the development of hypertension. Since green tea has numerous beneficial effects, we tested its effect on fructose-fed rats. The present study was therefore designed to further evaluate the effects of green tea supplementation on insulin resistance, hypertension, and the glucose transporters I and IV contents in adipose tissue in the fructose-fed rat model. The animals were divided into three groups and fed for 12 weeks with standard chow and water (control group), a high fructose diet and water (fructose group), or the same high fructose diet, but with green tea (0.5 g of lyophilized green tea powder dissolved in 100 mL of deionized distilled water) instead of water (fructose/green tea group). During the 12 weeks study period, fresh water or green tea was provided daily at 6:00 PM. Blood pressure was measured twice a week, and an oral glucose tolerance test performed after 12 weeks of diet supplementation. At the end of the experiment, plasma triglyceride (TG), free fatty acid (FFA), glucose, and insulin were assayed. The epididymal fat pads from all rats in the same group were pooled and adipocytes isolated and tested for insulin binding, glucose uptake, and their content of glucose transporters I (GLUT I) and IV (GLUT IV). Compared to the control group, the fructose group developed fasting hyperglycemia, hyperinsulinemia, and elevated blood pressure. Insulin-stimulated glucose uptake and insulin binding of adipocytes were significantly reduced, and the glucose transporter IV content of adipocytes also decreased. The fructose/green tea group showed improvement in all of these metabolic defects and in insulin resistance and blood pressure. Based on these results, we suggest that the amelioration of insulin resistance by green tea is associated with the increased expression of GLUT IV.
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              Involvement of the PI3K/Akt signal pathway in the hypoglycemic effects of tea polysaccharides on diabetic mice

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                Author and article information

                Contributors
                Journal
                International Journal of Food Science & Technology
                Int J Food Sci Technol
                Wiley
                09505423
                February 2019
                February 2019
                October 23 2018
                : 54
                : 2
                : 516-525
                Affiliations
                [1 ]Department of Healthcare Administration; Asia University; Taiwan No.500, Lioufeng Rd. Wufeng Taichung 41354 Taiwan
                [2 ]Taichung Armed Forces General Hospital, Taichung; Taiwan No.348, Sec. 2, Zhongshan Rd., Taiping Dist. Taichung City 411 Taiwan
                [3 ]National Defense Medical Center, Taipei; Taiwan No.161, Sec. 6, Minquan E. Rd., Neihu Dist. Taipei City 11490 Taiwan
                [4 ]Tsaotun psychiatric center ministry of Health and Welfare, Nantou; Taiwan No.161, Yuping Rd., Caotun Township Nantou County 542 Taiwan
                [5 ]Department of Oral Hygiene; College of Dental Medicine; Kaohsiung Medical University; Taiwan No.100, Shih-Chuan 1st Road Kaohsiung 80708 Taiwan
                [6 ]Department of Long Term Care; National Quemoy University, Kinmen County; Taiwan No. 1, University Rd., Jinning Township Kinmen County 892 Taiwan
                [7 ]Department of Medical Research; China Medical University Hospital; China Medical University, Taichung; Taiwan No.91, Hsueh-Shih Road Taichung 40402 Taiwan
                Article
                10.1111/ijfs.13966
                d25efdde-2b91-473e-9319-e08db870c095
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://creativecommons.org/licenses/by/4.0/

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