title: Matcha, a powdered green tea, ameliorates the progression of renal and hepatic damage in type 2 diabetic OLETF rats.
abstract: Matcha, a powdered green tea produced by grinding with a stone mill, has been popularly used in the traditional tea ceremony and foods in Japan. Matcha is well known to be richer in some nutritional elements and epigallocatechin 3-O-gallate than other green teas. In our previous study, epigallocatechin 3-O-gallate exhibited protective effects against renal damage in a rat model of diabetic nephropathy. In the present study, we investigated the preventive effects of Matcha (50, 100, or 200 mg/kg/day) on the progression of hepatic and renal damage in type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. OLETF rats were orally administered Matcha for 16 weeks, and we assessed biochemical parameters in the serum, liver, and kidney and expression levels of major products of advanced glycation end products (AGEs), N(6)-(carboxylmethyl)lysine (CML) and N(6)-(carboxylethyl)lysine (CEL), receptor for AGE (RAGE), and sterol regulatory element binding proteins (SREBPs)-1 and -2. Serum total protein levels were significantly increased by Matcha administration, whereas the serum albumin and glycosylated protein levels as well as the renal glucose and triglyceride levels were only slightly or not at all affected. However, Matcha treatment significantly lowered the glucose, triglyceride, and total cholesterol levels in the serum and liver, renal AGE levels, and the serum thiobarbituric acid-reactive substances levels. In addition, Matcha supplementation resulted in decreases in the renal CML, CEL, and RAGE expressions as well as an increase in hepatic SREBP-2 expression, but not that of SREBP-1. These results suggest that Matcha protects against hepatic and renal damage through the suppression of renal AGE accumulation, by decreases in hepatic glucose, triglyceride, and total cholesterol levels, and by its antioxidant activities.
authors.affiliation: Institute of Natural Medicine, University of Toyama, Toyama, Japan.
authors.forename: Noriko
authors.initials: N
authors.lastname: Yamabe
authors.forename: Ki Sung
authors.initials: KS
authors.lastname: Kang
authors.forename: Jong Moon
authors.initials: JM
authors.lastname: Hur
authors.forename: Takako
authors.initials: T
authors.lastname: Yokozawa
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D028241:Camellia sinensis; D002784:Cholesterol / Q000378:metabolism; D048909:Diabetes Complications / Q000188:drug therapy* / Q000503:physiopathology; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D008239:Lysine / Q000031:analogs & derivatives / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use*; D011208:Powders; D051381:Rats; D020334:Rats, Inbred OLETF; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism; D051782:Sterol Regulatory Element Binding Protein 2 / Q000378:metabolism; D013662:Tea; D013858:Thiobarbiturates / Q000097:blood; D014280:Triglycerides / Q000378:metabolism
chemical_list: D015415:Biomarkers; D001798:Blood Proteins; D017127:Glycation End Products, Advanced; D010936:Plant Extracts; D011208:Powders; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D012709:Serum Albumin; D051782:Sterol Regulatory Element Binding Protein 2; D013662:Tea; D013858:Thiobarbiturates; D014280:Triglycerides; C048496:N(6)-carboxymethyllysine; D002784:Cholesterol; D005947:Glucose; D008239:Lysine; C029684:thiobarbituric acid