title: Supplementation of persimmon leaf ameliorates hyperglycemia, dyslipidemia and hepatic fat accumulation in type 2 diabetic mice.
abstract: Persimmon Leaf (PL), commonly consumed as herbal tea and traditional medicines, contains a variety of compounds that exert antioxidant, α-amylase and α-glucosidase inhibitory activity. However, little is known about the in vivo effects and underlying mechanisms of PL on hyperglycemia, hyperlipidemia and hepatic steatosis in type 2 diabetes. Powered PL (5%, w/w) was supplemented with a normal diet to C57BL/KsJ-db/db mice for 5 weeks. PL decreased blood glucose, HOMA-IR, plasma triglyceride and total cholesterol levels, as well as liver weight, hepatic lipid droplets, triglycerides and cholesterol contents, while increasing plasma HDL-cholesterol and adiponectin levels. The anti-hyperglycemic effect was linked to decreased activity of gluconeogenic enzymes as well as increased glycogen content, glucokinase activity and its mRNA level in the liver. PL also led to a decrease in lipogenic transcriptional factor PPARγ as well as gene expression and activity of enzymes involved in lipogenesis, with a simultaneous increase in fecal lipids, which are seemingly attributable to the improved hyperlipidemia and hepatic steatosis and decreased hepatic fatty acid oxidation. Furthermore, PL ameliorated plasma and hepatic oxidative stress. Supplementation with PL may be an effective dietary strategy to improve type 2 diabetes accompanied by dyslipidemia and hepatic steatosis by partly modulating the activity or gene expression of enzymes related to antioxidant, glucose and lipid homeostasis.
authors.affiliation: Department of Food Science and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
authors.forename: Un Ju
authors.initials: UJ
authors.lastname: Jung
authors.forename: Yong Bok
authors.initials: YB
authors.lastname: Park
authors.forename: Sang Ryong
authors.initials: SR
authors.lastname: Kim
authors.forename: Myung-Sook
authors.initials: MS
authors.lastname: Choi
mesh_terms: D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001786:Blood Glucose / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D019587:Dietary Supplements; D029788:Diospyros; D050171:Dyslipidemias / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D005234:Fatty Liver / Q000235:genetics / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects / Q000235:genetics; D005941:Glucokinase / Q000235:genetics / Q000378:metabolism; D006003:Glycogen / Q000235:genetics / Q000378:metabolism; D006943:Hyperglycemia / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics; D050155:Lipogenesis / Q000187:drug effects / Q000235:genetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D008517:Phytotherapy / Q000379:methods*; D018515:Plant Leaves; D028321:Plant Preparations / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D014280:Triglycerides / Q000097:blood / Q000235:genetics / Q000378:metabolism
chemical_list: D052242:Adiponectin; D000975:Antioxidants; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D047495:PPAR gamma; D028321:Plant Preparations; D012333:RNA, Messenger; D014280:Triglycerides; D006003:Glycogen; D002784:Cholesterol; D005941:Glucokinase