Antihyperglycemic and antioxidant properties of caffeic acid in db/db mice.
This study investigated the blood glucose-lowering effect and antioxidant capacity of caffeic acid in C57BL/KsJ-db/db mice. Caffeic acid induced a significant reduction of the blood glucose and glycosylated hemoglobin levels than the control group. The plasma insulin, C-peptide, and leptin levels in caffeic acid group were significantly higher than those of the control group, whereas the plasma glucagon level was lower. Increased plasma insulin by caffeic acid was attributable to an antidegenerative effect on the islets. Caffeic acid also markedly increased glucokinase activity and its mRNA expression and glycogen content and simultaneously lowered glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities and their respective mRNA expressions, accompanied by a reduction in the glucose transporter 2 expression in the liver. In contrast to the hepatic glucose transporter 2, adipocyte glucose transporter 4 expression was greater than the control group. In addition, caffeic acid significantly increased superoxide dismutase, catalase, and glutathione peroxidase activities and their respective mRNA levels, while lowering the hydrogen peroxide and thiobarbituric acid reactive substances levels in the erythrocyte and liver of db/db mice. These results indicate that caffeic acid exhibits a significant potential as an antidiabetic agent by suppressing a progression of type 2 diabetic states that is suggested by an attenuation of hepatic glucose output and enhancement of adipocyte glucose uptake, insulin secretion, and antioxidant capacity.
Jung
Un Ju
UJ
Institute of Genetic Engineering, Kyungpook National University, Daegu, Korea.
Lee
Mi-Kyung
MK
Park
Yong Bok
YB
Jeon
Seon-Min
SM
Choi
Myung-Sook
MS
D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015415:Biomarkers; D001786:Blood Glucose / Q000378:metabolism; D015152:Blotting, Northern; D015153:Blotting, Western; D002109:Caffeic Acids / Q000494:pharmacology*; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism*; D004032:Diet; D005943:Gluconeogenesis / Q000187:drug effects / Q000235:genetics; D051246:Glucose Transport Proteins, Facilitative / Q000096:biosynthesis; D006019:Glycolysis / Q000187:drug effects / Q000502:physiology; D006706:Homeostasis / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000378:metabolism; D007004:Hypoglycemic Agents; D007150:Immunohistochemistry; D007328:Insulin / Q000097:blood / Q000502:physiology; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress / Q000187:drug effects; D010179:Pancreas / Q000187:drug effects / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D015430:Weight Gain / Q000187:drug effects
D000975:Antioxidants; D015415:Biomarkers; D001786:Blood Glucose; D002109:Caffeic Acids; D051246:Glucose Transport Proteins, Facilitative; D007004:Hypoglycemic Agents; D007328:Insulin; D012333:RNA, Messenger; D006861:Hydrogen Peroxide; C040048:caffeic acid