M S Choi1, U J Jung, J Yeo, M J Kim, M K Lee. 1. Department of Food Science and Nutrition, Kyungpook National University, Daegu, 702-701, Republic of Korea.
Abstract
BACKGROUND: Non-obese diabetic (NOD) mice are regarded as being excellent animal models of human type 1 diabetes or insulin dependent diabetes (IDDM). This study investigated the beneficial effects of genistein and daidzein on IDDM, an autoimmune disease. METHODS: Female NOD mice were divided into control, genistein (0.02%, w/w) and daidzein (0.02%, w/w) groups. Blood glucose level, plasma biomarkers, hepatic glucose and lipid regulating enzyme activities and pancreas immunohistochemistry analysis were examined after a 9-week experimental period. RESULTS: Blood glucose levels of genistein and daidzein groups were 40 and 36% of control value at the end of study (9th week). The genistein and daidzein supplements increased insulin/glucagon ratio and C-peptide level with preservation of insulin staining beta-cell of pancreas in the NOD mice. In the liver, genistein and daidzein supplements resulted in lowering glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) activities, while increasing two lipogenic enzymes activities, malic enzyme and glucose-6-phosphate dehydrogenase (G6PD), compared to the control group. Significantly, genistein and daidzein supplementation lowered the activities of fatty acid beta-oxidation and carnitine palmitoyltransferase (CPT) in these mice. Genistein and daidzein also improved plasma triglyceride and free fatty acid (FFA) concentrations compared to the control group. CONCLUSIONS: These results suggest that genistein and daidzein play important roles in regulation of glucose homeostasis in type 1 diabetic mice by down-regulating G6Pase, PEPCK, fatty acid beta-oxidation and CPT activities, while up-regulating malic enzyme and G6PD activities in liver with preservation of pancreatic beta-cells. The supplementation of genistein and daidzein are seemingly helpful for preventing IDDM onset. 2007 John Wiley & Sons, Ltd
BACKGROUND:Non-obese diabetic (NOD) mice are regarded as being excellent animal models of human type 1 diabetes or insulin dependent diabetes (IDDM). This study investigated the beneficial effects of genistein and daidzein on IDDM, an autoimmune disease. METHODS: Female NOD mice were divided into control, genistein (0.02%, w/w) and daidzein (0.02%, w/w) groups. Blood glucose level, plasma biomarkers, hepatic glucose and lipid regulating enzyme activities and pancreas immunohistochemistry analysis were examined after a 9-week experimental period. RESULTS:Blood glucose levels of genistein and daidzein groups were 40 and 36% of control value at the end of study (9th week). The genistein and daidzein supplements increased insulin/glucagon ratio and C-peptide level with preservation of insulin staining beta-cell of pancreas in the NOD mice. In the liver, genistein and daidzein supplements resulted in lowering glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) activities, while increasing two lipogenic enzymes activities, malic enzyme and glucose-6-phosphate dehydrogenase (G6PD), compared to the control group. Significantly, genistein and daidzein supplementation lowered the activities of fatty acid beta-oxidation and carnitine palmitoyltransferase (CPT) in these mice. Genistein and daidzein also improved plasma triglyceride and free fatty acid (FFA) concentrations compared to the control group. CONCLUSIONS: These results suggest that genistein and daidzein play important roles in regulation of glucose homeostasis in type 1 diabeticmice by down-regulating G6Pase, PEPCK, fatty acid beta-oxidation and CPT activities, while up-regulating malic enzyme and G6PD activities in liver with preservation of pancreatic beta-cells. The supplementation of genistein and daidzein are seemingly helpful for preventing IDDM onset. 2007 John Wiley & Sons, Ltd
Authors: Ling Shi; Heather Harker Ryan; Emily Jones; Tiffany A Moore Simas; Alice H Lichtenstein; Qi Sun; Laura L Hayman Journal: J Nutr Date: 2013-12-31 Impact factor: 4.798