Ginsenoside Re Ameliorates Brain Insulin Resistance and Cognitive Dysfunction in High Fat Diet-Induced C57BL/6 Mice.
Jong Min KimChang Hyeon ParkSeon Kyeong ParkTae Wan SeungJin Yong KangJeong Su HaDu Sang LeeUk LeeDae-Ok KimHo-Jin HeoPublished in: Journal of agricultural and food chemistry (2017)
The ameliorating effects of ginsenoside Re (G Re) on high fat diet (HFD)-induced insulin resistance in C57BL/6 mice were investigated to assess its physiological function. In the results of behavioral tests, G Re improved cognitive dysfunction in diabetic mice using Y-maze, passive avoidance, and Morris water maze tests. G Re also significantly recovered hyperglycemia and fasting blood glucose level. In the results of serum analysis, G Re decreased triglyceride (TG), total cholesterol (TCHO), low-density lipoprotein cholesterol (LDLC), glutamic-oxaloacetic transaminase (GOT), and glutamic-pyruvic transaminase (GPT) and increased the ratio of high-density lipoprotein cholesterol (HDLC). G Re regulated acetylcholine (ACh), acetylcholinesterase (AChE), malondialdehyde (MDA), superoxide dismutase (SOD), and oxidized glutathione (GSH)/total GSH by regulating the c-Jun N-terminal protein kinase (JNK) pathway. These findings suggest that G Re could be used to improve HFD-induced insulin resistance condition by ameliorating hyperglycemia via protecting the cholinergic and antioxidant systems in the mouse brains.
Keyphrases
- insulin resistance
- high fat diet induced
- high fat diet
- blood glucose
- diabetic rats
- adipose tissue
- metabolic syndrome
- skeletal muscle
- glycemic control
- polycystic ovary syndrome
- type diabetes
- high glucose
- oxidative stress
- low density lipoprotein
- protein kinase
- cell death
- endothelial cells
- blood pressure
- signaling pathway
- resting state
- drug induced
- multiple sclerosis
- functional connectivity
- white matter
- mouse model
- anti inflammatory
- amyotrophic lateral sclerosis
- weight loss
- transcription factor
- stress induced