The Root of Atractylodes macrocephala Koidzumi Prevents Obesity and Glucose Intolerance and Increases Energy Metabolism in Mice.
Mi Young SongSoo-Kyoung LimChang-Gue SonHojun KimPublished in: International journal of molecular sciences (2018)
Targeting energy expenditure offers a strategy for treating obesity more effectively and safely. In previous studies, we found that the root of Atractylodes macrocephala Koidzumi (Atractylodis Rhizoma Alba, ARA) increased energy metabolism in C2C12 cells. Here, we investigated the effects of ARA on obesity and glucose intolerance by examining energy metabolism in skeletal muscle and brown fat in high-fat diet (HFD) induced obese mice. ARA decreased body weight gain, hepatic lipid levels and serum total cholesterol levels, but did not modify food intake. Fasting serum glucose, serum insulin levels and glucose intolerance were all improved in ARA treated mice. Furthermore, ARA increased peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) expression, and the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) in skeletal muscle tissues, and also prevented skeletal muscle atrophy. In addition, the numbers of brown adipocytes and the expressions of PGC1α and uncoupling protein 1 (UCP1) were elevated in the brown adipose tissues of ARA treated mice. Our results show that ARA can prevent diet-induced obesity and glucose intolerance in C5BL/6 mice and suggests that the mechanism responsible is related to the promotion of energy metabolism in skeletal muscle and brown adipose tissues.
Keyphrases
- insulin resistance
- high fat diet induced
- skeletal muscle
- high fat diet
- adipose tissue
- blood glucose
- weight gain
- protein kinase
- glycemic control
- gene expression
- metabolic syndrome
- type diabetes
- body mass index
- birth weight
- high resolution
- weight loss
- drug delivery
- diabetic rats
- oxidative stress
- physical activity
- mass spectrometry
- mouse model
- signaling pathway
- cell cycle arrest
- cell proliferation
- fatty acid
- drug induced
- high glucose
- long non coding rna