Activity, Motor Control & Coordination
Pain - Thermal Allodynia / Hyperalgesia
Pain - Spontaneous Pain - Postural Deficit
Pain - Mechanical Allodynia / Hyperalgesia
Anxiety & Depression Disorder
Learning/Memory - Attention - Addiction
Physiology & Respiratory Research
Metabolism - Food & Drink Intake
Pain
Metabolism
Motor control
Neurodegeneration
Cross-disciplinary subjects
Muscular system
General activity
Mood Disorders
Other disorders
Joints
Central Nervous System (CNS)
Sensory system
Authors
D Xu, X Huang, HM Hassan, L Wang, S Li, Z Jiang
Lab
China Pharmaceutical University, Jiangsu Key Laboratory of Drug Screening, Nanjing, China
Journal
Applied Physiology, Nutrition, and Metabolism
Abstract
Type 2 diabetes mellitus is a major health problem and a societal burden. Individuals with pre-diabetes are at increased risk of type 2 diabetes mellitus. Catalpol, an iridoid glycoside, has been reported to exert a hypoglycaemic effect in db/db mice, but its effect on the progression of pre-diabetes is unclear. In this study, we established a mouse model of pre-diabetes and examined the hypoglycaemic effect, and the mechanism of any such effect, of catalpol. Catalpol (200 mg/kg/day) had no effect on glucose tolerance or the serum lipid level in a mouse model of impaired glucose tolerance (IGT)-stage pre-diabetes. However, catalpol (200 mg/kg/day) increased insulin sensitivity and decreased the fasting glucose level in a mouse model of impaired fasting glucose/impaired glucose tolerance-stage pre-diabetes. Moreover, catalpol increased the mitochondrial membrane potential (1.52-fold) and ATP content (1.87-fold) in skeletal muscle and improved skeletal muscle function. These effects were mediated by activation of the IRS-1/GLUT4 signalling pathway in skeletal muscle. Our findings will facilitate the development of a novel approach to suppressing the progression of diabetes at an early stage.
BIOSEB Instruments Used:
Grip strength test (BIO-GS3)
