Source:http://linkedlifedata.com/resource/pubmed/id/18080810
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4-6
|
pubmed:dateCreated |
2008-6-19
|
pubmed:abstractText |
In the present study, we investigated the mechanism(s) for glucose-lowering action of andrographolide in streptozotocin-induced diabetic rats (STZ-diabetic rats). Andrographolide lowered plasma glucose concentrations in a dose-dependent manner and increased plasma beta-endorphin-like immunoreactivity (BER) dose-dependently in diabetic rats. Both of these responses to andrographolide were abolished by the pretreatment of animals with prazosin or N-(2-(2-cyclopropylmethoxy) ethyl) 5-choro-alpha-dimethyl-1H-indole-3-thylamine (RS17053) at doses sufficient to block alpha1-adrenoceptors (ARs). Also, andrographolide enhanced BER release from isolated rat adrenal medulla in a concentration-related manner that could be abolished by alpha1-ARs antagonists. Bilateral adrenalectomy in STZ-diabetic rats eliminated the activities of andrographolide, including the plasma glucose-lowering effect and the plasma BER-elevating effect. Andrographolide failed to lower plasma glucose in the presence of opioid micro-receptor antagonists and in the opioid micro-receptor knockout diabetic mice. Treatment of STZ-diabetic rats with andrographolide resulted in the reduced expression of phosphoenolpyruvate carboxykinase (PEPCK) in liver and an increased expression of the glucose transporter subtype 4 (GLUT 4) in soleus muscle. These effects were also blocked by opioid micro-receptor antagonists. In conclusion, our results suggest that andrographolide may activate alpha1-ARs to enhance the secretion of beta-endorphin which can stimulate the opioid micro-receptors to reduce hepatic gluconeogenesis and to enhance the glucose uptake in soleus muscle, resulting in a decrease of plasma glucose in STZ-diabetic rats. However, the roles of other endogenous opioid peptides or the mixture of several opioid peptides in the activation of opioid micro-receptors associated with the plasma glucose-lowering action of andrographolide, should be considered and need more investigation in the future.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Diterpenes,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 4,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoglycemic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu,
http://linkedlifedata.com/resource/pubmed/chemical/Streptozocin,
http://linkedlifedata.com/resource/pubmed/chemical/andrographolide,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Endorphin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
0028-1298
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
377
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
529-40
|
pubmed:meshHeading |
pubmed-meshheading:18080810-Animals,
pubmed-meshheading:18080810-Blood Glucose,
pubmed-meshheading:18080810-Diabetes Mellitus, Experimental,
pubmed-meshheading:18080810-Diabetes Mellitus, Type 1,
pubmed-meshheading:18080810-Diterpenes,
pubmed-meshheading:18080810-Dose-Response Relationship, Drug,
pubmed-meshheading:18080810-Gene Expression Regulation,
pubmed-meshheading:18080810-Glucose Transporter Type 4,
pubmed-meshheading:18080810-Hypoglycemic Agents,
pubmed-meshheading:18080810-Liver,
pubmed-meshheading:18080810-Male,
pubmed-meshheading:18080810-Mice,
pubmed-meshheading:18080810-Mice, Knockout,
pubmed-meshheading:18080810-Muscle, Skeletal,
pubmed-meshheading:18080810-Rats,
pubmed-meshheading:18080810-Rats, Wistar,
pubmed-meshheading:18080810-Receptors, Opioid, mu,
pubmed-meshheading:18080810-Streptozocin,
pubmed-meshheading:18080810-beta-Endorphin
|
pubmed:year |
2008
|
pubmed:articleTitle |
Mediation of beta-endorphin in andrographolide-induced plasma glucose-lowering action in type I diabetes-like animals.
|
pubmed:affiliation |
Institute of Basic Medical Science, and Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan, 70101, Republic of China.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|