The plasma glucose lowering action of tetrandrine in streptozotocin-induced diabetic rats

Chen, Wang-Chuan; Hayakawa, Satoshi; Yamamoto, Tatsuo; Huang, Lee-Wen; Liu, I-Min

doi:10.1211/0022357023330

Cited by 17 publications

(10 citation statements)

References 25 publications

(26 reference statements)

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“…In the present study, we found that tetrandrine can dose-dependently increase the plasma BER in STZ-diabetic rats in a manner parallel to the lowering of plasma glucose as mentioned in our previous report (11). In STZ-diabetic rats, the deficiency of insulin has been documented (20).…”

Section: Discussionsupporting

confidence: 90%

“…Reduction in insulin-mediated glucose uptake resulting from decreased expression of GLUT4 mRNA and protein in diabetes has been reported (33). In a previous study, we found that the plasma glucose-lowering activity of tetrandrine was associated with the enhancement of glucose uptake and glycogen synthesis in STZ-diabetic rats (11). Moreover, we have demonstrated that endogenous β-endorphin via the activation of the opioid μ-receptors is a positive regulator of glucose utilization and a negative modulator of hepatic gluconeogenesis in the insulin deficient state (19,22).…”

Section: Discussionmentioning

confidence: 92%

“…Moreover, tetrandrine has been shown to prevent the development of spontaneous diabetes in BioBreeding rats (9) and protect pancreatic islet beta cells from the injuries caused by alloxan (10). In addition, we have observed that tetrandrine has the ability to improve glucose utilization in streptozotocin-induced diabetic rats (STZ-diabetic rats), the type 1 diabetes-like animal model (11). These results indicate that tetrandrine seems helpful in the prevention and/or management of diabetes.…”

Section: Introductionmentioning

confidence: 99%

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Mediation of Endogenous β‐Endorphin by Tetrandrine to Lower Plasma Glucose in Streptozotocin‐Induced Diabetic Rats

Hsu

Liou

et al. 2004

Evidence-Based Complementary and Alternative Medicine

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The role of β-endorphin in the plasma glucose-lowering action of tetrandrine in streptozotocin-induced diabetic rats (STZ-diabetic rats) was investigated. The plasma glucose concentration was assessed by the glucose oxidase method. The enzyme-linked immunosorbent assay was used to determine the plasma level of β-endorphin-like immunoreactivity (BER). The mRNA levels of glucose transporter subtype 4 (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver of STZ-diabetic rats were detected by Northern blotting analysis. The expressed protein of GLUT4 or PEPCK was characterized by Western blotting analysis. Tetrandrine dose-dependently increased plasma BER in a manner parallel to the decrease of plasma glucose in STZ-diabetic rats. Moreover, the plasma glucose-lowering effect of tetrandrine was inhibited by naloxone and naloxonazine at doses sufficient to block opioid μ-receptors. Further, tetrandrine failed to produce plasma glucose-lowering action in opioid μ-receptor knockout diabetic mice. Bilateral adrenalectomy eliminated the plasma glucose-lowering effect and plasma BER-elevating effect of tetrandrine in STZ-diabetic rats. Both effects were abolished by treatment with hexamethonium or pentolinium at doses sufficient to block nicotinic receptors. Tetrandrine enhanced BER release directly from the isolated adrenal medulla of STZ-diabetic rats and this action was abolished by the blockade of nicotinic receptors. Repeated intravenous administration of tetrandrine (1.0 mg/kg) to STZ-diabetic rats for 3 days resulted in an increase in the mRNA and protein levels of the GLUT4 in soleus muscle, in addition to the lowering of plasma glucose. Similar treatment with tetrandrine reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. The obtained results suggest that tetrandrine may induce the activation of nicotinic receptors in adrenal medulla to enhance the secretion of β-endorphin, which could stimulate opioid μ-receptors to increase glucose utilization or/and reduce hepatic gluconeogenesis to lower plasma glucose levels in STZ-diabetic rats.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Mediation of Endogenous β‐Endorphin by Tetrandrine to Lower Plasma Glucose in Streptozotocin‐Induced Diabetic Rats

Hsu

Liou

et al. 2004

Evidence-Based Complementary and Alternative Medicine

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“…Although aporphine alkaloids are not known to have hypoglycemic effects, other isoquinoline alkaloids, such as tetrandrine, fangchinoline, and berberine, have been shown to be effective in the treatment of diabetes (Lieberman et al, 1992;Pan et al, 2003;Tsutsumi et al, 2003;Chen et al, 2004). Tetrandrine and its 7-Odemethylated analog, fangchinoline, are bisbenzylisoquinoline alkaloids.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of intestinal glucose uptake by aporphines and secoaporphines

et al. 2006

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“…Tetrandrine has been used for the treatment of hypertension, cardiac arrhythmia, angina, diabetes and inflammation (Iturriaga‐Vasquez et al . 2003; Chen et al . 2004).…”

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confidence: 99%

Effect of Tetrandrine on Calcium‐Dependent Tumour Necrosis Factor‐α Production in Glia‐Neurone Mixed Cultures

Wang

Yang

Yan

et al. 2005

Basic Clin Pharma Tox

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Tumour necrosis factor-a is believed to have a deleterious role in the pathophysiology of brain injury. Tetrandrine has protective effect on neuronal cells, however, the mechanisms involved in its action have not been clearly established. The aim of this study was to investigate the role of tetrandrine on calcium-dependent tumour necrosis factor-a production in glia-neurone mixed cultures. Glia-neurone mixed cultures were treated by addition of Ca 2π regulating agents for a period of 6 hr. Tetrandrine or/and TMB-8 were added 30 min. before the stimulation. The supernatant tumour necrosis factor-a levels were quantified by enzyme-linked immunosorbent assay. Exposure of lipopolysaccharide 10 and 100 ng/ml caused significant increase in tumour necrosis factor-a production respectively, with no alteration in cultures treated with 1 ng/ml lipopolysaccharide. Glia-neurone mixed cultures exhibited a marked elevation in tumour necrosis factor-a production after exposure to CaCl 2 , KCl, thapsigargin, BHQ and norepinephrine in the presence of lipopolysaccharide at 1 ng/ ml respectively. Tetrandrine 0.3, 1, and 3 mM concentration-dependently reduced tumour necrosis factor-a production evoked by CaCl 2 or KCl. Tetrandrine preincubation had no significant effect on the response to Ca 2π -ATPase inhibitor thapsigargin or BHQ. Norepinephrine-induced tumour necrosis factor-a production was significantly reduced by tetrandrine and almost abolished by combination of tetrandrine and intracellular Ca 2π release inhibitor TMB-8. These results suggested that tetrandrine at a concentration of 0.3, 1, or 3 mM inhibited tumour necrosis factor-a production induced by Ca 2π entry in glia-neurone mixed cultures.

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The plasma glucose lowering action of tetrandrine in streptozotocin-induced diabetic rats

Cited by 17 publications

References 25 publications

Mediation of Endogenous β‐Endorphin by Tetrandrine to Lower Plasma Glucose in Streptozotocin‐Induced Diabetic Rats

Mediation of Endogenous β‐Endorphin by Tetrandrine to Lower Plasma Glucose in Streptozotocin‐Induced Diabetic Rats

Inhibition of intestinal glucose uptake by aporphines and secoaporphines

Effect of Tetrandrine on Calcium‐Dependent Tumour Necrosis Factor‐α Production in Glia‐Neurone Mixed Cultures

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