Endothelin A-receptor blockade in experimental diabetes improves glucose balance and gastrointestinal function

Balsiger, B; Rickenbacher, A; Boden, PJ; Biecker, E; Tsui, J; Dashwood, M; Reichen, J; Shaw, SG (2002). Endothelin A-receptor blockade in experimental diabetes improves glucose balance and gastrointestinal function. Clinical science, 48(103), 430S-433S.. London: Portland

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Secondary complications of diabetes mellitus often involve gastrointestinal dysfunction. In the experimental Goto Kakizaki rat, a model of Type II diabetes, hyperglycaemia and reduced glucose clearance is associated with elevated plasma endothelin (ET)-1 levels and selective decreases in nitric oxide synthase in circular muscle, longitudinal muscle and neuronal elements of the gastrointestinal tract. Functionally, this is accompanied by decreased nitrergic relaxatory responses of jejunal longitudinal muscle to tetrodotoxin-sensitive electrical field stimulation. Long-term treatment with a selective ET A-type receptor antagonist, markedly reduced hyperglycaemia and restored plasma glucose clearance rates towards normal. This was associated with a restoration of N(G)-nitro-L-arginine methyl ester-sensitive relaxatory responses of jejunal longitudinal muscle to electrical field stimulation. The results indicate that beneficial effects of ETA receptor blockade on gastrointestinal function may result from an improvement in insulin sensitivity with concomitant reduction of the severity of hyperglycaemia. ETA receptor blockade may represent a new therapeutic principle for improving glucose tolerance in Type II diabetes and could be beneficial in alleviating or preventing hyperglycaemia-related secondary complications in this condition.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DCR Unit Tiefenau Hospital [discontinued] > Forschungsgruppe Vasoaktive Peptide [discontinued]

UniBE Contributor:

Shaw, Sidney

ISSN:

0143-5221

ISBN:

12193138

Publisher:

Portland

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:58

Last Modified:

05 Dec 2022 14:18

PubMed ID:

12193138

Web of Science ID:

000178171300098

URI:

https://boris.unibe.ch/id/eprint/25004 (FactScience: 54604)

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