| Possible role of carbonic anhydrase in rat pancreatic islets: enzymatic, secretory, metabolic, ionic, and electrical aspects. | |
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MedLine Citation:
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PMID: 17284575 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The presence of carbonic anhydrase (type V) was recently documented in rat and mouse pancreatic islet beta-cells by immunostaining and Western blotting. In the present study, the activity of carbonic anhydrase was measured in rat islet homogenates and shown to be about four times lower than in rat parotid cells. The pattern for the inhibitory action of acetazolamide on carbonic anhydrase activity also differed in islet and parotid cell homogenates, suggesting the presence of different isoenzymes. NaN3 inhibited carbonic anhydrase activity in islet homogenates and both D-[U-14C]glucose oxidation and glucose-stimulated insulin secretion. Acetazolamide (0.3-10.0 mM) also decreased glucose-induced insulin output but failed to affect adversely D-[U-14C]glucose oxidation, although it inhibited the conversion of D-[5-3H]glucose to [3H]OH and that of D-[U-14C]glucose to acidic metabolites. Hydrochlorothiazide (3.0-10.0 mM), which also caused a concentration-related inhibition of the secretory response, like acetazolamide (5.0-10.0 mM), decreased H(14)CO3- production from D-[U-14C]glucose (16.7 mM). Acetazolamide (5.0 mM) did not affect the activity of volume-sensitive anion channels in beta-cells but lowered intracellular pH and adversely affected both the bioelectrical response to d-glucose and its effect on the cytosolic concentration of Ca2+ in these cells. The lowering of cellular pH by acetazolamide, which could well be due to inhibition of carbonic anhydrase, might in turn account for inhibition of glycolysis. The perturbation of stimulus-secretion coupling in the beta-cells exposed to acetazolamide may thus involve impaired circulation in the pyruvate-malate shuttle, altered mitochondrial Ca2+ accumulation, and perturbation of Cl- fluxes, resulting in both decreased bioelectrical activity and insulin release. |
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Authors:
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Abdullah Sener; Hassan Jijakli; Saleh Zahedi Asl; Philippe Courtois; Allen P Yates; Sylvain Meuris; Leonard C Best; Willy J Malaisse |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-02-06 |
Journal Detail:
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Title: American journal of physiology. Endocrinology and metabolism Volume: 292 ISSN: 0193-1849 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2007 Jun |
Date Detail:
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Created Date: 2007-06-05 Completed Date: 2007-07-30 Revised Date: 2008-05-05 |
Medline Journal Info:
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Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E1624-30 Citation Subset: IM |
Affiliation:
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Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium. abdsener@ulb.ac.be |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetazolamide
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pharmacology Animals Bicarbonates / metabolism Carbonic Anhydrase Inhibitors / pharmacology Carbonic Anhydrases / metabolism, physiology* Electrophysiology Female Glucose / metabolism Hydrogen-Ion Concentration Insulin / secretion* Intracellular Fluid / metabolism Islets of Langerhans / enzymology, metabolism, physiology* Male Parotid Gland / cytology, metabolism Rats Rats, Wistar Sodium Azide / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Bicarbonates; 0/Carbonic Anhydrase Inhibitors; 11061-68-0/Insulin; 26628-22-8/Sodium Azide; 50-99-7/Glucose; 59-66-5/Acetazolamide; EC 4.2.1.1/Carbonic Anhydrases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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