ArticleInternational journal of pancreatology : official journal of the International Association of Pancreatology1996
Stimulation of somatostatin secretion by 3-O-methylglucose in the perfused dog pancreas.
Article in International journal of pancreatology : official journal of the International Association of Pancreatology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Somatostatin secretion by NaNature metabolism · 2020Article
- The somatostatin-secreting pancreatic δ-cell in health and disease.Nature reviews. Endocrinology · 2018Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
conclusion3-O-methylglucose stimulates somatostatin secretion from the dog pancreas by a glucose-dependent and glucose-like effect. Therefore, it is possible that 3-O-methylglucose-stimulated somatostatin secretion is dependent on glucose metabolism.
backgroundSomatostatin secretion from the endocrine pancreas is stimulated by glucose, glyceraldehyde, and dihydroxyacetone but not affected by fructose, galactose, or ribose. Whether the nonmetabolizable glucose analog, 3-O-methylglucose affects somatostatin secretion is, however, not known.
methodWe therefore, examined whether the glucose analog affects somatostatin secretion in the perfused dog pancreas.
resultsWe found that when added to a medium containing 2.7 mM or 5.5 mM D-glucose, 3-O-methylglucose (10 mM) stimulated somatostatin secretion to the same extent as did an equivalent dose of D-glucose. The same stimulation was observed also with arginine at 2.5 mM in the perfusion medium. In contrast, 3-O-methylglucose did not stimulate somatostatin secretion in the absence of glucose in the perfusion medium. Mannoheptulose (5 mM), which inhibits glucose metabolism, completely blocked the secretion to both hexoses.
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