Stimulation of insulin output by monosaccharides and monosaccharide derivatives.

Content Provider	Semantic Scholar
Author	Pozza, Guido Galansino, G. Hoffeld, H. Foà, Piero P.
Copyright Year	1958
Abstract	POZZA, GUIDO, GIORGIO GALANSINO, HARVEY HOFFELD AND PIERO P. Foi. Stimulatim of insulin output by monosaccharides and monosaccharide derivatives. Am. J. Physiol. 192(s): 497-500. I@.-The ability of various sugars and closely related substances to stimulate insulin secretion was studied by means of pancreatic-femoral cross-circulation experiments between hepatectomized donor dogs and normal recipients. In other experiments, the test subs I tance was injected directly into the pancreatic ar tery of normal dogs. The admin istration of d -glucose, d-galactose or d-ribose was followed by a prompt hypoglycemia, suggesting insulin secretion; d-arabinose caused an unexplained delayed hypoglycemia, while d-fructose, d-mannose, d-xylose, I-arabinose, :j-methylglucose, d-glucosamine, galacturonic acid and saline had no effect. The tentative hypothesis that insulin secretion is stimulated by sugars which are both utilizable and insulin-sensitive is offered. No relationship between chemical structure and ability to cause insulin release was found. H YPERGLYCEMIA obtained by means of oral or parenteral administration of glucose, causes the release of insulin from the pancreas (for references see (I)). This statement is based on numerous experimental observations such as: a) the slow intravenous infusion of glucose is followed by hypoglycemia and increased tolerance for glucose (2, 3); b) the perfusion of an isolated pancreas with glucose solution causes the release of insulin into the perfusate (4); c) pancreatic venous blood from a hyperglycemic donor dog causes hypoglycemia in a recipient dog (5, 6); d) the injection of glucose into the pancreatic artery is followed by a fall in the systemic blood sugar concentration (7-9) ; e) the administration of glucose causes an apparent increase in plasma insulin activity (IO, I I). Recent evidence indicates that, in addition to glucose, prolactin (I 2), mesoxalate Received for publication August 20, 195 7. l Aided by grant A-522 from the National Institute of Arthritis and Metabolic Diseases. This paper was presented in part at the 1956 Fall Meeting of the American Physiological Society. 2 International Exchange Fellow. Permanent address: Clinica Medica, Universitk di Milano, Italy. (13) and the hypoglycemic sulfonamides (14, IS) may stimulate insulin release. Sugars other than glucose also may have this property, as suggested by the hypoglycemia frequently observed in galac tosemic children (I 6), especially following galactose administration (17, IS), by the hypoglycemia seen after the injection of d-ribose in man (19) and by the fact that several sugars cause the return of beta granules in pancreatic islets previously suppressed by insulin treatment (20). The purpose of this work was to investigate if a number of monosaccharides and monosaccharide derivatives can stimulate the release of insulin from the pancreas and if this property is related to their chemical structure.
Starting Page	497
Ending Page	500
Page Count	4
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://ajplegacy.physiology.org/content/192/3/497?ijkey=d42e97c392fcb359acaac557f3888aec319d7e96&keytype2=tf_ipsecsha
PubMed reference number	13520942v1
Volume Number	192
Issue Number	3
Journal	The American journal of physiology
Language	English
Access Restriction	Open
Subject Keyword	Arabinose Arthritis Canis familiaris Chemical Structure Diabetes Insipidus Foy Fructose Galactose Glucosamine Glucose Harvey murine sarcoma virus Hematological Disease Hypoglycemia Hypoglycemic Agents Islets of Langerhans Mannose Metabolic Diseases Monosaccharides Ribose Sugars Sulfonamides Xylose galacturonic acid insulin activity insulin secretion
Content Type	Text
Resource Type	Article