1978Acta Physiologica ScandinavicaRequires access

Insulin production by pancreatic islets of obese‐hyperglycemic mice cultured for one week in different glucose concentrations

Arne Andersson, Kjell Asplund, Richard G. Larkins

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Abstract

Abstract Anderson, A., K. Asplund and R. Larkins, Insulin production by pancreuric islets of obese‐hyperglycemic mice cultured for one week in different glucose concentrations. Acta physiol. scand. 1978. 104. 377–385. Culture of pancreatic islets isolated from obese‐hyperglycemic mice (gene symbol oh) for one week in media containing widely different concentrations of glucose (3.3, 5.6 or 16.7 mM) was found to markedly influence the functional behaviour of the islet B‐cells. Thus, the insulin content of islets cultured at 3.3 or 16.7 mM glucose (subphysiological or supraphysiological glucoce concentrations respectively) was markedly reduced. Islets cultured in 5.6 or 16.7 mM glucose displayed a normal insulin secretory response when stimulated with glucose, whereas islets cultured in a subnormal glucose concentration (3.3 mM) showed a reduced insulin response to glucose stimulation in batch type incubations and also lacked a second phase of insulin secretion in islet perifusion experiments. The rate of insulin biosynthesis of non‐cultured ob/ob islets was higher than that of islets from Lheir lean siblings but cuiture for one week in 3.3 mM glucose induced a pronounced impairment of the insulin biosynthesis in islets of obese as well as lean mice. The present data indicate that the hyperfunction of the islets of the ob/ob mouse at least in part is a reversible phenomenon, suggesting that inherent properties of islet B‐cells do not act as “primary” factors in the development of the obese‐hyperglycemic syndrome.

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Abstract Anderson, A., K. Asplund and R. Larkins, Insulin production by pancreuric islets of obese‐hyperglycemic mice cultured for one week in different glucose concentrations. Acta physiol. scand. 1978. 104. 377–385. Culture of pancreatic islets isolated from obese‐hyperglycemic mice (gene symbol oh) for one week in media containing widely different concentrations of glucose (3.3, 5.6 or 16.7 mM) was found to markedly influence the functional behaviour of the islet B‐cells. Thus, the insulin content of islets cultured at 3.3 or 16.7 mM glucose (subphysiological or supraphysiological glucoce concentrations respectively) was markedly reduced. Islets cultured in 5.6 or 16.7 mM glucose displayed a normal insulin secretory response when stimulated with glucose, whereas islets cultured in a subnormal glucose concentration (3.3 mM) showed a reduced insulin response to glucose stimulation in batch type incubations and also lacked a second phase of insulin secretion in islet perifusion experiments. The rate of insulin biosynthesis of non‐cultured ob/ob islets was higher than that of islets from Lheir lean siblings but cuiture for one week in 3.3 mM glucose induced a pronounced impairment of the insulin biosynthesis in islets of obese as well as lean mice. The present data indicate that the hyperfunction of the islets of the ob/ob mouse at least in part is a reversible phenomenon, suggesting that inherent properties of islet B‐cells do not act as “primary” factors in the development of the obese‐hyperglycemic syndrome.

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Available abstract

Abstract Anderson, A., K. Asplund and R. Larkins, Insulin production by pancreuric islets of obese‐hyperglycemic mice cultured for one week in different glucose concentrations. Acta physiol. scand. 1978. 104. 377–385. Culture of pancreatic islets isolated from obese‐hyperglycemic mice (gene symbol oh) for one week in media containing widely different concentrations of glucose (3.3, 5.6 or 16.7 mM) was found to markedly influence the functional behaviour of the islet B‐cells. Thus, the insulin content of islets cultured at 3.3 or 16.7 mM glucose (subphysiological or supraphysiological glucoce concentrations respectively) was markedly reduced. Islets cultured in 5.6 or 16.7 mM glucose displayed a normal insulin secretory response when stimulated with glucose, whereas islets cultured in a subnormal glucose concentration (3.3 mM) showed a reduced insulin response to glucose stimulation in batch type incubations and also lacked a second phase of insulin secretion in islet perifusion experiments. The rate of insulin biosynthesis of non‐cultured ob/ob islets was higher than that of islets from Lheir lean siblings but cuiture for one week in 3.3 mM glucose induced a pronounced impairment of the insulin biosynthesis in islets of obese as well as lean mice. The present data indicate that the hyperfunction of the islets of the ob/ob mouse at least in part is a reversible phenomenon, suggesting that inherent properties of islet B‐cells do not act as “primary” factors in the development of the obese‐hyperglycemic syndrome.

Key concepts: Internal medicine, Endocrinology, Insulin, Pancreatic islets, Islet, Medicine, Biology

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