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Biomedical subjects

B J Lin

Publications and source records attributed to B J Lin.

At least 91 records · Page 5Linked to original sources
PubMed1976

Effects of iodoacetate and fluoride on islate respiration and insulin biosynthesis.

Fluoride and iodoacetate inhibited the oxidation of glucose by islets of Langerhans isolated from the rat pancreas. Fifty % inhibition occurred with either 17 mM fluoride or 0.5 mM iodoacetate. The rate of insulin biosynthesis was more strongly inhibited by these inhibitors, especially fluoride. Fifty % inhibition occurred with approximately 1.5 mM fluoride. At high concentrations of iodoacetate and fluoride, the inhibitory effect on insulin synthesis was not reversed to a significant degree by the addition of pyruvate in the incubation medium. In addition to inhibiting the glycolysis and depriving islets of energy essential for the biosynthesis of insulin, fluoride probably exerts a direct inhibitory influence on the biosynthetic mechanism. A separate experiment with [6-14C]glucose indicated that 0.2 mM iodoacetate does not inhibit glycolysis completely.

Animals↗
PubMed1976

Interaction of alloxan and anomers of D-glucose on glucose-induced insulin secretion and biosynthesis in vitro.

The direct effects of alloxan on glucose-induced insulin secretion and biosynthesis and the interaction of alloxan and D-glucose anomers were studied in vitro by use of isolated islets from rat pancreas. Islets were pretreated by incubation for five minutes in media containing alloxan (0.2 mg./ml.) alone or alloxan with either the alpha or beta anomer of D-glucose (3 mg./ml.). After washing, batches of five islets were incubated in the medium supplemented with glucose (1.8 mg./ml.) for 60 minutes to observe insulin secretion and for 90 minutes to observe insulin biosynthesis. Prior exposure to alloxan alone produced marked inhibition of subsequent glucose-induced insulin secretion and biosynthesis. A significantly greater protection against these inhibitory effects of alloxan was observed by using the alpha anomer of D-glucose than the beta anomer. The anomeric preference of D-glucose for protecting islet cells from the inhibitory effect of alloxan on glucose-induced insulin secretion and biosynthesis was similar to that for triggering insulin secretion. Possible mechanisms of the inhibitory effect of alloxan and the protective effect of D-glucose anomers in connection with those of other sugars are discussed. It is suggested that a glucoreceptor, stereospecific to the alpha anomer of D-glucose, may exist for both insulin secretion and biosynthesis.

Alloxan↗
PubMed1975

Insulin biosynthesis: the monoaminergic mechanisms and the specificity of "glucoreceptor".

Islets of Langerhans, isolated from the rat, did not synthesize insulin in the presence of L-glucose, fructose, galactose, 3-0-methyl glucose or sorbitol. A small amount of insulin was synthesized in the presence of glucosamine. Addition of caffeine to these compounds did not enhance the biosynthesis of insulin. It is suggested that the specificity of the membrane surface "glucoreceptor", if it exists, may be rather narrow, at least with respect to insulin biosynthesis. Serotonin, dopamine and isoproterenol did not inhibit or enhance insulin biosynthesis induced by glucose. Propranolol also failed to modify insulin synthesis in the absence or presence of isoproterenol. It is concluded that the monoaminergic mechanisms do not affect insulin biosynthesis in spite of their significant regulatory influence on insulin release. Methysergide, at the concentration reported to potentiate insulin release induced by glucose and tolbutamide in rabbit, strongly inhibited insulin biosynthesis.

Amines↗