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Biomedical subjects

S Lenzen

Publications and source records attributed to S Lenzen.

113 records · Page 7Linked to original sources
PubMed1975

Thyroxine treatment and insulin secretion in the rat.

Thyroxine treatment increases blood glucose and plasma insulin levels in the rat. The hypoglycemic effect of tolbutamide is more pronounced in treated animals. The immediate insulin secretory response of the isolated perfused pancreas to maximal, but not to submaximal, glucose stimuli was increased after thyroxine treatment, especially in the lower dose range. However, as thyroxine treatment reduces insulin release during the prolonged late phase, the total amount of insulin released from the pancreas is reduced. Both the early response to tolbutamide and the subsequent basal secretion were increased after thyroxine treatment. When the pancreas of treated rats was exposed to glucose plus pyruvate the inhibition of the late phase was reversed. Isoprenaline did not overcome the inhibitory effect of thyroxine treatment on the late phase of glucose-induced insulin release. Thyroxine induces a selective inhibition of glucose induced insulin release which is reversed by pyruvate; this indicates that thyroxine interferes with the glycolysis in the beta cell.

Animals↗
PubMedDate not supplied

Effects of lysophosphatidylcholine and arachidonic acid on the regulation of intracellular Ca2+ transport.

The role of lysophosphatidylcholine and arachidonic acid in signal transduction was investigated using subcellular organelles and permeabilized cells from liver. Both substances can be generated intracellularly by the action of phospholipase A2 on phosphatidylcholine. Lysophosphatidylcholine as well as arachidonic acid raised the free Ca2+ concentration in the incubation media of permeabilized cells, isolated mitochondria and microsomes. The half maximally effective concentrations for Ca2+ release from mitochondria were 78 +/- 1 mumol/l for lysophosphatidylcholine and 80 +/- 11 mumol/l for arachidonic acid. Though isolated microsomes released Ca2+ in response to both agents, the combined presence of mitochondria and microsomes did not exhibit a synergism in Ca2+ release in response to arachidonic acid; the increase in the free Ca2+ concentration in response to lysophosphatidylcholine was even smaller than with mitochondria alone. It is concluded that the two reaction products of phospholipase A2 can raise the cytoplasmic Ca2+ concentration and therefore may participate in cellular signal transduction.

Animals↗