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P19, a group of 19,000 mol wt cytosolic proteins, with apparent isoelectric points of pI 5.9, pI 5.7, and pI 5.4, respectively, was identified in three peptide hormone-producing cell types: AtT20 mouse pituitary tumor cells, RIN-1122 rat insulinoma cells, and hamster insulinoma cells. Secretagogue-dependent phosphorylation of P19 was analyzed in 32P-labeled cells by two-dimensional electrophoresis and autoradiography. The results were quantitated by computer-assisted densitometry. Cellular levels of cAMP and hormone release were measured in parallel incubations. In addition to stimulating ACTH release, CRF raised the cellular level of cAMP and increased the 32P labeling of all three 19,000 mol wt proteins in AtT20 cells. Other agents known to act through cAMP, which included isoproterenol, forskolin, and 8-bromo-cAMP, mimicked the effect of CRF on both ACTH release and phosphorylation of P19. 12-O-Tetra-decanoylphorbol-13-acetate, a tumor-promoting phorbol ester, also stimulated both ACTH release and phosphorylation of P19. In contrast, although 40 mM K+ promoted ACTH release, it did not affect the phosphorylation of P19. Analogous findings were observed in insulinoma cells. Glucagon stimulated insulin release, increased cellular cAMP and promoted phosphorylation of P19 in RIN 1122 cells. 12-O-Tetradecanoylphorbol-13-acetate also enhanced insulin release and the phosphorylation of P19 in these cells. The results obtained with hamster insulinoma cells closely resembled the observations in RIN-1122 cells. In conclusion, P19, an apparently homologous set of cytosolic proteins, undergoes phosphorylation in three peptide hormone-producing cells in response to two groups of secretagogues, the effect of which is probably mediated, in one case, by cAMP-dependent protein kinase and, in the other, by protein kinase C. The data suggest the possibility that P19 participates in a secretory pathway activated by these two effector systems.

In the hyperglycemic black NIDDM population, two variants exist: one with insulin resistance and one with normal insulin sensitivity. This insulin-sensitive variant represents 40% of subjects with a BMI less than 30 kg/m2. Moreover, the insulin-sensitive group has a lower risk profile for cardiovascular disease.

Standard reflectance meters were modified by the addition of memory chips capable of storing 440 glucose determinations with corresponding time and date. These modified reflectance meters (MR) were given to 20 individuals with type I diabetes in an effort to determine the level of reliability and accuracy they could achieve on a self-monitoring regimen. During a 6-wk period these subjects measured their capillary blood glucose and recorded the results in a logbook (LB). At 2-wk intervals they visited the clinic. Data from the MR was offloaded onto an Apple IIe microcomputer (Apple Computer, Inc., Cupertino, California) and presented to the subjects in a graphic format, depicting the level of metabolic control over the previous 2 wk. The performance of subjects for the 6-wk period showed that they averaged 7 omissions from the LB for every 100 MR recordings; 1 added value in the LB for every 200 MR recordings; and 1 error in accurately copying the test value for every 100 determinations. In comparison with subjects who participated in an earlier study in which they were unaware of the memory function of the reflectance meter, performance during the current study improved in all categories. It was also observed that consistency in reliable and accurate record keeping did not diminish throughout the study period. Despite these positive changes in performance, no alteration in glycemic control was found.

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