Biological differences in a rat insulinoma cell line obtained from different laboratories do not affect binding of human anti-islet immunoglobulins.

An insulin-producing clone of rat insulinoma cells (RINm5F) has been used by several investigators as target cells for studies of both humoral and cell-mediated anti-islet immunity in diabetic animals and humans. We noted that the rate of proliferation of RINm5F cells obtained from different laboratories varied considerably, and, in the present study, we have compared the proliferation rates of RINm5F cells obtained from 3 laboratories (Uppsala, Sweden [UPP], Chicago [CHI] and New York [NY]). The cells were plated at 0.5 and 2.0 X 10(4)/cm2 and changes in cell number were measured over 5 days. Basal insulin release was also determined daily. In addition, binding of IgG from sera of human diabetics by each of the cell lines was also examined by a solid-phase, quantitative assay. Plating efficiency was significantly greater in the NY and CHI cells than UPP cells at both plating densities (p less than 0.025). When plated at 2 X 10(4)/cm2, the growth rate of the NY cells was faster than the others (NY: 100.1 +/- 7.8%/day, CHI: 72.2 +/- 8.1%/day, UPP: 78.3 +/- 14.0%/day, p less than 0.025). All growth rates were lower when cells were plated at 5 X 10(4)/cm2, and the differences in growth between the NY and the other cells was greater (NY: 94.1 +/- 12.2%/day, CHI: 61.8 +/- 5.8%/day, UPP: 58.1 +/- 5.6%/day). Insulin release also differed among the cells. More insulin was released by the NY cells than by the other cells on all days, and the CHI cells released more insulin than the UPP cells (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Triad of markers for identifying children at high risk of developing insulin-dependent diabetes mellitus.

A longitudinal investigation was conducted from 1977 to 1984 on 178 families in which one or more of the children had insulin-dependent diabetes mellitus. Of 351 nondiabetic sibs followed up for an average of 54 months, ten have, thus far, become diabetic. Eight sibs were HLA identical to their diabetic proband and nine had HLA-DR3 and/or HLA-DR4. Islet cell surface antibody and islet cell cytoplasmic antibody were found from two to 74 months before the onset of clinical diabetes in 100% and 90%, respectively, of the children. A decrease in insulin secretion was observed in all of these children on entry into the study and was detected in the absence of elevated plasma glucose concentrations. The data suggest that the triad of HLA identity, pancreatic islet cell antibodies, and depressed insulin secretion identifies those sibs who are at high risk of developing insulin-dependent diabetes mellitus.

Transient lipoprotein lipase deficiency with hyperchylomicronemia.

Type I hyperlipoproteinemia is a rare disorder characterized by the presence of chylomicrons in fasting plasma and dysfunction of the lipoprotein lipase system. The disease may result from primary genetic defects leading to the lack of the enzyme lipoprotein lipase or to a deficiency in the CII apoprotein activator of that enzyme. It may also appear secondary to underlying systemic diseases. We now describe a case of hyperchylomicronemia and pancreatitis with a lack of lipoprotein lipase activity as assessed by three different methods. The patient had no evidence of a plasma inactivator of lipoprotein lipase, and his plasma was able to activate the enzyme in control postheparin plasma. The postheparin plasma hepatic triglyceride lipase was normal. Tests for associated systemic diseases were negative. Six weeks after presentation, that patient's lipoprotein levels and postheparin plasma lipase activities were normal. This was a unique case of hyperchylomicronemia which for a limited time was indistinguishable from primary lipoprotein lipase deficiency by current biochemical techniques.