Lipids increase after solitary pancreas transplantation.

OBJECTIVE: The aims of this study were to determine 1) changes in lipids after solitary pancreas transplantation (SPTX) in patients with type 1 diabetes and 2) factors that influence those changes. RESEARCH DESIGN AND METHODS: Lipids were evaluated prospectively in 24 patients who underwent SPTX. Three were excluded because of early graft failure. The remaining patients (n = 21; 13 men, 8 women) were studied for changes in lipids over time (pre-SPTX, 0-2, 3-6, 7-12, and > 12 months). Glycohemoglobin, serum creatinine, BMI, and medications were also analyzed for their effects on lipid changes. RESULTS: Cholesterol, HDL, and LDL decreased in the immediate postoperative period (0-2 months), whereas triglycerides (TGs) increased (P < 0.05). At 3-6 months, cholesterol, HDL, and TG were higher than before the SPTX, whereas LDL returned to pre-SPTX levels. After 12 months, HDL and TG remained higher than their pre-SPTX levels (P < 0.05). During the study, systolic and diastolic blood pressure increased, renal function decreased, glyco-hemoglobin improved, and weight was unchanged. Changes in cholesterol/HDL ratio, HDL, and TG correlated with changes in prednisone dose (P < 0.05), and changes in TG correlated with changes in creatinine (P < 0.05). The same pattern of lipids occurred in patients prescribed or not prescribed hypolipidemic agents. CONCLUSIONS: Lipids do not improve within the 1st year after SPTX, despite improved glycemic control and blood pressure control, and renal function is worse. These results are in contrast to those reported for combined kidney-pancreas transplantation, where lipids, blood pressure, and renal function improved immediately after transplant. Further studies are needed to determine whether lipids continue to change with time after SPTX. The impact of these changes after SPTX on overall cardiovascular risk is unknown.

Insulin, insulin-like growth factors, and vascular endothelium.

Endothelial cells form the intimal lining of the entire vascular system. The vascular endothelium is continuously and directly bathed by components of the bloodstream and represents the initial fixed anatomical surface with which these components come in contact. In the past decade, the methodologies for studying endothelial cell functions have markedly advanced, enabling direct and detailed study of the vascular endothelium. From such studies, it is now apparent that the vascular endothelium represents an extraordinarily complex network of cells demonstrating a multitude of distinct anatomic, metabolic, and immunologic properties critical to such processes as angiogenesis, atherosclerosis, thrombosis, neoplasia, and a variety of metabolic disorders including homocystinuria and diabetes mellitus. This report will focus on the interactions of insulin and the insulin-like growth factors (IGFs) with vascular endothelium, based on studies with cultured endothelial cells, isolated microvessels, and perfused organ systems. Data will be presented relevant to the following concepts: (1) endothelial cells, in culture and in vivo, have specific receptors for insulin, IGF-I, and IGF-II; (2) insulin, IGF-I, and IGF-II have both distinct and overlapping functions in cultured endothelial cells; (3) cultured endothelial cells process receptor-bound insulin, IGF-I, and IGF-II, by distinct processes; (4) in vivo, capillary endothelial receptors are integrally involved in the transport of intact insulin to subendothelial sites of insulin action; and (5) vascular endothelium has specialized cellular features that are likely to contribute to the unique interactions of endothelial cells with insulin and the IGFs.

Iron and ferritin contents and distribution in human alveolar macrophages.

Previous investigations have shown that alveolar macrophages from cigarette smokers contain more iron than do macrophages obtained from nonsmokers. To localize intracellular iron and to help assess its potential for participation in the production of hydroxyl radicals, macrophages were fractionated and the ferritin and iron contents were measured in various cell fractions. Alveolar macrophages from seven smokers and six nonsmokers were lysed by nitrogen cavitation and centrifuged, first at 500 g and then at 11,000 g. Measured by radio-immunoassay, the total cellular ferritin was 133.8 +/- 33.2 ng and 782.0 +/- 177.8 ng per 1 x 10(6) macrophages (mean +/- SEM, p less than 0.01) obtained from nonsmokers and smokers, respectively. The total cellular iron contents were 7.5 +/- 0.6 nmol and 27.6 +/- 4.8 nmol per 1 x 10(6) macrophages (p less than 0.02) obtained from nonsmokers and smokers, respectively. The accumulation of iron by smokers' alveolar macrophages correlated with the number of cigarettes that had been smoked. Forty-two percent of the iron but only 9% of the ferritin was contained in the pellet obtained from centrifugation at 500 g. The pellet from the second centrifugation contained approximately 33% of the iron and 5% of the ferritin. The supernatant resulting from the second centrifugation contained 25% of the iron and 85% of the ferritin. Cigarette smoking did not appear to alter the intracellular distribution of either iron or ferritin. The ferritin content of bronchoalveolar lavage fluid was 0.10 +/- 0.04 micrograms/mg and 0.90 +/- 0.18 micrograms/mg albumin for nonsmokers and smokers, respectively (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)