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Lipid composition of glucose‐stimulated pancreatic islets and insulin‐secreting tumor cells
Author(s) -
Rustenbeck Ingo,
Matthies Alexander,
Lenzen Sigurd
Publication year - 1994
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02538912
Subject(s) - phospholipid , lysophosphatidylcholine , islet , pancreatic islets , medicine , phosphatidic acid , endocrinology , phosphatidylinositol , diacylglycerol kinase , chemistry , insulin , lipid metabolism , biochemistry , stimulation , biology , phosphatidylcholine , protein kinase c , kinase , membrane , enzyme
The effect of glucose stimulation (25 mM for 5 min) on the phospholipid and neutral lipid composition of isolated pancreatic islets was studied to find out whether there is a change in the mass of potential lipid mediators or modulators of insulin secretion. For comparison, the lipid compositions of homogenates and subcellular fractions from RINm5F insulin‐secreting tumor cells and of glucose‐stimulated streptozotocin/nicotinamide‐induced islet cell tumors were analyzed. After separation of the lipid extract into a neutral and an acidic fraction by anion‐exchange chromatography, lipids were separated by high‐performance thin‐layer chromatography and quantitated by in situ densitometry of the cupric sulfate‐charred bands. In glucose‐stimulated islets, the molar percentages of phosphatidic acid (PA) and of phosphatidylinositol were significantly increased (3.1 vs. 4.7 mol% and 8.6 vs. 11.8 mol%), while those of all other phospholipids and neutral lipids, including 1,2‐diacylglycerol, were not significantly changed. In stimulated islet cell tumors, an increase of PA was visible in the microsomal fraction, and there was an increase of lysophosphatidylcholine in the mitochondrial fraction. However, in both tumoral tissues, particularly in RINm5F cells, the lipid distribution pattern showed abnormalities which can be regarded as a loss of differentiation and which limit the usefulness of these tissues for the study of the physiological regulation of lipid metabolism during glucose stimulation. In conclusion, the data are in accordance with a role of PA early in stimulus‐secretion coupling. The well‐known stimulation of phospholipid synthesis in pancreatic islets during glucose‐induced insulin secretion does not result in an increase in the total phospholipid mass.