Abstract
Introduction: The lung surfactant dipalmitoylphosphatidylcholine (DPPC) leaks into the blood, settling on the luminal aspect of blood vessels to create active hydrophobic spots. Nanobubbles are formed at these spots from dissolved gas. We hypothesized that contact between a large molecule in the blood and a nanobubble at an active hydrophobic spot would disrupt the molecule’s tertiary structure. An exposed epitope may then prompt an autoimmune response.
Methods: DPPC content was determined in the heart of diabetic and healthy non-obese diabetic (NOD) mice and two control mice strains (C57/BL6 and Swiss-webster).
Results: The hearts from NOD mice contained more DPPC (47.6 ± 3.7 SE mg/g) than the control mice (36.9 ± 2.2 SE mg/g) (P < 0.018).
Discussion: It is probable that leakage of large β-cell molecules is the difference between affected and non-affected NOD mice. The Double Cause Hypothesis (DCH) is supported and the further research and applicability is discussed.