作者: Joseph Levy , James R. Gavin , James R. Sowers
DOI: 10.1016/0002-9343(94)90152-X
关键词: Homeostasis 、 Diabetes mellitus 、 Disease 、 Pathogenesis 、 Cataracts 、 Calcium metabolism 、 Medicine 、 Endocrinology 、 Insulin 、 Internal medicine 、 Premature aging
摘要: Although the pathogenesis of diabetes mellitus syndrome remains poorly understood, both insulin-dependent and non-insulin-dependent predispose individual to a similar spectrum complications, including hypertension, macrovascular microvascular disease, cataracts cardiomyopathy, neuropathy, premature aging, suggesting that these complications develop along pathway common diabetic conditions. Yet not all persons are affected by or same degree. What causes this marked variability in clinical manifestations an enigma. Accumulating data from animal models studying patients with reveal intracellular calcium levels increased most tissues. The activities membrane, adenosine triphosphatase (ATPase) associated cation pumps, which determine level (i.e., calcium-ATPase [sodium + potassium]-ATPase), also altered. nature alteration is often tissue specific may depend on blood glucose insulin, both. In review we discuss potential contribution changes regulation, whether acquired genetically determined, syndrome, abnormalities insulin secretion action (mainly diabetes), syndromes. Altered metabolism represent common, underlying abnormality linking metabolic, cardiovascular, ocular, neural disease process.