Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic nephropathy represents a major complication of diabetes mellitus (DM), and the origin of this complication is poorly understood. Vasopressin (VP), which is elevated in type I and type II DM, has been shown to increase glomerular filtration rate in normal rats and to contribute to progression of chronic renal failure in 5/6 nephrectomized rats. The present study was thus designed to evaluate whether VP contributes to the renal disorders of DM. Renal function was compared in Brattleboro rats with diabetes insipidus (DI) lacking VP and in normal Long-Evans (LE) rats, with or without streptozotocin-induced DM. Blood and urine were collected after 2 and 4 weeks of DM, and creatinine clearance, urinary glucose and albumin excretion, and kidney weight were measured. Plasma glucose increased 3-fold in DM rats of both strains, but glucose excretion was approximately 40% lower in DI-DM than in LE-DM, suggesting less intense metabolic disorders. Creatinine clearance increased significantly in LE-DM (P < 0.01) but failed to increase in DI-DM. Urinary albumin excretion more than doubled in LE-DM but rose by only 34% in DI-DM rats (P < 0.05). Kidney hypertrophy was also less intense in DI-DM than in LE-DM (P < 0.001). These results suggest that VP plays a critical role in diabetic hyperfiltration and albuminuria induced by DM. This hormone thus seems to be an additional risk factor for diabetic nephropathy and, thus, a potential target for prevention and/or therapeutic intervention.
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PMID:Vasopressin contributes to hyperfiltration, albuminuria, and renal hypertrophy in diabetes mellitus: study in vasopressin-deficient Brattleboro rats. 1046 19

Vasopressin is synthesized by neurons in the supraoptic nucleus of the hypothalamus and its release is controlled by action potentials produced by specific subtypes of voltage-gated sodium channels expressed in these neurons. The hyperosmotic state associated with uncontrolled diabetes mellitus causes elevated levels of plasma vasopressin, which are thought to contribute to the pathologic changes of diabetic nephropathy. We demonstrate here that in the rodent streptozotocin model of diabetes there are increases in expression of mRNA and protein for two sodium channel alpha-subunits and two beta-subunits in the neurons of the supraoptic nucleus. Transient and persistent sodium currents show parallel increases in these diabetic neurons. In the setting of chronic uncontrolled diabetes, these changes in sodium channel expression in the supraoptic nucleus may be maladaptive, contributing to the development of secondary renal complications.
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PMID:Sodium channel expression in hypothalamic osmosensitive neurons in experimental diabetes. 1216 78