Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been recommended that patients who perform self-blood glucose monitoring use the information gained from the test to alter their diabetic regimen. Skyler et al. have proposed algorithms for patients to adjust their insulin dosage when blood sugar is elevated. However, the clinical result of increasing insulin dosage may be the promotion of weight gain. We proposed that altering the regimen by decreasing caloric intake is an appropriate first approach for NIDDM patients for whom weight loss would be of considerable benefit. Results of an initial needs assessment showed that patients did not generally regard testing and adjusting therapy as important in taking care of diabetes. A recent study by Fox et al. reported similar results, showing that a large portion of patients using blood glucose self-monitoring do not make changes in their regimen when they know that their blood sugar is elevated. Consequently, we implemented a half-day seminar to instruct patients on making adjustments in their dietary regimen on the basis of results of glucose monitoring. Results suggest that our teaching methods were effective in teaching patients to follow the adjusting algorithm. Although we observed trends toward improved metabolic control and weight loss, further studies are required to document the clinical benefit of adjustment of caloric intake based on self-monitoring in diabetes.
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PMID:Adjustment of caloric intake based on self-monitoring in noninsulin-dependent diabetes mellitus: development and feasibility. 274 14

Plasminogen activator inhibitor-1 (PAI-1) is an important regulator of fibrinolysis. PAI-1 levels are elevated in type 2 diabetes, and this elevation correlates with macro- and microvascular complications of diabetes. However, the mechanistic link between insulin and up-regulation of PAI-1 is unclear. Here we demonstrate that overexpression of Forkhead-related transcription factor (Fox)O1, FoxO3a, and FoxC1 augment insulin's ability to activate the PAI-1 promoter. In addition, insulin treatment promotes the phosphorylation of nuclear and cytoplasmic Fox03a and an increase of cytoplasmic Fox03a. In contrast, insulin treatment led to the accumulation of phospho-Fox01 only in the cytoplasm. Furthermore, insulin also increased the ability of chimeric LexA-FoxO1, LexA-FoxO3a, and LexA-FoxC1 proteins to increase the activity of a LexA reporter, suggesting that the effect of insulin on FoxO3a was direct. Using small interfering RNA to specifically deplete each of the Fox transcription factors tested, we demonstrate that only reduction of FoxO3a inhibits insulin-increased PAI-1-Luc expression and PAI-1 mRNA accumulation. Finally, chromatin immunoprecipitation assays confirm the presence of FoxO3a on the PAI-1 promoter. These results suggest that FoxO3a mediates insulin-increased PAI-1 gene expression.
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PMID:Insulin acts through FOXO3a to activate transcription of plasminogen activator inhibitor type 1. 1960 44