Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnostic evidence or symptoms of gastroparesis develop in about 20% to 30% of patients with long-standing diabetes. Diabetic gastroparesis is likely caused by autonomic neuropathy involving the nerves that regulate gastric motor function. The following are necessary for diagnosis: thorough history taking and physical examination to eliminate factors that might further delay gastric emptying; esophagogastroduodenoscopy or barium contrast studies to exclude structural abnormalities; and a radionuclide gastric emptying study. The three main agents available for therapy in the United States are metoclopramide (Maxolon, Octamide, Reglan), erythromycin, and cisapride (Propulsid). All have been shown to offer benefit in improving gastric emptying and symptoms, although use of metoclopramide is limited by a significant incidence of side effects. Surgical intervention should be avoided if possible.
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PMID:Diabetic gastroparesis. What to do when gastric emptying is delayed. 815 43

Ultrasound registration of changes in gallbladder volume by the method of cylinder sum allows reliable means of studying gallbladder contractility in response to pharmacological load. Cerucal increased this activity in chronics with gastroduodenitis and diabetes mellitus, pentagastrin reduced the gallbladder volume. In duodenal ulcer patients a single dose of dalargin dilated the gallbladder for a short time, while in course treatment did not influence it. Gastrocepin inhibited motor activity of gallbladder as well as corinfar.
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PMID:[Drug effects on gallbladder motility (based on dynamic ultrasonic data)]. 913 11

Inflammation and endoplasmic reticulum (ER) stress are associated with the development of insulin resistance and diabetes. Developmental endothelial locus-1 (DEL-1) enhances efferocytosis by macrophage and suppresses inflammatory response. However, effects of DEL-1 on ER stress-mediated insulin resistance in skeletal muscle remain unclear. Here, DEL-1 treatment augmented SIRT1 expression in C2C12 myocytes, thereby increasing SERCA2 expression in a dose-dependent fashion, and attenuated ER stress and insulin resistance under palmitate treatment condition. SIRT1/SERCA2 knockdown abrogated effects of DEL-1 on palmitate-induced insulin resistance as well as ER stress. Pharmacological significance of DEL-1 was confirmed by in vivo experiments. DEL-1 administration suppressed ER stress, insulin resistance, and SIRT1/SERCA2 expression in skeletal muscle of high-fat diet (HFD)-fed mice. Additionally, siRNA transfection-mediated in vivo downregulation of SIRT1 suppressed the effects of DEL-1 on expression of SERCA2, ER stress, and insulin resistance in skeletal muscle of HFD-fed mice. DEL-1 attenuates palmitate-induced and HFD-induced skeletal muscle ER stress and insulin resistance via SIRT1/SERCA2-mediated signaling.
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PMID:DEL-1 ameliorates high-fat diet-induced insulin resistance in mouse skeletal muscle through SIRT1/SERCA2-mediated ER stress suppression. 3177 46