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)

A patient with insulin dependent adult onset diabetes presented with bilateral disc edema and minimal visual dysfunction. Initial work-up excluded an intracranial lesion, and a lumbar puncture revealed a normal opening pressure. The patient developed proliferative retinopathy, for which she received photocoagulation therapy. She subsequently developed an exacerbation and change of her disc swelling, associated with raised intracranial pressure. The differential diagnosis of diabetic papillopathy and papilledema is discussed.
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PMID:Disc swelling in an adult diabetic patient. 223 59

Diabetic retinopathy is one of the common complications of diabetes and is the leading cause for patients' visual dysfunction and sight loss. However, the mechanism of diabetic retinopathy is not clearly defined. The present study was undertaken to investigate neuroretinal apoptosis in different stages in a mouse model for type 2 diabetes mellitus and the mechanism of diabetic retinopathy. KKAY mouse with genetic diabetes, an animal model for type 2 diabetes, was used in this study. Mice were divided into a control group and a diabetic group. The mice in both groups were sacrificed at one month and three months, and the mouse eyeballs were used for making retinal histologic sections. We showed in this study that the apoptotic cell numbers for retinal neural cells in the ganglion cell layer were significantly greater in the diabetic group than in the control group (p<0.01), as determined by the TUNEL assay. In addition, many more apoptotic retinal neuronal cells were found in the retinal ganglion cell layer and medial part of the inner nuclear layer in the diabetic group when the mice were sacrificed at three months as compared to those sacrificed at one month (p<0.01). We also studied the ultrastructure of the retinal nerve cells and microvesseles by electron microscopy and demonstrated that the ultrastructure changes for retinal neural cells and retinal microangiopathy were observed in, as early as, the early stage of diabetes. These findings indicate that: i). retinal neuropathy and microangiopathy occur in the early stage of diabetes, ii). apoptosis may be an important mechanism through which retinal neurodegeneration is developed, and iii). both retinal neurodegeneration and retinal microangiopathy should be considered as the diabetic retinopathy.
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PMID:Neuro-optic cell apoptosis and microangiopathy in KKAY mouse retina. 1465 76

Increased expression of the peptide hormone retinol-binding protein 4 (RBP4) has been implicated in the development of insulin resistance, type 2 diabetes, and visual dysfunction. Prior investigations of the mechanisms that influence RBP4 synthesis have focused solely on changes in mRNA abundance. Yet, the production of many secreted proteins is controlled at the level of mRNA translation, as it allows for a rapid and reversible change in expression. Herein, we evaluated Rbp4 mRNA translation using sucrose density gradient centrifugation. In the liver of fasted rodents, Rbp4 mRNA translation was low. In response to re-feeding, Rbp4 mRNA translation was enhanced and RBP4 levels in serum were increased. In H4IIE cells, refreshing culture medium promoted Rbp4 mRNA translation and expression of the protein. Rbp4 mRNA abundance was not increased by either experimental manipulation. Enhanced Rbp4 mRNA translation was associated with activation of the kinase mTORC1 and enhanced phosphorylation of the translational repressor 4E-BP1. In H4IIE cells, expression of a 4E-BP1 variant that is unable to be phosphorylated by mTORC1 or suppression of mTORC1 with rapamycin attenuated activity of a luciferase reporter encoding the Rbp4 mRNA 5'-untranslated region (UTR). Purine substitutions to disrupt a terminal oligopyrimidine (TOP)-like sequence in the Rbp4 5'-UTRprevented the suppressive effect of rapamycin on reporter activity. Rapamycin also prevented upregulation of Rbp4 mRNA translation in the liver, and reduced serum levels of RBP4 in response to feeding. Overall, the findings support a model in which nutrient-induced activation of mTORC1 up regulates Rbp4 mRNA translation to promote RBP4 synthesis.
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PMID:Retinol binding protein 4 (Rbp4) mRNA translation in hepatocytes is enhanced by activation of mTORC1. 3328 85