| Complication | Evidence | PMID |
| Nephropathy | 1. In vivo, intrarenal delivery of adenovirus expressing SOCS1 and SOCS3 to diabetic rats significantly improved renal function and reduced renal lesions associated with diabetes, such as mesangial expansion, fibrosis, and influx of macrophages. Suppression of the JAK/STAT pathway by increasing intracellular SOCS proteins may have therapeutic potential in diabetic nephropathy. | 20185635 |
| Retinopathy | 1. The goal of this present study was to investigate a potential mechanism for retinal endothelial cell apoptosis in response to hyperglycemia.Increased TNF-alpha inhibits insulin signaling in 2 ways1) increased phosphorylation of IRS-1(Ser307), 2) increased SOCS3 levels to decrease total IRS-1 and increase IR(Tyr960), both of which block normal insulin signal transduction. | 22266116 |
| Tuberculosis | 1. We studied gene expression in peripheral blood cells of patients with diabetes (n = 10) and healthy endemic controls (EC, n = 11) both with and without MTB infection. Mycobacterial antigen (PPD) and mitogen-stimulated SOCS1, SOCS3, interferon-gamma (IFN-?), IL-6, and tumor necrosis factor alpha (TNF?) mRNA expression levels were determined using real-time polymerase chain reaction. | 28043584 |
| Insulin resistance and Inflammation | 1. Hepatocytes from control-fed SOCS3 LKO mice were protected from developing tumor necrosis factor ?-induced insulin resistance but also had increased lipogenesis and expression of sterol response element-binding protein-1c target genes. | 20799351 |
