| Complication | Evidence | PMID |
| Nephropathy | 1. The AKT-mTOR pathway is activated in diabetic nephropathy. 2. Diabetes increased activated forms of AKT and mTOR both in glomeruli and podocyte. In diabetic rats, losartan decreased phosphorylated/activated forms of AKT (Thr308) and mTOR (Ser2448) in glomeruli but decreased only activated mTOR in podocytes. | 23456824 |
| Cardiovascular | 1. GDF-15 protects heart, adipose tissue, and endothelial cells by inhibiting JNK (c-Jun N-terminal kinase), Bad (Bcl-2-associated death promoter), and EGFR (epidermal growth factor receptor) and activating Smad, eNOS, PI3K, and AKT signaling pathways. | 26273671 |
| Retinopathy | 1. PI3K-AKT signaling, L-VGCCs, and PMCA1 were down-regulated in obesity-induced prediabetic/early diabetic retinas, as well as in human DR retinas, suggesting that down-regulation of PI3K-AKT and impaired calcium homeostasis might contribute to the etiology of DR. | 25788653 |
| Atherosclerosis | 1. Using network analysis, we have identified several cellular network proteins like PTPN1, AKT1, INSR, LEPR, IRS1, IRS2, IL1R2, IL6R, PCSK9 and MYD88, which are responsible for regulating inflammation, insulin resistance, and atherosclerosis. We have identified three distinct sets of serum markers for diabetes, CAD and diabetes associated with CAD in Indian patients using nonparametric-based machine learning approach. These multiple marker classifiers may be useful for monitoring progression from a healthy person to T2DM and T2DM to T2DM_CAD. | 30674322 |
| Insulin resistance and inflammation | 1. Our comprehension of AKT regulation and functions is particularly important given the consequences of AKT dysfunction in diverse pathological settings, including developmental and overgrowth syndromes, cancer, cardiovascular disease, insulin resistance , type 2 diabetes and inflammatory disorders | 28431241 |
