The prevalence of diabetes is continuously increasing in the recent decades. Persistent hyperglycemia, hyperinsulinemia and the subsequent oxidative stress result in diabetic complications, primarily categorized as microvascular (nephropathy, retinopathy and neuropathy) and macrovascular (cardiomyopathy) complications. The complications are prevalent in both type 1 and type 2 diabetic patients. Polyol pathway, elevated AGE production, PKC activation and hexosamine pathway are indeed the critical pathways involved in the progression of diabetic complications. Silent information regulator 2 or SIR2 or more commonly known as sirtuins are NAD+ dependent histone deacetylase. SIRT1, a member of the sirtuin family has been extensively studied for its role in lifespan extension and needs to be explored for its beneficial effects in diabetic complications. Moreover, it is also known to regulate the activity of other proteins and transcription factors. One such substrate of SIRT1 is FOXOs transcription factor which has gained much attention as the mediator of various cellular processes such as cell cycle arrest and proliferation, DNA repair and metabolism. It has been reported that SIRT1 regulates the activity of FOXOs, whereas few recent advances also suggest a role FOXOs in governing the activity of SIRT1, which permits for a crosstalk between SIRT1 and FOXOs. Therefore, the focus of the present review is to describe and explore the interaction between SIRT1 and FOXOs, predominantly FOXO1 and FOXO3 and to understand the underlying mechanism of SIRT1-FOXOs in controlling and alleviating diabetic complications. Thus, this crosstalk suggests that SIRT1 and FOXOs may serve as potential therapeutic targets in treating diabetic complications. 

SIRT1-FOXOs activity regulates diabetic complications

Diabetic kidney disease (DKD) is an important public health problem. Podocyte injury is a central event in the mechanism of DKD development. Podocytes are terminally differentiated, highly specialized glomerular visceral epithelial cells critical for the maintenance of the glomerular filtration barrier. Although potential mechanisms by which diabetic milieu contributes to irreversible loss of podocytes have been described, identification of markers that prognosticate either the development of DKD or the progression to end-stage kidney disease (ESKD) have only recently made it to the forefront. Currently, the most common marker of early DKD is microalbuminuria; however, this marker has significant limitations: not all diabetic patients with microalbuminuria will progress to ESKD and as many as 30% of patients with DKD have normal urine albumin levels. Several novel biomarkers indicating glomerular or tubular damage precede microalbuminuria, suggesting that the latter develops when significant kidney injury has already occurred. Because podocyte injury plays a key role in DKD pathogenesis, identification of markers of early podocyte injury or loss may play an important role in the early diagnosis of DKD. Such biomarkers in the urine include podocyte-released microparticles as well as expression of podocyte-specific markers. Here, we review the mechanisms by which podocyte injury contributes to DKD as well as key markers that have been recently implicated in the development and/or progression of DKD and might serve to identify individuals that require earlier preventative care and treatment in order to slow the progression to ESKD.

/pdf/the-role-of-podocytes-and-podocyte-associated-biomarkers-in-4bf64svprh.pdf

The Role of Podocytes and Podocyte-Associated Biomarkers in Diagnosis and Treatment of Diabetic Kidney Disease.

Intestinal microbiota and diabetic kidney diseases: the Role of microbiota and derived metabolites inmodulation of renal inflammation and disease progression.

http://www.cell.com/article/S2405844023035478/pdf

Potential effects of bisphenol A on diabetes mellitus and its chronic complications: A narrative review

INTRODUCTION This study was conducted to compare parameters of kidney injury, oxidative stress and inflammation in people with diabetic nephropathy (DN) and type 2 diabetes mellitus (T2DM). METHODS In a cross-sectional study, 57 cases with DN and 57 cases with T2DM were included in the study. Fasting blood samples were obtained to determine parameters of kidney injury, oxidative stress and inflammation. RESULTS The current study showed that patients with DN had higher tumor necrosis factor-α (TNF-α) (167.0 ± 40.1 vs. 151.4 ± 37.4 ng/L, P .05). Furthermore, advanced glycation end products (AGEs) levels in patients with DN were higher than that of patients with T2DM (8511.7 ± 1799.9 vs. 7660.7 ± 1711.9 AU, P < .05), but the difference in malondialdehyde value was not significant. Finally, we found that total protein levels in cases with DN were enhanced compared with individuals with T2DM (7.1 ± 0.5 vs. 6.9 ± 0.6 mg/dL, P < .05); however, other markers of kidney injury did not change. CONCLUSIONS In conclusion, the results of present study revealed that few markers of inflammation and oxidative stress including TNF-α, MMP-2, AGEs levels and total protein levels in patients with DN were significantly higher than that of patients with T2DN. Further studies are necessary to confirm these findings.

Comparison Between Biomarkers of Kidney Injury, Inflammation, and Oxidative Stress in Patients with Diabetic Nephropathy and Type 2 Diabetes Mellitus.

/pdf/diabetic-nephropathy-from-pathophysiology-to-treatment-2i810yy4ba.pdf

Diabetic Nephropathy: From Pathophysiology to Treatment.

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Diabetic Nephropathy: From Pathophysiology to Treatment.