Is intervening inflammatory pathways a way to treat type 2-diabetes

Over the past few decades, the prevalence of type 2 diabetes (T2D) has rapidly increased. Cardiovascular kidney-metabolic (CKM) syndrome commonly arises from excessive or defective adipose tissue or combination of both. Proinflammatory mediators secreted by dysfunctional adipose tissue, especially visceral adipose tissue damage kidney, heart and artery tissues. Excessive storage of fatty acids disrupts the endocrine functions of adipose tissue, resulting in ectopic fat accumulation that induces lipotoxicity, thereby promoting low-grade inflammation and insulin resistance (IR) in the liver. Systemic inflammation and IR are exacerbated by the onset of metabolic dysfunction-associated steatotic liver disease, formerly known as non-alcoholic fatty liver disease (NAFLD). It is well established that low grade inflammation plays an important role in T2D and its associated microvascular complications like nephropathy, neuropathy, retinopathy and macrovascular complications like atherosclerosis. Accelerated atherosclerosis predisposes to cardiovascular diseases, which is the leading cause of mortality in these patients. Till date, various anti-inflammatory drugs have been tried in the setting of chronic disorders such as T2D and CVD (cardiovascular diseases). But too selective targeting may not have produced the desired outcomes. Multiple inflammatory pathways contribute to the pathogenesis of CVD and T2D, hydroxychloroquine (HCQ), a broad anti-inflammatory agent, demonstrates beneficial effects on glucose and lipid metabolism and is the only DCGI approved anti-inflammatory drug for T2D. Due to pleotropic benefits, HCQ has the potential of reducing prediabetes for diabetics, has antidiabetic properties and also reduces complications of diabetes, most importantly, CVD associated with T2D.