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Diabetes mellitus (DM) is a worldwide health threat affecting millions of people, which is associated with different micro- and macro-vascular complications. Type 2 diabetes mellitus (T2DM) is one of the different types of DM caused by insulin resistance and/or reduced secretion of insulin from the pancreas. A validated novel biomarker is required to enhance the accuracy of disease prediction, provide novel insights into pathophysiology and contribute to future prevention of T2DM. Various newer diagnostic methods have been developed by targeting endogenous proteins among which Adipsin is one of the promising target. Therefore, this review discusses Adipsin as a potential biomarker and its implication in T2DM. Adipsin is one of the adipokines secreted by adipose tissues which is involved in maintaining adipose tissue homeostasis and increasing insulin secretion in response to glucose. According to different experimental and clinical studies, plasma Adipsin concentrations are low in animals and patients with DM which support its use as a biomarker in combination to the other diagnostic modalities for DM. Additionally, the existence of Adipsin could be important in improving hyperglycemia by preserving β-cell mass through improving β-cell survival and maintaining their transcriptional identity.

Diabetes mellitus (DM) is a common metabolic disorder which is characterized by a persistent increment of blood glucose. Globally, DM affects millions of people and the prevalence is increasing alarmingly. The critical step in the pathophysiology of DM is the loss of β-cells of the pancreas, which are responsible for the secretion of insulin. Thioredoxin-interacting protein (TXNIP) is among the factors that control the production and loss of the pancreatic β-cells. TXNIP is an α-arrestin that can bind and inhibit thioredoxin (the antioxidant protein) which is produced in the pancreatic islet after glucose intake. Numerous studies illustrated that elevated TXNIP levels were found to induce β-cell apoptosis; whereas TXNIP deficiency protects against type I and type II diabetes by promoting β-cell survival. Nowadays, TXNIP depletion is becoming a key factor in pancreatic β-cell survival enhancement. In the present review, targeting TXNIP is found to be relevant as a unique therapeutic opportunity, not only to improve insulin secretion and sensitivity, but also ameliorating the long term microvascular and macrovascular complications of the disease. Thus, TXNIP inhibitors that could reduce the expression and/or activity of TXNIP to non-diabetic levels are promising agents to halt the alarming rate of diabetes and its related complications.