The role of Dermcidin isoform-2 in the occurrence and severity of Diabetes

Abstract

Diabetes is now epidemic worldwide. Several hundred-million peoples are presently suffering from this disease with other secondary-disorders. Stress, hypertension, sedentary life-style, carbohydrate/lipid metabolic-disorders due to genetic or environmental factors attributes to type-1 and/or type-2 diabetes. Present investigation demonstrates that stress-induced protein dermcidin isoform-2 (DCN-2) which appears in the serum of diabetic-patients play a key-role in this disease pathogenesis/severity. DCN-2 suppresses insulin production-release from liver/pancreas. It also increases the insulin-resistance. Stress-induction at the onset/progression of this disease is noticed as the high-level of lipid peroxides/low-level of free-thiols in association with increase of inflammatory-markers c-reactive protein and TNF-α. DCN-2 induced decrease in the synthesis of glucose-activated nitric oxide synthase (GANOS) and lower production of NO in liver has been shown here where NO is demonstrated to lower the expression of glucose trabsporter-4 (GLUT-4) and its translocation on liver membrane surface. This finally impairs glucose transport to organs from the extracellular fluid. Low level of glucose uptake further decreases glucose-induced insulin synthesis. The central role of DCN-2 has been demonstrated in type-1/type-2 diabetic individuals, in rodent hepatocytes and pancreatic-cell, tissue-slices, in-vitro and in-vivo experimental model. It can be concluded that stress-induced decrease in insulin synthesis/function, glucose transport is an interactive consequence of oxidative threats and inflammatory events.

Effects of Lactobacillus acidophilus on the growth performance, immune response, and intestinal barrier function of broiler chickens challenged with Escherichia coli O157

“…CRP is an acute phase protein and a component of the innate immune system. It is always regarded as a metabolic inflammatory marker ( Wang et al., 2014 ; Bhattacharya et al., 2017 ). DAO is located mainly in the small intestinal mucosa.…”

Chemerin and Dermcidin in Human Milk and Their Alteration in Gestational Diabetes

“…It has been difficult to determine whether metformin or insulin treatments modulate milk and blood chemistry, including dermcidin concentrations. The concentrations of chemerin (Zhang et al, 2018) and dermcidin (Bhattacharya et al, 2017) are related to insulin resistance. The molecular mechanism of insulin action initiates the activation of kinases to generate a signal that eventually results in insulin’s action on glucose, lipid, and protein metabolism (Ramasarma & Rafi, 2016).…”

“…Another molecule, dermcidin, is a peptide consisting of 110 amino acids with antibacterial and antifungal properties (especially protecting against pathogenic gram-positive bacteria) secreted by human eccrine sweat glands (the major sweat glands of the human body that are found in virtually all areas of skin, with the highest density in the palms and soles; Burian & Schittek, 2015; Zeth & Sancho-Vaello, 2017). It has been suggested that dermcidin is part of the innate host defense in the immune system; dermcidin also suppresses pancreatic insulin secretion and increases insulin resistance (Bhattacharya, Khan, Ghosh, Bank, & Maiti, 2017). In a study of patients with diabetes, the detection of dermcidin isoform-2 (DCN-2) in serum ( n = 5 male, n = 15 female) showed that dermcidin plays a key role in the pathogenesis and severity of diabetes (Bhattacharya et al, 2017).…”

“…It has been suggested that dermcidin is part of the innate host defense in the immune system; dermcidin also suppresses pancreatic insulin secretion and increases insulin resistance (Bhattacharya, Khan, Ghosh, Bank, & Maiti, 2017). In a study of patients with diabetes, the detection of dermcidin isoform-2 (DCN-2) in serum ( n = 5 male, n = 15 female) showed that dermcidin plays a key role in the pathogenesis and severity of diabetes (Bhattacharya et al, 2017).…”

Silencing cyclophilin A improves insulin secretion, reduces cell apoptosis, and alleviates inflammation as well as oxidant stress in high glucose-induced pancreatic β-cells via MAPK/NF-kb signaling pathway

“…T1D is attributed to destruction of the pancreatic β cells or inhibition of glucose uptake [ 12 , 13 ]. T2D is due to pancreatic β cells function decline together with insulin resistance [ 14 ]. Ninety-five percent of diabetic patients suffered from T2D [ 15 , 16 ].…”