New Aspects in Obesity and Diabetes: Involvement in Regucalcin, a Suppressor Protein of Cell Signaling

Abstract

Obesity and diabetes (type 1 and 2 diabetes) are currently a major health problem worldwide with growing in prevalence. The incidence of metabolic disease, including type 2 diabetes with obesity, has increased to epidemic levels. Obesity and diabetes induce secondary diseases with various pathophysiologic states, which are important in clinical aspects including cardiovascular disease, neural disturbance, kidney disease, osteoporosis and cancer [1-6]. Obesity is based on stimulation of adipogenesis. Bone marrow mesenchymal stem cells are multipotent cells, which among other cell lineages, and give to differentiate into adipocytes, osteoblasts, chondrocytes and myoblasts [1]. This occurs through cross talk between complex signaling pathways including those derived from bone morphogenic proteins, winglesstype MMTV integration site (Wnt) proteins, hedgehogs, delta/ jagged proteins, fibroblastic growth factors, insulin, insulin-like growth factors, and transcriptional regulators of adipocyte and osteoblast differentiation including peroxisome proliferators-activated receptorgamma (PPARγ) and runt-related transcription factor 2 (Runx2) [13]. Insulin, which is secreted by feeding, stimulates adipogenesis from bone marrow mesenchymal stem cells. In addition, bone marrow adiposity and mature adipocytes with obesity greatly produces tumor necrosis factor-α (TNF-α), an inflammatory cytokine [4]. This TNF-α may cause insulin resistance that leads to type 2 diabetes.