Inhibition of RANKL and Sema4D improves residual ridge resorption in mice.

Residual ridge resorption (RRR) is a chronic and progressive bone resorption following tooth loss. It causes deterioration of the oral environments and leads to the pathogenesis of various systemic diseases. However, the molecular mechanisms and risk factors for RRR progression are still unclear and controversial.

Comparison of the prognosis of the remaining teeth between implant-supported fixed prostheses and removable partial dentures in partially edentulous patients: A retrospective study.

Background: There have been several reports about the prognosis of teeth adjacent to edentulous spaces for implant-supported fixed prostheses (ISFPs) and removable partial dentures (RPDs). However, there are few reports about the prognosis of the other remaining teeth comparing ISFPs with RPDs.

Purpose: The aim of this study was to evaluate and compare the prognosis of the remaining teeth for ISFPs and RPDs in terms of survival and complication-free rates.

Diacylglycerol kinase δ functions as a proliferation suppressor in pancreatic β-cells.

Although an aberrant reduction in pancreatic β-cell mass contributes to the pathogenesis of diabetes, the mechanism underlying the regulation of β-cell mass is poorly understood. Here, we show that diacylglycerol kinase δ (DGKδ) is a key enzyme in the regulation of β-cell mass. DGKδ expression was detected in the nucleus of β-cells.

Myristic acid specifically stabilizes diacylglycerol kinase δ protein in C2C12 skeletal muscle cells.

Decreased levels of the δ isozyme of diacylglycerol kinase (DGK) in skeletal muscle attenuate glucose uptake and, consequently, are critical for the pathogenesis of type 2 diabetes. We recently found that free myristic acid (14:0), but not free palmitic acid (16:0), increased the DGKδ protein levels and enhanced glucose uptake in C2C12 myotube cells. However, it has been unclear how myristic acid regulates the level of DGKδ2 protein.

Chronic administration of myristic acid improves hyperglycaemia in the Nagoya-Shibata-Yasuda mouse model of congenital type 2 diabetes.

Aims/hypothesis: Previously, we demonstrated that myristic acid (14:0) increases levels of diacylglycerol kinase (DGK) δ, a key enzyme involved in type 2 diabetes exacerbation, and enhances glucose uptake in C2C12 myotube cells. Moreover, results from a population-based cohort study suggest that consumption of high-fat dairy products, which contain high amounts of myristic acid, is associated with a lower risk of developing type 2 diabetes. Taken together, we hypothesised that intake of myristic acid reduces type 2 diabetes risk in vivo.