Ting Yuan

TL;DR: MST1 is identified as a proapoptotic kinase and key mediator of apoptotic signaling and beta cell dysfunction and suggested that it may serve as target for the development of new therapies for diabetes.

TL;DR: Elevated mTORC1 activation is a striking pathogenic hallmark of islets in type 2 diabetes, contributing to impaired beta cell function and survival in the presence of metabolic stress and under high-glucose conditions in metabolically stressed human islets.

TL;DR: Recent emerging advances on the contribution of mTORC2 and its associated signaling on the regulation of glucose metabolism and functional β-cell mass under physiological and pathophysiological conditions in type 2 diabetes are summarized.

TL;DR: Investigation of the combined effects of high fat/high sucrose diet feeding, ageing and TLR4-deficiency on tissue inflammation, insulin resistance and β-cell failure in mice shows that ageing exacerbates HFD-induced impairment of glucose homeostasis and pancreatic β- cell function and survival, and deteriorates H FD-induced induction of mRNA expression of inflammatory cytokines and pro-inflammatory macrophage markers.

TL;DR: Elevated macrophage-associated inflammation in human islets in obesity could be an initiating factor to the pro-inflammatory intra-islet milieu and contribute to the higher susceptibility to T2D in obese individuals.