Umut Ozcan

TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).

TL;DR: It is demonstrated that chemical chaperones enhance the adaptive capacity of the ER and act as potent antidiabetic modalities with potential application in the treatment of type 2 diabetes.

TL;DR: It is shown that increased endoplasmic reticulum stress and activation of the unfolded protein response in the hypothalamus of obese mice inhibits leptin receptor signaling and chemical chaperones, 4-phenyl butyric acid, and tauroursodeoxycholic acid, act as leptin-sensitizing agents, which may provide the basis for a novel treatment of obesity.

TL;DR: It is discovered that Celastrol, a pentacyclic triterpene extracted from the roots of Tripterygium Wilfordi (thunder god vine) plant, is a powerful anti-obesity agent and a promising agent for the pharmacological treatment of obesity.

TL;DR: In this article, it was shown that loss of tuberous sclerosis complex genes (TSC1 or TSC2) leads to constitutive activation of mTOR and downstream signaling elements, resulting in the development of tumors, neurological disorders, and severe insulin/IGF-1 resistance.