Philipp Hammerschmidt

TL;DR: CerS6 inhibition is highlighted as a specific approach for the treatment of obesity and type 2 diabetes mellitus, circumventing the side effects of global ceramide synthesis inhibition.

TL;DR: The results suggest that AgRP neurons in mice induce not only eating, but also insulin resistance by stimulating expression of muscle-related genes in BAT, revealing a mechanism by which these neurons rapidly coordinate hunger states with glucose homeostasis.

TL;DR: The experiments reveal an unprecedented specificity of sphingolipid signaling depending on specific synthesizing enzymes, provide a mechanistic link between hepatic lipid deposition and mitochondrial fragmentation in obesity, and define the CerS6-derived sphingoipid/Mff interaction as a therapeutic target for metabolic diseases.

TL;DR: Ceramide profiling of high-fat diet-fed animals revealed increased skeletal muscle C18:0 ceramide content, concomitant with increased expression of ceramide synthase (CerS)1, revealing the tissue-specific function of distinct ceramide species during the development of obesity-associated insulin resistance.

TL;DR: A maternally expressed, imprinted lncRNA, H19, that increases BAT oxidative metabolism and energy expenditure is identified and it is demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper.