Motoharu Awazawa

TL;DR: A critical timing is revealed, when altered maternal metabolism disrupts metabolic homeostasis in the offspring via impairing neuronal projections, and it is shown that abnormal insulin signaling contributes to this effect.

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.

TL;DR: Although sustained weight loss improves systemic glucose homeostasis, primarily through improved inflammation and insulin action in liver, a remarkable obesogenic memory can confer long-term increases in adipose tissueinflammation and insulin resistance in mice as well as in a significant subpopulation of obese patients.