Constitutional Thinness: tALKing the tALK or wALKing the wALK?

Abstract

The role of the carbohydrate response element-binding protein in male fructose-fed rats. Endocrinology 154, 36-44.

Olanzapine Modulate Lipid Metabolism and Adipose Tissue Accumulation via Hepatic Muscarinic M3 Receptor-Mediated Alk-Related Signaling

“…Following the recent identification of Alk as a key gene in the regulation of thinness, it has been proposed that Alk inhibition is a potential target for obesity therapy [9]. In fact, a number of Alk inhibitors (e.g., Crizotinib, Ceritinib, and Lorlatinib) have been used for treating some types of cancers for decades, but with a number of adverse effects [10,[67][68][69]. This study provides novel evidence of a regulatory role of the hepatic M3R in Alk-modulated lipid metabolism and adipose tissue accumulation, which provides a new direction for the development of drugs for use in modulating hepatic Alk signaling that warrant further investigation.…”

“…Recently, Orthofer et al reported that the sympathetic control of adipose tissue lipolysis was linked to the Alk pathway modulating energy expenditure [9]. This finding came under the spotlight [10], and was supported by a recent study which found that Augmentor α (Augα), one of newly discovered ligands of Alk, appeared to control body weight through a hypothalamic pathway [11]. Since the sympathetic system and the parasympathetic system are the two arms of the autonomic nervous system [12].…”