Bruce M. Spiegelman

TL;DR: Exercise-induced AHN improved cognition along with reduced Aβ load and increased levels of brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), fibronectin type III domain–containing protein–5 (FNDC5), and synaptic markers, however, AHN activation was also required for exercise-induced improvement in memory.

TL;DR: Data strongly suggest that PPARgamma is the predominant receptor regulating adipogenesis; however, they also suggest thatPPARalpha may play a role in differentiation of certain adipose depots in response to a different set of physiologic activators or in certain disease states.

TL;DR: Novel synthetic compounds are described that have a unique mode of binding to PPARγ, completely lack classical transcriptional agonism and block the Cdk5-mediated phosphorylation in cultured adipocytes and in insulin-resistant mice, and one such compound, SR1664, has potent antidiabetic activity while not causing the fluid retention and weight gain that are serious side effects of many of the PParγ drugs.

TL;DR: Deletion analysis of promoter-linked transfection assays and competition of these constructions in cells with a synthetic FSE2 element suggest that trans-acting factors bind to this region and act as negative regulators of aP2 gene activity in preadipocytes.

TL;DR: Fibroblastic cell lines that express PPARgamma ectopically can be induced to differentiate into fat cells by a variety of lipids and lipid-like activators of PPARs, suggesting that this protein may function to link adipogenesis with systemic lipid metabolism.