Androgen receptor function depends on its interaction with heat shock proteins and their co-chaperones. DNAJB1 acts as a co-chaperone in a number of pathways including androgen receptor and glucocorticoid receptor signaling. An androgenic protein co-chaperone, DNAJB1 is under transcriptional regulation by insulin, with increased hepatic expression demonstrated under conditions of reduced insulin. DNAJB1 may thus represent a common factor at the nexus of both the androgenic and insulin pathways that are frequently dysfunctional in PCOS. Throughout evolution, the ability of humans to convert glucose to triglyceride for long-term storage has provided a competitive advantage during times of famine. However, in our current Western society where food is abundantly available,Erlotinib this thrifty phenotype has resulted in excess fat accumulation leading to 65% of adults in the United States being overweight and 30% being obese. Clearly, a proper balance of the synthesis and breakdown of lipids is essential for reaching metabolic homeosta- sis, but the mechanisms responsible for controlling these processes are still not fully understood. The regulation of lipid metabolism is a very complex process, utilizing a number of signals and pathways leading to lipid synthesis, breakdown or both. Recent research has focused on understanding the regulation of lipid metabolism in liver and adipose tissue by the brain. In mammals, the arcuate nucleus of the hypothalamus serves as a main regulator of energy homeostasis by integrating signals from many circulating hormones. The ARC also receives neural inputs from other regions of the hypothalamus, one of these being the suprachiasmatic nucleus, the site of the central circadian clock. The circadian system is, in fact, known to be a major regulator of metabolic activity,Everolimus with profound metabolic pheno-types reported in clock mutant animals. However, analysis of underlying mechanisms has focused on autonomous effects of clocks located in metabolic tissues such as the control of gene expression by such clocks as well as interactions between clock proteins and metabolic factors in these tissues. Despite the connection between the ARC and the SCN, little is known about the contribution of the central clock to metabolic processes. The fruit fly, Drosophila melanogaster, is a well-established model of circadian rhythms and has recently become a powerful model to study the regulation of metabolism. In Drosophila, as in mammals, the central clock is found in specific neurons of the brain, but clocks also exist in other body tissues. However, effects of these different clocks on metabolic activity are poorly understood. We showed recently that the Drosophila fat body contains a circadian clock, which regulates the storage of glycogen and triglycerides. Clocks in neurons also affect glycogen storage, but the specific neurons responsible were not identified and the control of triglyceride levels by neuronal clocks was not assessed. Here, we sought to explore a role of the central clock neurons in the accumulation of lipids. We report that knocking down the function of the circadian gene, Clock in central clock cells leads to increased triglycerides in the fly’s fat body. We observe a similar phenotype when we trigger premature degeneration in these neurons. However, triglyceride levels are normal in arrhythmic flies that express the heat-sensitive ion channel dTRPA1 in the PDF neurons and in Pdf01 mutants, suggesting that these neurons control fat storage independently of the circadian rest:activity output.