News

Zsofia was chosen to be one of three new Scholars on the MSK T32 training grant. She will begin looking at neuronal-non-neuronal crosstalk in the hypothalamus in regulating bone mass.

I will be accepting this award 4/2025 @APS Summit in Baltimore

                                   WHAT AN HONOR!

The latest group effort between the Julius/Ingraham/Bayrer/Brierley Labs highlights the importance of EC cells in sex-differences in gut visceral pain and anxiety.

Link to Paper and Figures 

In lactating mothers, the high calcium (Ca²⁺) demand for milk production triggers significant bone resorption. While estrogen would normally counteract excessive bone loss and maintain sufficient bone formation during this postpartum period, this sex steroid drops precipitously after giving birth. Here, we report that brain-derived CCN3 (Cellular Communication Network factor 3) secreted from KISS1 neurons of the arcuate nucleus (ARC^KISS1) fills this void and functions as a potent osteoanabolic factor to promote bone mass in lactating females. Read More in our Nature Paper.

Bill will be leveraging his earlier findings in the VMHvl, where he identified an estrogen-dependent activity node. Now he will ask how chronic activation of these neurons affect aging and brain health.

Muriel is set to pursue her interests in bone biology and metabolism. She has been awarded a 5 year K08 grant so that she can take the next steps in becoming an independent faculty member.  Can't wait to see what she does.

Part of the lab celebrating after Joni signed his offer letter to join the faculty at UCB - he is starting his lab in the Department of Integrative Sciences in the College of Natural Resources. He hopes to be in his lab in late Fall after renovations. Check out his plans for the new lab and exciting research program aimed at understanding how the brain control lipid homeostasis (Link to website).

ABSTRACT

Adaptations to infectious and dietary pressures shape mammalian physiology and disease risk. How such adaptations affect sex-biased diseases remains understudied. Here, we show that sex-dependent hepatic gene programs confer a robust (~300%) survival advantage for male mice during lethal bacterial infection. The transcription factor BCL6, which masculinizes hepatic gene expression at puberty, is essential for this advantage. However, protection by BCL6 comes at a cost during conditions of dietary excess, resulting in overt fatty liver and glucose intolerance in males. Deleting hepatic BCL6 reverses these phenotypes but markedly lowers male survival during infection, thus establishing a sex-dependent tradeoff between host defense and metabolic systems. Our findings offer strong evidence that some current sex-biased diseases are rooted in ancient evolutionary trade-offs between immunity and metabolism.

Accepted 8/29/22 Science

NIDDK Mission Statement

The program will provide supplementary funds to support advanced research opportunities for exceptional emerging physician-scientists (hereafter, "candidates") holding an MD or equivalent or MD/PhD degrees, and who are early in their research careers. The supplement is intended to allow candidates to expand their research experience to help them transition beyond their clinical training to the next stage of their research careers as physician-scientists.