This study shows Gβγ-signaling exerting control over physiology by regulating neurohormone exocytosis. The Gβγ-SNAP25 interaction is a potential drug target, and targeting this pathway that modulates neuroendocrine signals would be a unique approach to treating metabolic disease.
Zack Zurawski and Simon Alford developed a method to measure norepinephrine release from sympathetic neurons in inguinal adipose depots. Using this method, we show that inguinal fat pad sympathetic neurons from SNAP25Δ3/Δ3 mice have enhanced and prolonged norepinephrine release.
Check out our new JCI paper (a thread)
Gβγ-SNAP25 exocytotic brake removal enhances insulin action, promotes adipocyte browning, and protects against diet-induced obesity
jci.org/articles/view/…@hamm_heidi
Researchers, including senior authors @hamm_heidi and Sheila Collins, PhD, have uncovered a potential new way to help curb the rapidly rising worldwide prevalence of metabolic disorders, including obesity and diabetes.
Published in @jclinicalinvest.
spr.ly/6015PIoRB