Postdoc Profiles


Name: Ruiz, Henry H.
Year you started at ISMMS: 2014
Lab: Christoph Buettner

 
Lab Mailing Address:

One Gustave L Levy Place, Box 1234
ATRAN 4-23
New York, NY 10029

Phone: 212-241-0887
E-mail: henry.ruiz@mssm.edu

Project/Research Interests:

My primary research interest is to study the role of central nervous system (CNS) signaling on regulating immunity and endocrine homeostasis. Specifically, I am interested in studying the contribution of the autonomic nervous system (ANS) to the chronic low-grade white adipose tissue (WAT) inflammation observed in obesity and diabetes. Since my graduate training focused on the neuroscience of neuropsychological and autoimmune disorders, for my postdoctoral work I sought to develop an expertise in endocrinology. To this end, I joined Christoph Buettner’s laboratory where I have learned techniques that allowed me to study the link between obesity/diabetes and Alzheimer’s disease (AD). This work resulted in a manuscript that is currently under review for publication in the journal of Alzheimer’s and Dementia.
Using the Cre-Lox Recombination technique, I am actively engaged in the development of a mouse model of inducible genetic sympathectomy that is peripherally restricted. When complete, these mice would allow us to determine the contribution of the sympathetic nervous system to carbohydrate and lipid metabolism and immunity. Furthermore, in collaboration with Dirik Homann and using bone marrow transplant techniques, the role of the sympathetic nervous system (SNS) on obesity/diabetes-induced inflammation as well as other models can be addressed.
In addition, I am currently studying the role of alcohol binge-induced unrestrained lipolysis on hepatic steatosis. To assess this, we are using mice genetically altered to selectively knock out (KO) adipose triglyceride lipase (ATGL) in WAT, an enzyme necessary for lipolysis, thereby rendering these mice unable to undergo lipolysis from WAT. We have found that ATGL KO mice are protected from alcohol binge-induced hepatic steatosis. This finding suggests that excess fatty acid flux from WAT to the liver as a result of unrestrained lipolysis may be an important contributor to fatty liver and further suggests lipolysis inhibition as a potential therapeutic target to for the treatment of fatty liver. A manuscript regarding these findings is currently being drafted for publication submission.
Moving forward, I expect to learn and perform experiment using the euglycemic clamp technique (and its variations), which is a main area of Dr. Buettner’s expertise as this will allow me to examine the effect of different brain manipulations on endocrine homeostasis and inflammation.

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