Associate Professor

Contact Information Hide Contact Information

Address: MRB 413
PO Box 245218
Tucson, AZ 85724
Phone: (520) 626-7702
E-Mail: brooksh@email.arizona.edu

Additional Information Hide Additional Information

Faculty Homepage

Research Interests

Find out more about our research at the following links

Brooks Lab on Arizona Illustrated, KUAT
http://ondemand.azpm.org/videoshorts/watch/2009/7/2/kuat-youth-in-science/

Brooks Lab in UA News
http://uanews.org/node/26052

Focus on Faculty: Dr Brooks
http://www.facultyaffairs.med.arizona.edu/FocusOnFaculty/Brooks/H_Brooks.cfm

Arizona Diabetes Program
http://www.medicine.arizona.edu/Diabetes_Program/index.cfm

Kidney and Diabetes Research in the Brooks Lab

Diabetes and congestive heart failure are diseases that have been associated with defects in the handling of salt and water by the kidney. Common in individuals with these disorders are elevated circulating levels of vasopressin, the peptide hormone that regulates renal water excretion. Circulating vasopressin plays a critical role in extra-cellular fluid expansion and development of hypertension, thus contributes to the pathogenesis of the disease.

      Vasopressin has clear long-term actions in the kidney, associated with regulatory processes at a transcriptional level as demonstrated by vasopressin-induced increases in aquaporin-2 transcription and translation. Circulating vasopressin also increases the concentrating capacity of the renal medulla by activating the counter current mechanism. The result is an increase in medullary osmotic stress that can directly activate renal cell signaling pathways and gene transcription. Thus specific effects of vasopressin on gene expression are not delineated from secondary alterations associated with this change in medullary osmolality.

      This is clinically important as patients with diabetes and heart failure have high levels of circulating vasopressin, but when treated with diuretics to reduce hypertension have decreased renal function and local osmolality.

       Our laboratory has been utilizing microarray technology to study the effects of vasopressin on gene expression in renal medullary cells. Using water restriction (WR) protocols to raise circulating vasopressin, we have identified vasopressin responsive genes in both wild type and AQP1 knockout mice. Due to the lack of a concentrating mechanism in the AQP1 knockout mice osmotically regulated transcripts should not be differentially expressed when vasopressin was increased in these mice. Our aim in applying microarray technology to the KO’s and normal mice was to rapidly identify vasopressin-responsive genes in common between the two physiological models. Our analysis revealed that 25 genes were significantly increased in both studies, i.e. increased in the water restricted wild type mice and increased in water restricted AQP1 KO animals. 15 genes were identified in common as significantly decreased following water restriction. We have focused our studies on two specific pathways that were identified as differentially expressed by in vivo increases in vasopressin: ER stress protein GRP78 and 3beta HSD steroid hormone enzymes

2) Diabetes, Menopause and Metabolic Syndrome : We are studying how sex differences effect the onset of metabolic syndrome and diabetes, focusing on diabetic kidney disease and renal function. Specifically we are identifying the role that the steroid hormones testosterone and estrogen have on glucose impairment, insulin resistance, in addition to their effect on renal salt and water transport, and regulation of extracellular fluid balance

Honours and Awards

2009 Astra Zeneca Young Investigator, American Physiological Society
2007 Lazaro Mandel Young Investigator Award, American Physiological Society
2006 APS New Investigator Award, Renal Section, American Physiological Society
2002 Research Recognition Award, American Physiological Society, Renal Section
1999 Award for Excellence in Renal Physiology (Hoechst Marion Roussel Postdoctoral Award) American Physiological Society

Selected Publications

Romero-Aleshire MJ, Diamond-Stanic MK, Hasty AH, Hoyer PB, Brooks HL. May 2009. Loss of ovarian function in the VCD mouse-model of menopause leads to insulin resistance and a rapid progression into the metabolic syndrome. Am J Physiol Regul Integr Comp Physiol,2009 May 13;

Rivera Z, Christian PJ, Marion SL, Brooks HL, Hoyer PB. Feb 2009. Steroidogenic capacity of residual ovarian tissue in 4-vinylcyclohexene diepoxide-treated mice. Biol Reprod, 80:328-36