Marguerite Hatch, Ph.D.

Professor

Hatch

UF Department of Pathology, Immunology and Laboratory Medicine
College of Medicine
P.O. Box 100275
Gainesville, FL 32610

Office Location and Express Mail
UF Department of Pathology, Immunology and Laboratory Medicine
College of Medicine

1395 Center Drive, D6-33A
Gainesville, FL 32610

Administrative Support AST I: Ethan Maia de Needell
  • Phone: 352.294.8493
  • Fax: 352.294.5433

Dr. Hatch’s general interests are focused on the mechanisms and control of electrolyte and solute transport across epithelial membranes. She is particularly interested in transport mechanisms for the oxalate anion across intestinal and renal epithelial in the context of calcium oxalate kidney stone disease and primary hyperoxaluria.

Current investigations in Dr. Hatch’s laboratory are focused on several anion exchangers in the SLC26A gene family that are involved in epithelial oxalate transport. Using a variety of transport physiology and molecular biology approaches and studies that include whole animal (mouse knockout models) and tissue (intestine and kidney), in addition to cell culture studies, her team evaluates the contribution of specific transport proteins to epithelial movements of oxalate. Dr. Hatch also focuses on the physiological interaction between the gut-resident oxalobacter formigenes and the enterocyte, which results in alterations of intestinal oxalate transport and enteric elimination of oxalate and leads to reduced renal excretion of this stone-forming compound.

Curriculum Vitae

Publications

  • Hatch, M., Allison, M.J., Yu, F, and Farmerie, W. 2017. The Genome Sequence of Oxalobacter formigenes Strain HC-1. Genome A 5: #27.
  • Hatch, M., Allison, M.J., Yu, F, and Farmerie, W. 2017. The Genome Sequence of Oxalobacter formigenes Strain OXCC13. Genome A 5: #28.
  • Whittamore J.M., and Hatch M. 2017. Loss of the Cl-/HCO3- exchanger, DRA (Slc26a3), enhances ileal sulfate absorption and alters sulfate homeostasis in a model of congenital chloride diarrhea. Am. J. Physiol. Gastrointest. Liver Physiol. Sep 1;313 (3):G166-G179.
  • Canales, B.K. and Hatch, M. 2017. Oxalobacter formigenes colonization normalizes oxalate excretion in a gastric bypass model of hyperoxaluria. (Surg Obes Relat Dis. 2017 Jul;13(7):1152-1157.
  • Hatch, M. 2017. Gut microbiota and oxalate homeostasis. Invited Perspective. Annals of Translational Medicine. 5 (2): 36.
  • Whittamore J.M., and Hatch M. 2017. The role of intestinal oxalate transport in hyperoxaluria and the formation of kidney stones in animals and man. Invited Review. Urolithiasis 45: 89-108.
  • Hatch, M. and Canales, B.K. 2016. The mechanistic basis of hyperoxaluria following gastric bypass in obese rats. Urolithiasis 44: 221-230.
  • Whittamore J.M., and Hatch M. 2015. Chronic metabolic acidosis reduces urinary oxalate excretion and promotes intestinal oxalate secretion in the rat. Urolithiasis. Nov;43(6):489-99 (Epub ahead of print 07/2015).
  • Whittamore J.M., Frost S.C., Hatch M. 2015. Effects of acid-base variables and the role of carbonic anhydrase on oxalate secretion by the mouse intestine in vitro. Physiol Rep. Feb 25;3(2).
  • Klimesova, K., Whittamore, J.M., and Hatch, M. 2015. Bifidobacterium animalis subsp. lactis decreases urinary oxalate excretion in a mouse model of Primary Hyperoxaluria. Urolithiasis. 43:107-117. e-pub October 2014.
  • Hatch, M. 2014. Intestinal Adaptations in Chronic Kidney Disease and the Influence of Gastric Bypass Surgery. Exp. Physiol. 99(9):1163-7.
  • Canales, B.K. and Hatch, M. 2014. Kidney stone incidence and metabolic urinary changes after modern bariaric surgery: Review of clinical studies, experimental studies, and preventative methods. Surg. Obes. Rel. Dis. oxalate. Surg Obes Relat Dis. 10(4):734-742