Premium
Quantitative pancreatic β cell MRI using manganese‐enhanced Look‐Locker imaging and two‐site water exchange analysis
Author(s) -
Antkowiak Patrick F.,
Vandsburger Moriel H.,
Epstein Frederick H.
Publication year - 2012
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.23139
Subject(s) - intracellular , chemistry , relaxation (psychology) , nuclear magnetic resonance , cell , proton , biophysics , medicine , biochemistry , biology , physics , quantum mechanics
Pancreatic β‐cell imaging would be useful in monitoring the progression of and therapies for diabetes. The purpose of this study was to develop and evaluate quantitative β‐cell MRI using manganese (Mn 2+ ) labeling of β cells, T1 mapping, and a two‐site water exchange model. Normal, pharmacologically‐treated, and severely diabetic mice underwent injection of MnCl 2 . Pancreatic water proton T1 relaxation was measured using Look‐Locker MRI, and two‐site water exchange analysis was used to estimate model parameters including the intracellular water proton relaxation rate constant (R1 ic ) and the intracellular fraction as indicators of β‐cell function and mass, respectively. Logarithmic plots of T1 relaxation revealed two distinct proton pools relaxing with different T1s, and the two‐site water exchange model fit the measured T1 relaxation data better than a monoexponential model. The intracellular R1 ic time course revealed the kinetics of β‐cell Mn 2+ labeling. Pharmacological treatments with nifedipine, tolbutamide, and diazoxide altered R1 ic , indicating that beta cell function was a determinant of Mn 2+ uptake. Intracellular fraction was significantly higher in mice with normal β cell mass than in diabetic mice (14.9% vs. 14.4%, P < 0.05). Two‐site water exchange analysis of T1 relaxation of the Mn 2+ ‐enhanced pancreas is a promising method for quantifying β cell volume fraction and function. Magn Reson Med, 2011. © 2011 Wiley‐Liss, Inc.