Quantitative Radioautography of Sugar Transport in Intestinal Biopsies from Normal Humans and a Patient with Glucose-Galactose Malabsorption

Charles E. Stirling; Albert J. Schneider; Ming-Der Wong; William B. Kinter

doi:10.1172/JCI106830

^{Department of Physiology, State University of New York Upstate Medical Center, Syracuse, New York 13210}

^{Department of Pediatrics, State University of New York Upstate Medical Center, Syracuse, New York 13210}

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^{Department of Physiology, State University of New York Upstate Medical Center, Syracuse, New York 13210}

^{Department of Pediatrics, State University of New York Upstate Medical Center, Syracuse, New York 13210}

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^{Department of Physiology, State University of New York Upstate Medical Center, Syracuse, New York 13210}

^{Department of Pediatrics, State University of New York Upstate Medical Center, Syracuse, New York 13210}

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^{Department of Physiology, State University of New York Upstate Medical Center, Syracuse, New York 13210}

^{Department of Pediatrics, State University of New York Upstate Medical Center, Syracuse, New York 13210}

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Published in Volume 51, Issue 2 on February 1, 1972
J Clin Invest. 1972;51(2):438–451. https://doi.org/10.1172/JCI106830.
© 1972 The American Society for Clinical Investigation

Published February 1, 1972 - Version history

Both galactose accumulation and phlorizin binding by columnar epithelial cells have been investigated in vitro with a recently developed technique for high-resolution, plastic-section radioautography which is particularly suited to small quantities of biopsy tissue. Grain density analysis of the radioautographs provides definitive support for the view that the cellular mechanisms underlying glucose-galactose absorption in laboratory animals are fully applicable to the small intestine of man. Even the number of sugar carriers at the microvillar membrane appears similar and the major quantitative difference, lower affinity for phlorizin in man, correlates with the finding that phlorizin is also a less potent inhibitor of uphill, galactose transport at the microvilli. In addition, radioautographs of biopsies taken 2 yr apart from a patient with glucose-galactose malabsorption provide evidence that the cellular defect in this inborn error of transport is a persistent reduction in the number of functioning sugar carriers at the microvillar membrane.

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