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Research Article Free access | 10.1172/JCI105521
Gastroenterology Laboratory, Mallory Institute of Pathology, Boston, Mass.
Second and Fourth [Harvard] Medical Services, Boston City Hospital, Boston, Mass.
Department of Medicine, Harvard Medical School, Boston, Mass.
Department of Microbiology, Boston University School of Medicine, Boston, Mass.
Department of Pathology, Boston University School of Medicine, Boston, Mass.
†Present address: Dept. of Medicine, State University of New York (Downstate) and Dept. of Medicine, Maimonides Hospital, Brooklyn, N. Y.
‡Address requests for reprints to Dr. N. Zamcheck, Boston City Hospital, Boston, Mass. 02118.
*Submitted for publication June 6, 1966; accepted October 20, 1966.
This investigation was supported by research grants T1 AM 5320, National Institute of Arthritis and Metabolic Diseases; CA 02090 and CA 04486, National Cancer Institute; and GMO 9628, National Institute of General Medical Sciences, National Institutes of Health, Bethesda, Md. A preliminary report appeared in Fed. Proc. 1965, 24, 403.
Find articles by Deren, J. in: JCI | PubMed | Google Scholar
Gastroenterology Laboratory, Mallory Institute of Pathology, Boston, Mass.
Second and Fourth [Harvard] Medical Services, Boston City Hospital, Boston, Mass.
Department of Medicine, Harvard Medical School, Boston, Mass.
Department of Microbiology, Boston University School of Medicine, Boston, Mass.
Department of Pathology, Boston University School of Medicine, Boston, Mass.
†Present address: Dept. of Medicine, State University of New York (Downstate) and Dept. of Medicine, Maimonides Hospital, Brooklyn, N. Y.
‡Address requests for reprints to Dr. N. Zamcheck, Boston City Hospital, Boston, Mass. 02118.
*Submitted for publication June 6, 1966; accepted October 20, 1966.
This investigation was supported by research grants T1 AM 5320, National Institute of Arthritis and Metabolic Diseases; CA 02090 and CA 04486, National Cancer Institute; and GMO 9628, National Institute of General Medical Sciences, National Institutes of Health, Bethesda, Md. A preliminary report appeared in Fed. Proc. 1965, 24, 403.
Find articles by Broitman, S. in: JCI | PubMed | Google Scholar
Gastroenterology Laboratory, Mallory Institute of Pathology, Boston, Mass.
Second and Fourth [Harvard] Medical Services, Boston City Hospital, Boston, Mass.
Department of Medicine, Harvard Medical School, Boston, Mass.
Department of Microbiology, Boston University School of Medicine, Boston, Mass.
Department of Pathology, Boston University School of Medicine, Boston, Mass.
†Present address: Dept. of Medicine, State University of New York (Downstate) and Dept. of Medicine, Maimonides Hospital, Brooklyn, N. Y.
‡Address requests for reprints to Dr. N. Zamcheck, Boston City Hospital, Boston, Mass. 02118.
*Submitted for publication June 6, 1966; accepted October 20, 1966.
This investigation was supported by research grants T1 AM 5320, National Institute of Arthritis and Metabolic Diseases; CA 02090 and CA 04486, National Cancer Institute; and GMO 9628, National Institute of General Medical Sciences, National Institutes of Health, Bethesda, Md. A preliminary report appeared in Fed. Proc. 1965, 24, 403.
Find articles by Zamcheck, N. in: JCI | PubMed | Google Scholar
Published February 1, 1967 - More info
The administration of a carbohydrate-containing diet for 24 hours to rats previously fasted for 3 days led to a twofold increase in total intestinal sucrase and sucrase specific activity. The specific activity of maltase was similarly increased, but lactase activity was unaffected. The sucrose-containing diet led to a greater increase in sucrase than maltase activity, whereas the converse was true of the maltose-containing diet. A carbohydrate-free isocaloric diet led to a slight increase in the total intestinal sucrase, but sucrase specific activity was unchanged. Assay of sucrase activity of mixed homogenates from casein-fed and sucrose-fed rats or fasted and sucrose-fed animals yielded activities that were additive. The Michaelis constant (Km) of the enzyme hydrolyzing sucrose was similar in the fasted, casein-fed, and sucrose-fed rats. The maximal velocity (Vmax) was twice greater in sucrose-fed as compared to casein-fed or fasted rats, suggesting an increased quantity of enzyme subsequent to sucrose feeding.
Adrenalectomized rats maintained on 1.0% salt intake had sucrase and maltase levels comparable to those of controls. Steroid administration did not significantly increase their activities. The response to sucrose feeding was similar in both control and adrenalectomized rats, indicative of the absence of steroidal control on sucrase and maltase activity in the adult animal.
Studies using intestinal ring preparations indicated that sucrose hydrolysis by the intact cells proceeded more rapidly when animals were fed sucrose. Additional corroboration of the physiologic significance of the increased enzyme levels in homogenates was afforded by intestinal perfusion studies. Sucrose hydrolysis increased twofold and fructose absorption fourfold in animals fed sucrose when compared to either fasted or casein-fed rats.