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1 Departments of Medicine, Harvard Medical School and Peter Bent Brigham Hospital; Baker Clinic Research Laboratories, New England Deaconess Hospital; and Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts
Free fatty acid mobilization and glucose metabolism to CO2, to glyceride-glycerol, to fatty acids and to glycogen by adipose tissue in vitro were studied in genetically obese hyperglycemic mice (O-H), in goldthioglucose-injected obese Swiss mice and in their respective nonobese littermates. Tissue from O-H mice metabolizes less glucose than tissue from their nonobese littermates in absence of added hormone or in the presence of insulin (0.1 unit/ml) or epinephrine (104 m). In addition, there is also a diminished ability for insulin to inhibit and for epinephrine to augment free fatty acid release. No such differences were observed between tissues from goldthioglucose-injected obese Swiss mice and tissues from their lean littermates. Possible significance of these in vitro results with regard to the pathogenesis of the obese hyperglycemic syndrome is discussed.
Submitted on January 16, 1961
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