Some aspects of the metabolism of obesehyperglycemic mice are presented in the light of recent observations on the Swedish colony of these animals. A screening procedure has been elaborated, which allows early detection of those growing mice that will later develop the obese-hyperglycemic syndrome. The observation that intraperitoneal glucose injections induce a higher frequency of glucosuria in those suckling mice which are homozygous for the obese-hyperglycemic gene furthermore suggests that the impairment of the glucose metabolism represents a primary lesion in these animals. The obese-hyperglycemic syndrome is associated with a reduced endocrine activity of the testis. Quantitative microscopic analyses of the testis, both from obese-hyperglycemic mice kept on a restricted food intake and from mice in which hyperphagia and obesity had been induced by injections of gold thioglucose, revealed that other factors than overeating and/or obesity are responsible for the depression of the testis function. An increased activity of β-glucuronidase has been reported in serum and arteries from inviduals with diabetes or severe arteriosclerosis. However, among the various tissues analysed in the obese-hyperglycemic mice only the adrenals displayed a significantly higher β-glucuronidase activity than the lean litter mates. Studies of the enzymatic dehydrogenation of isocitrate revealed considerably higher ratios between the NADP+- and NAD+-specific enzyme activities in the skeletal muscle and liver from the obese-hyperglycemic mice. The observation that the liver dehydrogenation of isocitrate was more dependent on NADP+ in the latter animals must not necessarily be attributed to the presence of a hyperlipogenesis, since similar ratios were recorded for the NADP+- and NAD+-linked isocitric dehydrogenase activities when the adipose tissue from the obese-hyperglycemic mice was compared with that from the lean sibling controls. © 1967 Springer-Verlag.
CITATION STYLE
Hellman, B. (1967). Some metabolic aspects of the obese-hyperglycemic syndrome in mice. Diabetologia, 3(2), 222–229. https://doi.org/10.1007/BF01222199
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