Glucose oxidation in white adipose tissue from BIO 14.6 dystrophic hamsters

Abstract

In studies of glucose oxidation in white retroperitoneal adipose tissue of BIO 14.6 dystrophic and FIB normal hamsters aged 55–67 and 368–379 days, no difference was found in the basal state of radiolabelled 14CO2 production using either D-[6-14C]glucose or D-[1-14C]glucose. When C6-labelled glucose was used, insulin induced a slightly greater increase in glucose oxidation in dystrophic adipose tissue at both ages. When C1-labelled glucose was used, insulin enhanced glucose oxidation in dystrophic tissue more than twice normal in tissues from young animals and five times normal in tissues from the old ones. The increase in oxidation with D-[1-14C]glucose likely represents enhanced activity of the pentose phosphate pathway, which has also been observed in certain tissues of other animals with inherited skeletal-muscle degeneration. The change can probably be classified as being compensatory, an attempt by tissues to maintain functional integrity.