Effect of riboflavin deficiency on lipid metabolism of liver and brown adipose tissue of sucking rat pups.

An increase in liver: body-weight and in hepatic triacylglycerol content, together with changes in the fatty acid profiles of hepatic phospholipids, were observed as a result of moderate riboflavin deficiency in sucking rat pups. Oxygen consumption by hepatic mitochondria, with palmitoyl L-carnitine as substrate, was not significantly impaired. Mitochondria from interscapular brown adipose tissue, however, showed a marked impairment of O2 consumption, with palmitoyl L-carnitine as substrate, in the riboflavin-deficient pups. This impairment was also apparent after uncoupling with carbonyl cyanide p-trifluoromethoxyphenylhydrazone, but was not consistently observed after the addition of GDP to suppress uncoupled oxidation. It was much less evident, and did not reach statistical significance, for the mitochondria of brown adipose tissue of the corresponding deficient dams. Binding of 3H-labelled GDP by brown adipose tissue mitochondria was unaffected by riboflavin deficiency in the pups, suggesting that the effect on O2 consumption is more likely to be due to impaired integrity of the mitochondrial respiratory chain, than to impairment of the specific capacity for uncoupling of respiration which is characteristic of brown adipose tissue mitochondria. Total cytochrome c oxidase (EC 1.9.3.1) activity of the brown adipose tissue of riboflavin-deficient pups was not significantly reduced. A small but significant impairment was observed in the stimulation of whole-body O2 consumption by injected noradrenaline in the riboflavin-deficient pups, suggesting that the impairment of brown adipose tissue mitochondrial function may be accompanied by impaired physiological capacity in vivo.