The effect of digitonin and altered thyroid status on palmitic acid oxidation by isolated rat liver mitochondria.
The effect of altered thyroid status and food-deprivation on palmitic acid oxidation in isolated rat liver mitochondria was studied in the absence and presence of digitonin. Mitochondria prepared from triiodothyronine-treated (hyperthyroid) and food-deprived rats metabolized palmitic acid at the same rate as the untreated controls (euthyroid). Mitochondria prepared from thyroidectomized (hypothyroid) rats metabolized palmitic acid at a rate lower than was that seen with mitochondria from euthyroid controls in either the fed or fasted state. Fasting had no effect on palmitic acid oxidation by mitochondria prepared from euthyroid rats but diminished the rates seen in both hyper- and hypothyroid states. Digitonin (0.04 mg/mg mitochondrial protein) increased the sensitivity of the rate of fatty acid oxidation to inhibition by alpha-bromopalmitic acid. The addition of digitonin to the incubation mixture resulted in two-fold increases in the rate of palmitic acid oxidation in all states. This study shows that the limitations imposed by hypothyroidism on fatty acid oxidation in intact liver are preserved in isolated mitochondria.[1]References
- The effect of digitonin and altered thyroid status on palmitic acid oxidation by isolated rat liver mitochondria. Pointer, R.H., Gipson, V.A., Mitchell, W.A. Endocr. Res. (1993) [Pubmed]
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