Koletsky Rats Research Articles

Adrenal hydroxylations in genetically obese and hypertensive rats

The separate steps in the formation of aldosterone from cholesterol were studied in a strain of spontaneously hypertensive rats in which phenotypic obesity is inherited as a recessive trait (Koletsky rats). The obese and hypertensive state had little or no effect on side-chain cleavage of cholesterol, formation of progesterone from pregnenolone or 21-hydroxylation. Mitochondrial 18-hydroxylation of endogenous and exogenous corticosterone, however, as well as 18- and 11β-hydroxylation of deoxycorticosterone, were increased in obese hypertensive rats, both when compared with non-obese hypertensive siblings and when compared with healthy Sprague-Dawley rats. 18-Hydroxylation of corticosterone was increased more than 18-hydroxylation of deoxycorticosterone. In non-obese hypertensive rats, the adrenal content of mitochondrial cytochrome P-450 was lower than that in obese hypertensive rats but higher than that in rats of the conventional Sprague-Dawley strain. The results are discussed with respect to possible heterogeneity of adrenal cytochrome P-450 and to possible explanations for the changes observed.

Genetics of obesity in zucker rats and koletsky rats

The breeding data on Zucker rats and on Koletsky rats confirm that the obesity in these two strains of rats is inherited recessively and results from single gene mutations. Mating a Zucker heterozygote to a Koletsky heterozygote produced obese F1 progeny. Inter-stock breeding results indicate that the obesity in the Zucker-Koletsky hybrid stock is also inherited in a recessive manner. The gene that controls obesity in the Zucker rats, fatty (fa), and the gene that controls obesity in the Koletsky rats, f, are thus alleles at the same locus. We propose that f be renamed fak until it can be proven that fa and fak are identical.