AJP - Endocrinology and Metabolism, Vol 240, Issue 6 669-E676, Copyright © 1981 by American Physiological Society
Effects of hypophysectomy and thyroidectomy on leucine metabolism in adipose tissue
V. Coiro, G. P. Frick, L. E. Braverman and H. M. Goodman
Hypophysectomy doubled the rate of oxidation of L-[1-14C]leucine to 14CO2
by segments of rat epididymal adipose tissue. Thyroidectomy, but not
adrenalectomy, produced identical results. Acceleration of leucine
oxidation occurred even in the presence of glucose and saturating
concentrations of insulin and leucine, suggesting that thyroidectomy
increased the capacity to degrade leucine. Treatment of thyroidectomized
rats with triiodothyronine (T3) decreased leucine oxidation, but at least 4
days were required. Treatment of hypophysectomized rats with T3 for 6 days
was ineffective unless growth hormone was also given. A similar
acceleration was also seen in the rate of oxidation of
alpha-keto[1-14C]isocaproate, the deaminated analogue of leucine, but
neither hypophysectomy nor thyroidectomy accelerated the rate of oxidation
of isovalerate, the next metabolite in the degradative sequence. These
observations suggested that hypothyroidism, whether primary or secondary,
might increase the activity of the mitochondrial reaction responsible for
the decarboxylation of alpha-ketoisocaproate. Because thyroidectomy failed
to modify the rate of oxidation of [1-14C]pyruvate that occurs by an
analogue reaction and requires the same cofactors, an effect of
thyroidectomy on cofactor availability was ruled out. Direct assay in a
cell-free homogenate revealed a nearly twofold increase in the activity of
the alpha-ketoisocaproate dehydrogenase enzyme complex. The findings
support the conclusion that hypothyroidism increases the amount or activity
of the mitochondrial enzyme complex responsible for decarboxylation of
branched-chain alpha-keto acids.
