Cytochemical studies of adipose tissue-associated blood vessels in untreated and thyroxine-treated hypophysectomized pig fetuses.

Fetal hypophysectomy (hypox) slightly enhances lipid accretion in adipose tissue and markedly increases fat cell size and de novo lipogenesis. Thyroxine (T4) treatment (14 to 20 d) had no influence on fat cell size but markedly increased lipogenesis, lipid accretion, and apparent fat cell number in hypox fetuses. Although vascular development is intimately associated with preadipocyte development in the fetus, little is known concerning the regulation of vascular development per se by T4 and other adipogenic hormones. Therefore, the purpose of the present study was to evaluate the development of qualitative traits of the adipocyte-associated vasculature after fetal hypox with and without T4 treatment. Type IV collagen immunoreactivity of and lectin binding by capillaries in large fat cell clusters was reduced by hypox, and binding of the soybean agglutinin lectin was completely lost. Reactivity for cytosolic markers in capillaries was also reduced by fetal hypox. These blood vessel traits were not influenced by T4 treatment. The qualitative aspects of capillary development in large fat cell clusters were not influenced by hypox or T4 treatment. On a qualitative basis, blood vessels in the skin and in small fat cell clusters were not affected by hypox. Lectin binding by adipocytes was enhanced by hypox regardless of the size of clusters, and T4 augmented this response to hypox. These studies demonstrate that endocrine regulation of the differentiation of the adipocyte-associated vasculature is more complex than the endocrine regulation of adipocyte differentiation per se.