EFFECT OF THYROIDECTOMY ON THE ACTIVITY OF Α-Glucosidases AND ACID HYDROLASES IN THE SMALL INTESTINE OF RATS DURING WEANING

Abstract

Adrenalectomy performed on 14-day-old rats delayed the usual increase of sucrase and maltase activity as well as the decrease of acid beta-galactosidase, beta-glucuroindase and N-acetyl-beta-glucosaminidase activity during the third postnatal week. Since these changes were only delayed, the role of the thyroid was explored. Thyroidectomy performed simultaneously with adrenalectomy on 14-day-old rats did not influence the increase in body weight and growth of the small intestine (already slowed down by adrenalectomy), but caused a further substantial delay in the maturation of the enzyme profile of the small intestine. Our results indicate that the thyroid is involved in regulation of the hydrolases studied.

Alterations in Intestinal Function in Response to Thyroxine and Cortisone Administration in Undernourished Rats

“…The administration of thyroxine or cor tisone to undernourished rats during the 3rd week of postnatal development stimulated the sucrase and alkaline phosphatase activi ties (3-to 6-fold) while lactase activity was significantly reduced under these conditions. The role of thyroxine and corticosteroids in the regulation of sucrase activity has been well documented in experimental animals [5], Adrenalectomy or thyroidectomy results in a delay in the appearance of sucrase activ ity in rats [15,16]. During early postnatal life, lactase activity is maximum and it falls con siderably at the end of the 3rd week of post natal life when sucrase activity begins to ap pear and gradually increases to a constant level [22], The development of alkaline phos phatase is also reported to be affected with steroids [20].…”

Intestinal Development in Suckling Rats: Direct or Indirect Spermine Action?

“…The litter with adrenalectomized pups was given 0.9% NaCl solution instead of tap water in drinking bottles [23]. In the present study, all adrenalectomized rats received a daily intraperitoneal injection of aldosterone (8 pg/100 g body weight) because previous investigations showed that without mineralocorticoid replacement following adre nalectomy, the mortality of rats is extremely high [5,24], On day 11, some adrenalectomized animals received orally administered sper mine (8 pmol/50 pi NaCl 0.9%), once a day for 3 days, and others received NaCl (0.9%).…”

Development of the gastrointestinal tract

“…However, the question of whether intestinal maturation is absolutely dependent on glucocorticoids has not been adequately addressed in the literature. Several studies have shown that enzymic development is delayed but not abolished in adrenalectomized rat pups (Moog, 1953;Koldovsky et al 1965Koldovsky et al , 1975). The problem with these studies was that none of them included either mineralocorticoid replacement or measurement of serum corticosterone following the adrenalectomy.…”

“…Thyroxine (T,) has received considerable attention as a candidate for regulation of intestinal development in the rat because its circulating concentration rises significantly during the second postnatal week (Henning, 198 I). Administration of T, or triiodothyronine has been shown to cause precocious decline of jejunal lactase activity (Paul & Flatz, 1983) and ileal lysosomal hydrolases (Koldovsky et al 1974), and precocious increases of jejunal sucrase and maltase (Jumawan & Koldovsky, 1978). Conversely, hypothyroidism delays but does not prevent the usual decline of lactase and lysosomal hydrolases and the usual increases of sucrase and maltase activities (Yeh & Moog, 1974Koldovsky et al 1975;Henning, 1978a,b).…”

“…Administration of T, or triiodothyronine has been shown to cause precocious decline of jejunal lactase activity (Paul & Flatz, 1983) and ileal lysosomal hydrolases (Koldovsky et al 1974), and precocious increases of jejunal sucrase and maltase (Jumawan & Koldovsky, 1978). Conversely, hypothyroidism delays but does not prevent the usual decline of lactase and lysosomal hydrolases and the usual increases of sucrase and maltase activities (Yeh & Moog, 1974Koldovsky et al 1975;Henning, 1978a,b). The significance of findings such as these must be questioned in view of the fact that administration of T, causes a precocious increase in plasma corticosterone and that hypothyroidism virtually abolishes the developmental rise of corticosterone (Malinowska et al 1974;Yeh & Moog, 1977; D'Agostino .…”