Hormonal regulation of the fibre growth and moult cycle in cashmere goats
The role of selected hormones in the control of hair follicle activity, fibre growth and moult in cashmere goats was investigated by manipulation of prolactin (PRL), thyroid hormones, and growth hormone (GH) individually or in combination. In experiment 1, the effect of different doses of the anti-thyroid drug "propylthiouracil" (PTU), on thyroxine (T4) and triiodothyronine (T3) profiles and deiodinase enzyme activities in liver, kidney and skin tissues was determined. Types II and III deiodinase enzymes were found to be present in goat skin but not type I. It was concluded that the supply of T3 within the skin was partly independent of circulating hormone profiles. In experiment 2, goats were treated with PTU, triiodothyronine (T3) and bromocriptine (Br) to decrease T3 availability to tissues and circulating PRL concentrations, respectively. Treatment with Br delayed the spring rise in plasma PRL concentrations (P=0.06) and primary (P<0.05) hair follicle activity, and delayed moult onset (P<0.01). PTU treatment did not significantly affect hair follicle activity but generally delayed the time of moult onset (P<0.05). The effects of the treatments were not additive, indicating that the actions of the two hormones were not independent. The effects of PTU and Br treatments were not exerted through changes in IGF-I binding activity in the skin, but binding was greater (P<0.01) in April than November. In experiment 3, treatment with bovine somatotropin (bST), T4 or metoclopramide to increase circulating concentrations of GH, T4 or PRL, failed to prolong the period of anagen in hair follicles, but bST increased fibre growth rate (P<0.05) and this was associated with higher circulating IGF-I concentrations. It is concluded that manipulation of the cycle of the cashmere-producing hair follicle is unlikely to be achieved through manipulation of circulating hormone concentrations alone and that much regulation of hair follicle activity occurs within the skin itself, possibly through changes in enzymes that control the supply of T3 to the follicles, in hormone receptor activity, and in the rate of synthesis of IGF-I and other growth factors within the skin.