Responses of sheep to annual cycles in nutrition. 2. Effects of diet and endogenous growth hormone during replenishment

Abstract

AbstractThe rôle of growth hormone (GH) in normal growth is well established, but its rôle during recovery after live-weight loss in adults is less defined. This study examined the interaction of endogenous GH with energy or protein supplements during re-feeding of ewes in low body condition. Control ewes and ewes immunized against growth hormone-releasing hormone were housed in individual pens and given food below maintenance for 107 days, before re-feeding was initiated by supplementing half of each group with either fish meal or barley for 28 days (P1), after which the supplements were switched for a further 28 days (P2). Following supplementation, the ewes grazed abundant green pasture for 92 days before slaughter. Immunization reduced plasma concentrations of GH, insulin, insulin-like growth factor 1 (IGF-1) and prolactin. Production responses to the two food supplements were similar in the control and immunized ewes, but when grazed at pasture immunized ewes gained live weight more slowly (P = 0·06), grew less wool (P<0·01), and had heavier fat depots, but lighter carcass, skin and liver weights at slaughter. The sequence of re-feeding treatments affected subsequent wool production in both control and immunized ewes. During P2, and for 52 days after supplementation ceased, ewes supplemented with fish meal then barley (F/B) produced less wool (P < 0·05) than those supplemented with barley followed by fish meal (B/F). At slaughter, the F/B ewes had lighter omental and kidney fat depots than the B/F ewes (P < 0·05). It is concluded that during live-weight regain, endogenous GH initially affected fat deposition, which in turn affected food intake and wool growth. Furthermore, provision of supplements with a high protein to energy ratio to sheep in low body condition, followed by supplements with a low protein to energy ratio, caused a prolonged suppression of wool growth. This effect was not mediated by endogenous GH.