1. Diets of fresh kale (Brassica oleracea) and ryegrass (Loliumperenne) – elover (Trifolium repens) herbage were fed to growing sheep in three experiments. In Expts 1 and 3 the sheep were confined indoors and fed at hourly intervals, and all were given supplementary iodine to counteract kale goitrogens. Lambs grazed the two forages for 24 weeks in Expt 2, with and without intramuscular injections of iodized oil. The kale and herbage contained respectively 11 and <0.1 g S-methyl-L-cysteine sulphoxide (SMCO)/kg dry matter (DM) and values for readily fermentable: structural carbohydrate (CHO) were 3.1 and 0.8, respectively.
2. Blood samples were withdrawn from indwelling catheters (Expts 1 and 3) or venipuncture (Expt 2) and the plasma analysed for a range of hormones using radioimmunoassay procedures. Glucose irreversible loss (GIL) was measured in Expt 1 using primed continuous infusions of D-[U-14C]glucose. Samples of adipose tissue were removed from the shoulder area in Expt 3, and rates of D-[U-14C]glucose and [U-14C]acetate incoporation and oxidation were measured in vitro, together with the rate of glycerol release.
3. In the presence of supplementary I2, kale feeding was associated with an elevation in plasma concentration of free thyroxine (T4) Regardless of I2 supplementation, sheep fed on kale had much higher plasma growth hormone concentrations than sheep fed on ryegrass-clover herbage, and this was accompanied by reduced plasma somatostatin concentrations.
4. Plasma insulin and glucagon concentrations were similar for sheep fed on the two diets; GIL tended to be slightly but not significantly greater (9.4%) for sheep fed on kale than for those fed on ryegrass-clover herbage.
5. Kale feeding was associated with increased uptakes of acetate and glucose into adipose tissue, reduced rates of oxidation of both substrates and no difference in rate of glycerol release. Each 1 nmol increase in glucose uptake was associated with 8.7 nmol acetate uptake ( P < 0.001).
6. It is proposed that ruminants counteract protein inactivation, caused by production of dimethyl disulphide from SMCO in the rumen, through increasing circulating concentrations of growth hormone and T4, which then stimulate synthesis of replacement body proteins.