Wool strength is a heritable trait and varies widely between individuals even when they are maintained under equivalent conditions nutritionally. Consequently, it is valid to search for genetic markers of wool strength with the aim of using them in improving fleece quality. Wool strength is closely related to winter wool growth (Geenty et al. 1984). It is thought that the diminished follicle activity at this time reduces fibre diameter (Ross et al. 1965). This thesis investigates some of the mechanisms which may control wool growth. Such understanding will consequently aid a future search for genetic markers of wool strength. Blood plasma from eighty-six sheep was assayed for a number of metabolites and growth factors including glucose, urea, β-hydroxybutyrate, creatinine, insulin, insulin-like growth factor I, growth hormone, cortisol and melatonin. A correlation was observed between elevated plasma insulin and reduced plasma glucose and wool strength. Some changes in peripheral tissue sensitivity to insulin were also found. For example, in an indoor treatment high wool strength animals showed some peripheral tissue resistance to insulin. These data suggest that the control of and/ or mechanisms of glucose uptake vary between high and low wool strength animals. Insulin binding by the skin was investigated. No significant differences in insulin receptor binding were found between the skin of high and low wool strength animals. Although it is possible that differences could have been masked by the variable nature of the data, the evidence available from this and previous studies suggest that highly variable insulin binding between individuals by ovine tissues is a 'normal' observation. The lack of correlation between insulin receptor binding and wool strength was consequently thought to be real. Differences in tissue sensitivity to insulin were therefore hypothesised to lie with a post-receptor mechanism. The expression of glucose transporters 1 and 4 was assessed in tissues of high and low wool strength sheep using human cDNA probes. Appropriate human cDNA probes were also used to evaluate the expression of the insulin and insulin-like growth factor I receptor genes and the gene for ribosomal protein S6. Except for the ribosomal protein S6 gene, low to nil expression of these genes was observed in all the tissues examined when compared to the constitutively expressed B-actin gene. Expression could not be stimulated by chronic (5 hour) insulin infusion. Low expression was not thought to be due solely to a lack of homology between ovine and human sequences suggesting the expression of genes involved in glucose uptake is extremely low in sheep. The glucose transporter 1 gene was expressed at low levels in skin, wool follicles and brain tissue but not in muscle and fat tissue. This suggests that skin, like brain tissue, has an absolute requirement for glucose, a situation not found in adipose and muscle tissue. Glucose transporter I is generally reported to be associated with non-insulin dependent glucose uptake. From this it was concluded that elucidation of the mechanisms by which glucose is taken up into different tissues provides the key to understanding the controlling factors by which glucose is partitioned to the wool follicle. Such a mechanism could be influenced by insulin either directly by its action on the wool follicle, or indirectly, by causing insulin resistance in muscle and adipose tissues which partitions glucose to the skin where it is taken up in an insulin-independent manner. [Show full abstract]

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