The influence of cobalt and vitamin 8 /12 deficiency on reproductive, adrenal and thyroid function of the female goat

Abstract

Twenty normocyclic female East African short horned goats were divided into four groups of 5 each and were made Vitamin deficient (3 groups) by feeding them cobalt deficient rhode grass hay from the Rift l/alley of Kenya, Maximal reduction in plasma 8 (determined by competitive inhibition radioassay kit) occured after 8 weeks parallel with reduction in body weight, and onset of macrocytic normochromic (i.e. pernicious) anaemia. The oestrous cycles became progressively irregular and finally ceased after the fifth oestrus. Blood was collected at 2 day intervals during the first month and at 3 day intervals thereafter up to 23 weeks (except at oestrus where collection was at 3 hourly intervals). Plasma progesterone, oestrogens, LH and pituitary LH, plasma corticosteroid and thyroid hormones (T^ and T^) were determined by respective radioimmunoassays. Peak plasma progesterone (Day + 9 to Day - 4) and oestrogens (Day - 1 to Day + 1 ) remained comparable to controls at 6 to 7 ng/ml for progesterone, and 60 to 80 pg/ml oestrogens for the first cycle, rising in the second cycle and thereafter declining sharply and progressively until cessation of cyclic activity. Oestrous Day 0 LH surge showed an initial rise to peak values during the first,second and third oestrus before declining to values comparable to controls. There was pituitary acidophil hyperplasia concomitant with hypoplasia of delta basophils there was hyperplasia of beta basophils . Total pituitary LH was less than one third of control values at the end of 23 weeks (30 vs 101 ug/gland for deficient and control, respectively). Pituitary weights for deficient animals were, however, higher. The primordial follicles as well as the cells of secondary and tertially follicles in the ovary showed marked atrophy. The adrenal cortex was markedly hypertrophic and there was consequently elevated corticosteroid levels (2.2 + 0.6 ng/ml for controls vs 7.5 +_ 1.5 ng/ml for deficient). Similarly the thyroid gland was hypertrophic and hyperplastic and was mirrored by increase in plasma T^ and T^ values and free thyroxine index (4,7 + 0.6 vs 11*5 +_ 1.4 for control and deficient, respectively). After 15 weeks, energy supplementation to group 3 and protein to group 4 for 8 weeks reduced the above changes but did not lead to recovery. It is concluded that vitamin deficiency probably acts by an initial overproduction of hypothalamic liberins (LRH, CRH and TRH) which in turn cause initial increases in LH, ACTH and TSH in plasma before pituitary exhaustion leads to decreases in the trophic hormones. Vitamin deficiency may, howover, have an additional direct effect on the ovary as it has been show n- in this study that decrease in ovarian functions precedes a decline in plasma LH. The observed symptoms, however, were essentially those of severe malnutrition.