Control and management of ovarian follicles in cattle to optimize fertility.

Experiments were designed to elucidate the control of ovarian follicle turnover and the impact of follicular dynamics on the subsequent fertility of dairy cattle. An experimental model was established to examine the interrelationships of gene expression for steroid enzymes, the insulin-like growth factor system and inhibin production as associated with follicle selection, dominance and atresia. Follicular dynamics during the postpartum period and the oestrous cycle are shown to be altered markedly by the metabolic demands of lactation. The feeding of ruminally-inert fat stimulated follicular development and improved reproductive performance. The development of persistent follicles during oestrus synchronization causes a reduction in fertility that can be corrected by recruitment and selection of a new ovulatory follicle after the injection of a gonadotrophin-releasing hormone agonist. Present systems of oestrus synchronization need to consider both synchronization of follicular development and corpus luteal regression in order to optimize fertility. With current systems manipulating follicle development, the potential to implement a timed insemination programme to improve reproductive management exists. Ovulation of the first-wave dominant follicle with human chorionic gonadotrophin provides a means to markedly enhance concentrations of plasma progesterone in the luteal phase.

Sorbitol, myo-inositol, and rod outer segment phagocytosis in cultured hRPE cells exposed to glucose. In vitro model of myo-inositol depletion hypothesis of diabetic complications.

The "myo-inositol depletion hypothesis" remains a leading but still controversial contender among proposed pathogenetic mechanisms for the chronic complications of diabetes. The multifaceted interrelationships among altered tissue myo-inositol content and metabolism and tissue function have been difficult to elucidate in diabetic animal models due in part to the complex, heterogeneous nature of tissues prone to diabetic complications. The retinal pigment epithelium consists of a homogenous cell monolayer that exhibits related alterations in myo-inositol metabolism and function in diabetic animals. Nontransformed human retinal pigment epithelial (hRPE) cells, which retain their general phenotypic and morphological characteristics during monolayer culture in vitro, were examined for parallel alterations in myoinositol metabolism and cell function when grown under carefully controlled conditions in medium containing hyperglycemic concentrations of glucose. Exposure of hRPE cells to 20-40 mM glucose produced time- and dose-dependent increases in sorbitol content and decreases in myo-inositol content that were partially blocked by the aldose reductase inhibitor sorbinil. myo-Inositol was taken up by two Na-dependent transport systems, at least one of which was competitively inhibited by glucose. Exposure to 20 mM glucose impaired the ability of hRPE cells to take up human retinal rod outer segments, an important physiological function of these cells. The impairment of rod outer segment uptake by high glucose levels was prevented by an aldose reductase inhibitor or elevated medium myo-inositol that corrected the fall in myo-inositol content. Thus, hRPE cells provide a new in vitro model in which to examine the biochemical-functional interrelationships of the myo-inositol depletion hypothesis.