Pituitary adenomas are a common form of endocrine neoplasia in man, and cause clinical problems resulting from syndromes of hormone hypersecretion, hypofunction of the residual normal pituitary gland, or from mass effects from the tumour bulk itself. They can now be treated by surgery, by irradiation or by endocrine therapies such as dopamine or somatostatin agonists, but none of these options has proved entirely satisfactory. After intense scrutiny of pituitary physiology and biochemistry, only now are some of the causes of pituitary tumour formation becoming understood, and this short review will discuss some recent advances in the field.

Pituitary tumours generally arise from a single differentiated cell type expressing its appropriate mature pituitary hormone product (such as prolactin, growth hormone (GH), adrenocorticotrophin (ACTH) or thyroid-stimulating hormone (TSH), and the hormone hypersecretion often leads to a clinically recognized syndrome. About 25% of adenomas are clinically 'non-functioning', but most of these in

This study examined the pattern of circulating leptin in age-matched sheep during adolescent pregnancy, and its relationship with maternal dietary intake, body composition and tissue expression of the leptin gene. Overfeeding the adolescent pregnant ewe results in rapid maternal growth at the expense of the placenta, leading to growth restriction in the fetus, compared with normal fed controls. Our results demonstrate that, in the adolescent ewe, overfeeding throughout pregnancy was associated with higher maternal leptin concentrations, when compared with moderately fed controls (P<0.05), with no peak in circulating leptin towards the end of pregnancy. There was a close correlation between indices of body composition and circulating leptin levels at day 104 of gestation and at term (P<0.03). Further, when the dietary intake was switched from moderate to high, or high to moderate, at day 50 of gestation, circulating leptin levels changed rapidly, in parallel with the changes in dietary intake. Leptin mRNA levels and leptin protein in perirenal adipose tissue samples, taken at day 128 of gestation, were higher in overfed dams (P<0.04), suggesting that adipose tissue was the source of the increase in circulating leptin in the overnourished ewes. Leptin protein was also detected in placenta but leptin gene expression was negligible. However, leptin receptor gene expression was detected in the ovine placenta, suggesting that the placenta is a target organ for leptin. A negative association existed between maternal circulating leptin and fetal birth weight, placental/cotyledon weight and cotyledon number. In conclusion, in this particular ovine model, hyperleptinaemia was not observed during late pregnancy. Instead, circulating leptin concentrations reflected increased levels of leptin secretion by adipose tissue primarily as a result of the increase in body fat deposition, due to overfeeding. However, there appears to be a direct effect of overfeeding, particularly in the short term. In the nutritional switch-over study, circulating leptin concentrations changed within 48 h of the change in dietary intake. The presence of leptin protein and leptin receptor gene expression in the placenta suggests that leptin could be involved in nutrient partitioning during placental and/or fetal development.