Showing papers on "Adrenocortical hyperfunction published in 2000"
88 citations
TL;DR: Acromegaly, in cats, is a relatively uncommon endocrine disorder and hyperadrenocorticism is even less common, but there is interest in their clinical signs, diagnosis and treatment.
Abstract: The two most common endocrine disorders in cats are diabetes mellitus and hyperthyroidism. Each of these conditions has been described as the most common endocrine disorder in geriatric cats of North America and each, separately, has been described as one of the most common conditions in geriatric cats of North America. It would seem that all other endocrine disorders of cats are uncommonto-rare. Acromegaly, in cats, is a relatively uncommon endocrine disorder and hyperadrenocorticism is even less common. However, there is interest in their clinical signs, diagnosis and treatment.
30 citations
TL;DR: It is suggested that, in intact TG females, enhanced ovarian estrogen synthesis causes increased secretion of prolactin (PRL), which elevates LHR expression, which triggers elevated adrenal function in LH overexpressing bLHbeta-CTP female mice.
Abstract: Transgenic (TG) female mice expressing bLHβ-CTP (a chimeric protein derived from the β-subunit of bovine luteinizing hormone [LH] and a fragment of the β-subunit of human chorionic gonadotropin [hCG]) exhibit elevated serum LH, infertility, polycystic ovaries, and ovarian tumors. In humans, increased LH secretion also occurs in infertility and polycystic ovarian syndrome, often concomitant with adrenocortical dysfunction. We therefore investigated adrenal function in LH overexpressing bLHβ-CTP female mice. The size of their adrenals was increased by 80% with histological signs of cortical stimulation. Furthermore, adrenal steroid production was increased, with up to 14-fold elevated serum corticosterone. Primary adrenal cells from TG and control females responded similarly to ACTH stimulation, but, surprisingly, the TG adrenals responded to hCG with significantly increased cAMP, progesterone, and corticosterone production. LH receptor (LHR) expression and activity were also elevated in adrenals from female TG mice, but gonadectomized TG females showed no increase in corticosterone, suggesting that the dysfunctional ovaries of the intact TG females promote adrenocortical hyperfunction. We suggest that, in intact TG females, enhanced ovarian estrogen synthesis causes increased secretion of prolactin (PRL), which elevates LHR expression. Chronically elevated serum LH, augmented by enhanced PRL production, induces functional LHR expression in mouse adrenal cortex, leading to elevated, LH-dependent, corticosterone production. Thus, besides polycystic ovaries, the bLHβ-CTP mice provide a useful model for studying human disorders related to elevated LH secretion and adrenocortical hyperfunction.