Endocrine Abstracts

Leptin, a key metabolic signal controlling both energy intake and energy reserves, informs the brain about energy stores of the body to initiate reproductive processes at puberty. Thyroid hormones are important determinant of overall energy expenditure, basal metabolic rate and thermogenesis. The present study examined the relationship between leptin and thyroxine (T4) and triiodothyronine (T3) in boys (n=540) between the age of 1 and 20 years. B...

Congenital adrenal hyperplasia (CAH), caused by lack of 21-hydroxylase, impairs cortisol secretion, which increases ACTH release that results in hyperplasia of adrenal glands and increased secretion of adrenal androgens. Elevated androgen concentration leads to increased skeletal maturation, early pubertal development and diminished pubertal growth. Treatment with glucocorticoids averts early puberty but may abruptly slow down growth. The effect of exogenous glucocorticoids on...

Congenital adrenal hyperplasia (CAH) is an autosomal recessive disorder caused by deficiency of 21-hydroxylase (CYP21), which inhibits adrenal synthesis of cortisol and aldosterone. The reduced cortisol synthesis leads to increased ACTH secretion, which results in adrenal gland hyperplasia, accumulation of steroid precursors and excessive adrenal androgen production, causing pseudoprecocious puberty. The study aimed at determining variance in two SNPs, I172N and V281L, of CYP2...

The signaling of G protein-coupled receptor 54 (GPR54) is a key regulator of the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamic GnRH neurons, whereas GnRH is a crucial neurohormone regulating the secretion of FSH and LH at the time of puberty. The deficiency in the release or action of GnRH leads to hypogonadotropic hypogonadism (HH) characterized by low FSH, LH and testosterone (T) and results in absent or impaired sexual development at puberty. In b...