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Mini-puberty is a transient hormonal activation of the hypothalamic-pituitary-gonadal (HPG) axis that occurs in infants shortly after birth. This period is characterized by a surge in the secretion of gonadotropins (LH and FSH) and sex steroids (testosterone in males and estradiol in females), similar to but less intense than the hormonal changes that occur in puberty during adolescence.
The goal is to normalize the production of 21-hydroxylase, the enzyme encoded by CYP21A2. Providing a working copy of this gene may improve adrenal hormone synthesis and subsequently normalize cortisol and aldosterone production. [253] Currently, gene replacement therapy for CAH is still at an early stage of research and development.
The human Y chromosome showing the SRY gene which codes for a protein regulating sexual differentiation. Sexual differentiation in humans is the process of development of sex differences in humans. It is defined as the development of phenotypic structures consequent to the action of hormones produced following gonadal determination. [1]
Mutations in genes such as LIN28, [25] [26] and LEP and LEPR, which encode leptin and the leptin receptor, [27] have been associated with precocious puberty. The association between LIN28 and puberty timing was validated experimentally in vivo, when it was found that mice with ectopic over-expression of LIN28 show an extended period of pre ...
5α-reductase deficiency (5-ARD) – an autosomal recessive condition caused by a mutation of the 5-alpha reductase type 2 gene. It only affects people with Y chromosomes, namely genetic males. People with this condition are fertile, with the ability to father children, but may be raised as females due to ambiguous or feminized genitalia. [18] [19]
This is an accepted version of this page This is the latest accepted revision, reviewed on 6 January 2025. Procreative biological processes of humanity Part of a series on Sex Biological terms Sexual dimorphism Sexual differentiation Feminization Virilization Sex-determination system XY XO ZW ZO Temperature-dependent Haplodiploidy Heterogametic sex Homogametic sex Sex chromosome X chromosome Y ...
The aetiology of 46,XY gonadal dysgenesis can be caused by mutations in the genes involved in testis development such as SRY, SOX9, WT1, SF1, and DHH. [9] [13] If a single or combination of these genes are mutated or deleted, downstream signalling is disrupted, leading to atypical penis and scrotum. [14]
Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis, [1] is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty. [2] Signs of puberty can develop as early as an age of 1 year.