The main functions of luteinizing hormone (LH) are concerned with regulation of gonadal function, and these functions are today well delineated through previous physiological studies. However, novel information of less well-known aspects of actions of this hormone is currently emerging from studies on genetically modified mouse models, with either enhanced or suppressed LH/LH receptor (LHR) function. The novel functions of LH include its role, in specific situations, as promoter of formation and growth of gonadal and extragonadal tumors. Chronically elevated LH levels in transgenic (TG) mice can also induce responses to this hormone in extragonadal tissues. The knockout (KO) mouse for the LHR has elucidated various less well-known details in the function of LH during ontogeny and adult life. Finally, studies on LHR promoter function have revealed that the expression of this gene occurs in age, sex and tissues-specific fashion. The purpose of this brief review is to summarize some of our recent findings upon studies of TG and KO mice with altered function of LH or its receptor.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0303-7207(01)00698-0DOI Listing

Publication Analysis

Top Keywords

luteinizing hormone
12
knockout mouse
8
mouse models
8
function
6
hormone
5
transgenic knockout
4
models study
4
study luteinizing
4
hormone luteinizing
4
hormone receptor
4

Similar Publications

Toxoplasma gondii (T. gondii) causes obvious reproductive toxicity in male by inducing inflammation and apoptosis in testicular tissue. Ginseng polysaccharide (GP) is an active compound in ginseng, known for its remarkable anti-inflammatory and antioxidant properties.

View Article and Find Full Text PDF

Hypothyroidism causes ovarian dysfunction and infertility in women and animals and impairs the hypothalamic expression of kisspeptin (Kp). However, kisspeptin is also expressed in the genital system, and the lack of the Kp receptor (Kiss1r) in the uterus is linked to reduced implantation rates. This study investigated the impact of hypothyroidism on the uterine expression of Kp and Kiss1r in female rats throughout the estrous cycle and the associated changes in uterine activity modulators.

View Article and Find Full Text PDF

Polycystic ovary syndrome (PCOS) is a common cause of infertility in women, characterized by metabolic and hormonal irregularities. We investigated the effects of placenta-derived mesenchymal stem cells (PDMSCs) and platelet-rich plasma (PRP), as well as their combination on follicular development, hormonal profile, inflammatory parameters, and insulin resistance in a model of PCOS. In this study, 25 female Wistar rats were randomly allocated into five groups: Sham (given a dose of 1 mL of a 0.

View Article and Find Full Text PDF

Undernutrition has increased worldwide in recent years and it is known that environmental factors to which individuals are exposed in early life can result in metabolic and reproductive changes that remain in adult life. In this context, the litter size expansion is a classic model used to induce undernutrition early in development. Thus, this study aimed to evaluate the effects of neonatal undernutrition induced by the litter size expansion on metabolic and reproductive parameters of female rats.

View Article and Find Full Text PDF

Background: Proper planning of reproductive health needs for HIV-infected adolescents requires a clear understanding of the effects of HIV infection on adolescents' pubertal development.

Objective: To assess the effects of HIV infection on the hypothalamic-pituitary-ovarian (HPO) axis, ovarian reserve and pubertal development in adolescent girls at a tertiary hospital in Zimbabwe.

Methods: This was a cross-sectional survey of HIV-infected adolescent girls aged 10-19 years, with available CD4 + count results at a tertiary hospital in Zimbabwe.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!