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Wybrane czynniki podwzgórzowe integrujące rozród i kontrolę bilansu energetycznego u zwierząt

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Kirsz K. , Zieba D. A.

nr 01

Mammalian reproduction is the most energy-consuming biological process. However, chronic dietary energy deficits, as well as energy surpluses can impair reproductive capacity, including the ability to produce viable gametes, and interrupt pregnancy or lactation. Thus, there is no doubt that the mechanisms controlling energy balance are integrated with those that control reproduction. There is functional evidence for a crucial connection between those mechanisms in the gonadotropin-releasing hormone (GnRH) cells of the hypothalamus, which are part of the hypothalamo-pituitary-gonadal (HPG) axis. Recent research has shown that the multiple hypothalamic peptidergic systems responsible for the homeostatic control of energy balance are involved in signaling to GnRH neurons. This group includes neuropeptyd Y (NPY), melanin-concentrating hormone (MCH), proopiomelanocortin (POMC), as well as periphery factors, such as leptin, ghrelin and insulin. However, the discovery of kisspeptin and gonadotropin-inhibitory hormone (GnIH) sheds a new light on mechanisms by which reproductive activity is regulated, also in the context of diurnal and annual photoperiod-driven cycles of mammals’ energy requirements. Thus, it seems clear that those two peptides are very important in linking the processes of energy balance maintenance and reproduction.

Transcript abundances of the prolactin receptor, the leptin receptor and their major suppressor in the sheep mammary gland during pregnancy and lactation

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Szczesna M. , Kirsz K. , Nowakowski M. , Zieba D. A.

2020

tom 20

nr 4

Gestational profile of suppressor of cytokine signaling-3 (SOCS-3) transcripts in ovine brain and anterior pituitary

80%

Szczesna M. , Kirsz K. , Zieba D. A.

nr Suppl.1

Induction of the secretion of LH and GH by orexin A and ghrelin is controlled in vivo by leptin and photoperiod in sheep

70%

Kirsz K. , Szczesna M. , Molik T. , Misztal T. , Zieba D. A.

nr 1