Research into the Kisspeptin-10 peptide suggests that the compound may act as a mediator of endocrine signaling during crucial reproductive or developmental stages. It may potentially impact development and regulation of blood vessels and renal function, and some studies have suggested it may mitigate cancer cell proliferation and metastasis. Also known as Metastin, this peptide also appears to impact the gonadotropin-releasing hormone or GnRH.[1]
OTHER KNOWN TITLES: KISS-1, Protein KISS-1, Metastin, Kp-10 peptide
SEQUENCE: YNWNSFGLRF
MOLECULAR FORMULA: C63H83N17O14
MOLECULAR WEIGHT: 1302.4 g/mol
KISSPEPTIN-10 AND GONADOTROPIN-RELEASING HORMONES, TESTOSTERONE
The Hypothalamus in the brain is considered to be responsible for the production and secretion of Gonadotropin-Releasing Hormones (GnRH). It appears to be secreted at the top of the hypothalamic-pituitary-gonadal axis, and may control the downstream production of follicle-stimulating hormone (FSH) and luteinizing hormones (LH). Primarily, these hormones are associated with the maturation of ova and sperm in the female and male reproductive organs, respectively. Researchers have posited that Kisspeptin may affect the hypothalamic-pituitary-gonadal axis, possibly resulting in an increase of LH and FSH release in the bloodstream. Studies suggest that this release may induce a ~3x increase in testosterone concentration within the bodies of male animals.[2] In addition, it the peptide has been suggested to hold potential in regulating the normal pulsatile release of sex hormones. These effects seem to be directly proportional to the concentration of Kisspeptin present in the organism. Kisspeptin is suggested to obscure individual pulses at extremely high concentrations, appearing to cause a continuous release of LH from the anterior pituitary glands.
KISSPEPTIN-10 AND ENERGY METABOLISM
The nutrient or energetic status of an organism appears to affect neurons which secrete endogenous Kisspeptin-10, potentially resulting in suppression of GnRH release. Extreme variations in this balance have been associated with infertility.[3] Researchers conclude that “the novel role of kisspeptin neurons as active players within the neuronal circuits that govern energy balance is discussed, offering evidence of a bidirectional role of these neurons as a nexus between metabolism and reproduction.” Kisspeptin may be responsible for the regulation of energy, and depleting the Kisspeptin receptor (Kiss1r) may augment lipid retention, simultaneously reducing energy consumption.
KISSPEPTIN-10 AND CANCER CELLS
Kisspeptin has been suggested to influence the malignancy of melanomas. This assumption has been contributed to the peptide’s potential to impact the migration of cancerous cells through reducing the adhesive capacity of these cells. Cancer cell cultures taken from organs such as the breast, urinary bladder, gastrointestinal tract, prostate, pancreas, ovaries, epidermis, and thyroid, all appear to exhibit reduced expression of Kisspeptin, which may support environments for metastasis. Research has also linked the levels of natural Kisspeptin and melatonin production to sunlight.[4] Upon extensive sun exposure, murine models were assessed, reporting excess Kisspeptin and melatonin production. When tumorigenic cells were introduced in these mice, heightened tumor growth and volume were reported following extended sun exposure.
KISSPEPTIN-10 AND MOOD
Reproductive activites, energy levels, and certain behavioral factors are considered to be influenced by hormonal release cycles. Researchers posit that reproduction and energy homeostasis may be affected by Kisspeptin levels. Recent studies have observed enhanced limbic brain activity such as increased reward-seeking behavior and enthusiasm upon increased Kisspeptin exposure.[5] Research in this area is ongoing.
KISSPEPTIN-10 AND KIDNEY, HEART
Other than its potential mitigatory role in tumor metastasis, Kisspeptin appears to have regulatory capacity within the kidney and heart. Kisspeptin-10 and its receptors appear to be expressed in renal tissues, and studies have reported that the Kiss-1 receptor knockouts fail to regulate glomerular development.[6] The scientists report that “Kisspeptins and kisspeptin receptor are altered in the kidney tissues of chronic renal impairment, raising the possibility of their pathophysiological roles in chronic renal failure.” Furthermore, Kisspeptin has been observed to control vasoconstriction and sometimes cardiac output under specific laboratory conditions.[7] Such regulation may be related to Kisspeptin’s potential to impact vascular development and response to injury, the exact mechanism of which remains to be elucidated.
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