Kisspeptins and the control of gonadotrophin secretion

Dedes, Ioannis

doi:10.3109/19396368.2011.651555

Cited by 40 publications

(31 citation statements)

References 62 publications

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“…A similar synergistic effect on ovarian cycling occurred in response to combinations of food restriction and psychosocial stress in cynomolgus monkeys (792). Increased activity and decreased eating combine to inhibit kisspeptin or GnRH neurons in the hypothalamus, which leads to reductions in LH and estrogens (175,456,666). Whether the reduced estrogen secretion is related to the weaker anorectic effect in female rats compared with male rats (185) is unknown.…”

Section: Physiological Sex Differences In Disordered Human Eatingmentioning

confidence: 92%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

414

349

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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Section: Physiological Sex Differences In Disordered Human Eatingmentioning

confidence: 92%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

414

349

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“…The results demonstrated that the kisspeptin levels of girls in the ICPP group prior to treatment were significantly higher than those of the other groups, which supports the hypothesis that kisspeptin is an activating effector of the HPG axis. Significant increases in Kiss-1 gene expression trigger the pulsed release of GnRH, activate the HPG axis and initiate pubertal development, thereby causing the occurrence of PP (10).…”

Section: Discussionmentioning

confidence: 99%

Testing of kisspeptin levels in girls with idiopathic central precocious puberty and its significance

Yang

Xiong

Yang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to explore the significance of plasma kisspeptin levels in diagnosis and therapeutic evaluation through the analysis of the kisspeptin levels of girls diagnosed with idiopathic central precocious puberty (ICPP) prior to treatment and after 6-months of treatment and those with simple premature thelarche (PT). A total of 70 girls including 24 girls diagnosed with ICPP, 21 girls with PT and 25 normal girls were enrolled in the study. ELISA analysis was conducted to detect the plasma levels of kisspeptin. The kisspeptin level of the ICPP group prior to treatment (1.80±0.13 ng/ml) was significantly higher than those of the other two groups. The kisspeptin level of the ICPP group after 6 months of treatment (1.49±0.21 ng/ml) was significantly lower than that prior to treatment (P<0.05). It may be concluded that the plasma level of kisspeptin is associated with the initiation of pubertal development, and it may serve as an important parameter in the diagnosis of ICPP and the evaluation of therapeutic effects.

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“…Continuous administration of kisspeptins downregulates the hypothalamic-gonadal-pituitary (HPG) axis (26). Kisspeptin is a potent peptide that initiates luteinizing hormone (LH) release in male and female mice (27), in both prepubertal and adult rats (28) and in prepubertal donkeys (29).…”

Section: Discussionmentioning

confidence: 99%

The effect of kisspeptin on spermatogenesis and apoptosis in rats

et al. 2017

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IntroductionKisspeptins, the peptide products of the KiSS-1 gene, bind to the G protein-coupled receptor 54 (GPR54), a critical regulator of GnRH secretion. The N-terminally truncated peptide metastin 45-54 exhibits 10-fold higher receptorbinding affinity than full-length metastin; it also shows agonistic KISS-1R activity (1).Kisspeptins are known to play a role in puberty, cancer metastasis, and vasoconstriction (2,3-7). They are synthesized in the arcuate and anteroventral periventricular hypothalamic neurons and in the perioptic area (8). Kisspeptin expression is variable according to sex in rats; its expression is more marked in female animals (9). Its known derivatives are kisspeptin-10, kisspeptin-13, kisspeptin-14, and kisspeptin-54 (10-12). All kisspeptins seem to have the same interactions under in vitro conditions. Kiss-10 is well characterized in mammals, in which it is found in large concentrations (10,11). It has been suggested, however, that Kiss-54 is the most effective form (12). Kisspeptin has been reported to also be synthesized in the testes, ovaries, pancreas, gut, liver, lung, muscle tissue, kidney, nervous system, and most densely in the placenta (13,14). As for its receptor, G protein-coupled receptor-54 (GPR54) is mostly expressed in the hypophysis, placenta, and pancreas (10,15,16). Kisspeptins are highly potent neuropeptides that stimulate the secretion of LH and FSH from the hypophysis, an effect exerted through the release of GnRH (7,17). While this pathway has been satisfactorily defined in several mammal species, the molecular and cellular events at the proencephalic origin of this process are incompletely elucidated. In recent years, studies have indicated that kisspeptin plays a role in the transition to puberty (18,19). Kiss-1 knockout mice showed hypogonadism and low Background/aim: To study the effect of kisspeptin, a gonadotropin release stimulator, on the testicular tissue of the rat.Materials and methods: Four groups were formed as follows: control, Kiss-10 50 nmol administration for 1 day, Kiss-10 administration for 13 days, and one last group kept for 7 days following Kiss-10 applied for 13 days. Testicular tissues were stained with hematoxylineosin, periodic acid Schiff, Masson trichrome staining, terminal deoxynucleotidyl transferased UTP nick-end labeling, and Ki-67 immune staining. Serum testosterone levels were determined.Results: Serum testosterone level increased following acute application, while it was reduced by chronic treatment. Spermatogenic cells as stained by Ki-67 and TUNEL increased in the treated groups compared to the controls. Following a 7-day rest after treatment, a decrease in testosterone levels and Ki-67-stained cell numbers and an increase in TUNEL-stained cells were observed. Leydig cells showed increased vacuolization in the Kiss-1 group. Leydig cell vacuolization continued in the Kiss (13) group and was reduced in the Kiss (13 + 7) group. Conclusion:Kiss-10 increased spermatogenic cell proliferation, while testosterone level and proliferation de...

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Kisspeptins and the control of gonadotrophin secretion

Cited by 40 publications

References 62 publications

Sex differences in the physiology of eating

Sex differences in the physiology of eating

Testing of kisspeptin levels in girls with idiopathic central precocious puberty and its significance

The effect of kisspeptin on spermatogenesis and apoptosis in rats

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