KiSS-1 mRNA in adipose tissue is regulated by sex hormones and food intake

Brown, Russell E.; Imran, Syed Ali; Ur, Ehud; Wilkinson, Michael

doi:10.1016/j.mce.2007.10.011

Cited by 116 publications

(102 citation statements)

References 53 publications

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“…Kisspeptin has pivotal roles in fertility,1 which are being utilised by kisspeptin‐based therapies now in development for common reproductive disorders 2, 3, 4, 5. Kisspeptin ( kiss1 ) and its receptor ( kiss1r ) are expressed in the hypothalamus, pancreatic β‐cells, liver and adipose tissue,6, 7, 8, 9 suggesting roles in key autocrine and paracrine metabolic processes. Kisspeptin has recently been reported to increase glucose‐stimulated insulin secretion (GSIS) in rats10 and monkeys,11 and this is supported by in vitro islet studies which demonstrate enhancement of GSIS by kisspeptin 8, 10, 12, 13.…”

Section: Introductionmentioning

confidence: 99%

The effects of kisspeptin on β‐cell function, serum metabolites and appetite in humans

Izzi‐Engbeaya

Comninos

Clarke

et al. 2018

Diabetes Obesity Metabolism

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AimsTo investigate the effect of kisspeptin on glucose‐stimulated insulin secretion and appetite in humans.Materials and methodsIn 15 healthy men (age: 25.2 ± 1.1 years; BMI: 22.3 ± 0.5 kg m−2), we compared the effects of 1 nmol kg−1 h−1 kisspeptin versus vehicle administration on glucose‐stimulated insulin secretion, metabolites, gut hormones, appetite and food intake. In addition, we assessed the effect of kisspeptin on glucose‐stimulated insulin secretion in vitro in human pancreatic islets and a human β‐cell line (EndoC‐βH1 cells).ResultsKisspeptin administration to healthy men enhanced insulin secretion following an intravenous glucose load, and modulated serum metabolites. In keeping with this, kisspeptin increased glucose‐stimulated insulin secretion from human islets and a human pancreatic cell line in vitro. In addition, kisspeptin administration did not alter gut hormones, appetite or food intake in healthy men.ConclusionsCollectively, these data demonstrate for the first time a beneficial role for kisspeptin in insulin secretion in humans in vivo. This has important implications for our understanding of the links between reproduction and metabolism in humans, as well as for the ongoing translational development of kisspeptin‐based therapies for reproductive and potentially metabolic conditions.

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Section: Introductionmentioning

confidence: 99%

The effects of kisspeptin on β‐cell function, serum metabolites and appetite in humans

Izzi‐Engbeaya

Comninos

Clarke

et al. 2018

Diabetes Obesity Metabolism

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“…Experimental evidence suggests that a decrease in the activity of kisspeptin is the main cause of the inhibition of reproductive function observed in subnutritional conditions. Hypothalamic Kiss1 mRNA expression is reduced in acute food-deprived female rodents , Luque et al 2007, Brown et al 2008) and streptozotocin-induced diabetic male rats (Castellano et al 2006), and hypogonadotropic hypogonadism can be restored in these animals by the administration of kisspeptin , Luque et al 2007). On the other hand, the effects of FD on Kiss1r are disputed.…”

Section: Introductionmentioning

confidence: 99%

Sensitivities of mRNA expression levels of Kiss1 and its receptor, Kiss1r, to nutritional status are changed during the developmental period in female rats

Iwasa

Matsuzaki²,

Murakami³

et al. 2010

Journal of Endocrinology

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Decreased activity of kisspeptin, the product of the hypothalamic Kiss1 gene, is the major cause of the suppression of reproductive function in subnutritional conditions. The sensitivities of the endocrine and the hypothalamic neuronal systems to nutritional status develop during the neonatal period. We examined the developmental changes in the sensitivity of hypothalamic mRNA expression of Kiss1 and its receptor, Kiss1r, to nutritional status in female rats. Kiss1 mRNA expression was reduced by 24 h food deprivation (24 h FD) at postnatal day 25, but not at postnatal day 5 or 15. Kiss1r mRNA expression was reduced by the 12 or 24 h FD at postnatal days 5 and 25, but not at postnatal day 15. Kiss1r mRNA level was found to be correlated with the plasma leptin level, and the administration of leptin, which increased the serum leptin concentration above the physiological range, restored the acute FD-induced suppression of Kiss1r mRNA expression. These data suggest that the hypothalamic Kiss1 and Kiss1r mRNA expression is differentially affected by the nutritional condition at different age points. It is speculated that the sensitivity of Kiss1 mRNA, which is expressed in kisspeptin neuron, to nutritional status develops during the neonatal period. On the other hand, it seems that the sensitivity of Kiss1r mRNA, which is expressed in GnRH neuron, to nutritional status has been already established during the early neonatal period. These data also show that hypoleptinemia plays a role in the reduction of hypothalamic Kiss1r mRNA expression under subnutritional conditions.

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“…Humans, mice, and rats with mutations in these genes show impaired puberty, hypogonadism, and infertility (1)(2)(3)(4)(5)(6). In addition to being expressed in reproductive areas of the brain, kisspeptin is also expressed in multiple peripheral tissues (7)(8)(9)(10). The receptor, Kiss1r, is also expressed in multiple non-GnRH brain areas and in several peripheral tissues (9 -11), including metabolic tissues such as fat, liver, and pancreas.…”

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confidence: 99%

Metabolism and Energy Expenditure, But Not Feeding or Glucose Tolerance, Are Impaired in Young Kiss1r KO Female Mice

et al. 2016

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Kisspeptin regulates reproduction via signaling through the receptor, Kiss1r, in GnRH neurons. However, both kisspeptin and Kiss1r are produced in several peripheral tissues, and recent studies have highlighted a role for kisspeptin signaling in metabolism and glucose homeostasis. We recently reported that Kiss1r KO mice display a sexually-dimorphic metabolic phenotype, with KO females displaying obesity, impaired metabolism, and glucose intolerance at 4 -5 months of age. However, it remains unclear when this metabolic phenotype first emerges in development, or which aspects of the pleiotropic phenotype underlie the metabolic defects and which are secondary to the obesity. Here, we studied Kiss1r KO females at different ages, including several weeks before the emergence of body weight differences and later when obesity is present. We determined that at young adult ages (6 weeks old), KO females already exhibit altered adiposity, leptin levels, metabolism, and energy expenditure, despite having normal body weights at this time. In contrast, food intake, water intake, and glucose tolerance are normal at young ages, and only show impairments at older adult ages, suggesting that these impairments may be secondary to earlier alterations in metabolism and adiposity. We also demonstrate that, in addition to body weight, all other facets of the adult metabolic phenotype persist even when gonadal sex steroids are similar between genotypes. Collectively, these data highlight the developmental emergence of a metabolic phenotype induced by disrupted kisspeptin signaling, and reveal that multiple-but not all-aspects of this phenotype are already disrupted prior to detectable changes in body weight.

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KiSS-1 mRNA in adipose tissue is regulated by sex hormones and food intake

Cited by 116 publications

References 53 publications

The effects of kisspeptin on β‐cell function, serum metabolites and appetite in humans

The effects of kisspeptin on β‐cell function, serum metabolites and appetite in humans

Sensitivities of mRNA expression levels of Kiss1 and its receptor, Kiss1r, to nutritional status are changed during the developmental period in female rats

Metabolism and Energy Expenditure, But Not Feeding or Glucose Tolerance, Are Impaired in Young Kiss1r KO Female Mice

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