ArticlePloS one2015
Insulin and Leptin Signaling Interact in the Mouse Kiss1 Neuron during the Peripubertal Period.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 62 citations in OpenAlex.
- Kisspeptin as a test of hypothalamic dysfunction in pubertal and reproductive disorders.Andrology · 2026Review
- IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism.Molecular metabolism · 2026Article
- Melanocortin-responsive Kiss1 neurons of the arcuate nucleus drive energy expenditure through glutamatergic signaling to the dorsomedial hypothalamus.bioRxiv : the preprint server for biology · 2025Article
- Hypothalamic kisspeptin alleviates myasthenia gravis by regulating Th1/Th17/Treg balance through Inhibition of NF-κB signaling pathway.Journal of neuroinflammation · 2025Article
- Shared Pathophysiological Mechanisms and Genetic Factors in Early Menarche and Polycystic Ovary Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- IGF-1 Acts through Kiss1-expressing Cells to Influence Metabolism and Reproduction.bioRxiv : the preprint server for biology · 2024Article
- Metabolic hormones are integral regulators of female reproductive health and function.Bioscience reports · 2024Review
- Review
- Article
- Novel Insight into the Role of the Kiss1/GPR54 System in Energy Metabolism in Major Metabolic Organs.Cells · 2022Review
- Hyperinsulinemia induces early and dyssynchronous puberty in lean female mice.The Journal of endocrinology · 2022Article
- Neuroendocrine control of gonadotropin-releasing hormone: Pulsatile and surge modes of secretion.Journal of neuroendocrinology · 2022Review
- The Network Pharmacology Study of Dahuang Fuzi Decoction for Treating Incomplete Intestinal Obstruction.BioMed research international · 2022Article
- The Role of Pediatric Nutrition as a Modifiable Risk Factor for Precocious Puberty.Life (Basel, Switzerland) · 2021Review
- Article
- Multiple Leptin Signalling Pathways in the Control of Metabolism and Fertility: A Means to Different Ends?International journal of molecular sciences · 2021Review
- Early Postnatal Genistein Administration Affects Mice Metabolism and Reproduction in a Sexually Dimorphic Way.Metabolites · 2021Article
- Article
- Metabolic regulation of kisspeptin - the link between energy balance and reproduction.Nature reviews. Endocrinology · 2020Review
- Novel insights into the metabolic action of Kiss1 neurons.Endocrine connections · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Reproduction requires adequate energy stores for parents and offspring to survive. Kiss1 neurons, which are essential for fertility, have the potential to serve as the central sensors of metabolic factors that signal to the reproductive axis the presence of stored calories. Paradoxically, obesity is often accompanied by infertility. Despite excess circulating levels of insulin and leptin, obese individuals exhibit resistance to both metabolic factors in many neuron types. Thus, resistance to insulin or leptin in Kiss1 neurons could lead to infertility. Single deletion of the receptors for either insulin or the adipokine leptin from Kiss1 neurons does not impair adult reproductive dysfunction. However, insulin and leptin signaling pathways may interact in such a way as to obscure their individual functions. We hypothesized that in the presence of genetic or obesity-induced concurrent insulin and leptin resistance, Kiss1 neurons would be unable to maintain reproductive function. We therefore induced a chronic hyperinsulinemic and hyperleptinemic state in mice lacking insulin receptors in Kiss1 neurons through high fat feeding and examined the impact on fertility. In an additional, genetic model, we ablated both leptin and insulin signaling in Kiss1 neurons (IR/LepRKiss mice). Counter to our hypothesis, we found that the addition of leptin insensitivity did not alter the reproductive phenotype of IRKiss mice. We also found that weight gain, body composition, glucose and insulin tolerance were normal in mice of both genders. Nonetheless, leptin and insulin receptor deletion altered pubertal timing as well as LH and FSH levels in mid-puberty in a reciprocal manner. Our results confirm that Kiss1 neurons do not directly mediate the critical role that insulin and leptin play in reproduction. However, during puberty kisspeptin neurons may experience a critical window of susceptibility to the influence of metabolic factors that can modify the onset of fertility.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.