ArticleThe Journal of clinical investigation2014
Impaired kisspeptin signaling decreases metabolism and promotes glucose intolerance and obesity.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
91 citing papers in PubMed, 189 citations in OpenAlex.
- The Effects of Kisspeptin on Brain Response to Food Images and Psychometric Parameters of Appetite in Healthy Men.The Journal of clinical endocrinology and metabolism · 2021Trial
- The effects of kisspeptin on β-cell function, serum metabolites and appetite in humans.Diabetes, obesity & metabolism · 2018Trial
- Enzymatic Stability and Comparative Effects of Kisspeptin-14, Kisspeptin-13 and Kisspeptin-10 on Beta-Cell Function, Glucose Homeostasis and Appetite Regulation.Metabolites · 2026Article
- Kisspeptin Restores Placental mTOR Signaling and Improves Glucose Homeostasis Mediators Disrupted by Maternal Hypothyroidism in Rats.Acta physiologica (Oxford, England) · 2026Article
- GPCR Biased Signaling in Metabolism.Handbook of experimental pharmacology · 2026Review
- Kisspeptin mediates the impact of chronic psychological stress on reproductive and metabolic dysregulation in polycystic ovary syndrome: evidence from human and rat models.Journal of ovarian research · 2025Article
- Circadian Clock Deregulation and Metabolic Reprogramming: A System Biology Approach to Tissue-Specific Redox Signaling and Disease Development.International journal of molecular sciences · 2025Review
- 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
- Kisspeptin Receptor Agonists and Antagonists: Strategies for Discovery and Implications for Human Health and Disease.International journal of molecular sciences · 2025Review
- Kisspeptin and neurokinin B: roles in reproductive health.Physiological reviews · 2025Review
- Review
- Kisspeptin a potential therapeutic target in treatment of both metabolic and reproductive dysfunction.Journal of diabetes · 2024Review
- The kisspeptin system in and beyond reproduction: exploring intricate pathways and potential links between endometriosis and polycystic ovary syndrome.Reviews in endocrine & metabolic disorders · 2024Review
- The Emerging Therapeutic Potential of Kisspeptin and Neurokinin B.Endocrine reviews · 2024Review
- Airway-associated adipose tissue accumulation is increased in a kisspeptin receptor knockout mouse model.Clinical science (London, England : 1979) · 2023Article
- Review
- Effects of obesity on the serum BMP15, GDF9, and kisspeptin concentrations in women of reproductive age.Journal of medical biochemistry · 2023Article
- The effects of kisspeptin on food intake in women with overweight or obesity.Diabetes, obesity & metabolism · 2023Article
- The role of oestrogen in determining sexual dimorphism in energy balance.The Journal of physiology · 2023Review
- Sexually dimorphic pubertal development and adipose tissue kisspeptin dysregulation in the obese and preeclamptic-like BPH/5 mouse model offspring.Frontiers in physiology · 2023Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The neuropeptide kisspeptin regulates reproduction by stimulating gonadotropin-releasing hormone (GnRH) neurons via the kisspeptin receptor KISS1R. In addition to GnRH neurons, KISS1R is expressed in other brain areas and peripheral tissues, which suggests that kisspeptin has additional functions beyond reproduction. Here, we studied the energetic and metabolic phenotype in mice lacking kisspeptin signaling (Kiss1r KO mice). Compared with WT littermates, adult Kiss1r KO females displayed dramatically higher BW, leptin levels, and adiposity, along with strikingly impaired glucose tolerance. Conversely, male Kiss1r KO mice had normal BW and glucose regulation. Surprisingly, despite their obesity, Kiss1r KO females ate less than WT females; however, Kiss1r KO females displayed markedly reduced locomotor activity, respiratory rate, and energy expenditure, which were not due to impaired thyroid hormone secretion. The BW and metabolic phenotype in Kiss1r KO females was not solely reflective of absent gonadal estrogen, as chronically ovariectomized Kiss1r KO females developed obesity, hyperleptinemia, reduced metabolism, and glucose intolerance compared with ovariectomized WT females. Our findings demonstrate that in addition to reproduction, kisspeptin signaling influences BW, energy expenditure, and glucose homeostasis in a sexually dimorphic and partially sex steroid-independent manner; therefore, alterations in kisspeptin signaling might contribute, directly or indirectly, to some facets of human obesity, diabetes, or metabolic dysfunction.
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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.