Imperial College London

ProfessorKevinMurphy

Faculty of MedicineDepartment of Metabolism, Digestion and Reproduction

Professor of Endocrinology & Metabolism
 
 
 
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Contact

 

+44 (0)20 3313 2156k.g.murphy Website

 
 
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Location

 

6N2DCommonwealth BuildingHammersmith Campus

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Summary

 

Publications

Publication Type
Year
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179 results found

Alamshah A, Spreckley E, McGavigan AK, Cheong W, Ghatei MA, Bloom SR, Murphy KGet al., 2014, L-Arginine Promotes Gut Hormone Release and Reduces Appetite in Rodents, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X

Journal article

Kinsey-Jones JS, Beale KE, Cuenco J, Li XF, Bloom SR, O'Byrne KT, Murphy KGet al., 2014, Quantification of Rat Kisspeptin Using a Novel Radioimmunoassay, PLoS ONE, Vol: 9, ISSN: 1932-6203

Kisspeptin is a hypothalamic peptide hormone that plays a pivotal role in pubertal onset and reproductive function. Previous studies have examined hypothalamic kisspeptin mRNA expression, either through in situ hybridisation or real-time RT-PCR, as a means quantifying kisspeptin gene expression. However, mRNA expression levels are not always reflected in levels of the translated protein. Kisspeptin-immunoreactivity (IR) has been extensively examined using immunohistochemistry, enabling detection and localisation of kisspeptin perikaya in the arcuate nucleus (ARC) and anteroventral periventricular nucleus (AVPV). However, quantification of kisspeptin-IR remains challenging. We developed a specific rodent radioimmunoassay assay (RIA) capable of detecting and quantifying kisspeptin-IR in rodent tissues. The RIA uses kisspeptin-10 as a standard and radioactive tracer, combined with a commercially available antibody raised to the kisspeptin-10 fragment. Adult female wistar rat brain samples were sectioned at 300 µm and the ARC and AVPV punch micro-dissected. Brain punches were homogenised in extraction buffer and assayed with rodent kisspeptin-RIA. In accord with the pattern of kisspeptin mRNA expression, kisspeptin-IR was detected in both the ARC (47.1±6.2 fmol/punch, mean±SEM n = 15) and AVPV (7.6±1.3 fmol/punch, mean±SEM n = 15). Kisspeptin-IR was also detectable in rat placenta (1.26±0.15 fmol/mg). Reverse phase high pressure liquid chromatography analysis showed that hypothalamic kisspeptin-IR had the same elution profile as a synthetic rodent kisspeptin standard. A specific rodent kisspeptin-RIA will allow accurate quantification of kisspeptin peptide levels within specific tissues in rodent experimental models.

Journal article

Basharat S, Parker JA, Murphy KG, Bloom SR, Buckingham JC, John CDet al., 2014, Leptin fails to blunt the lipopolysaccharide-induced activation of the hypothalamic-pituitary- adrenal axis in rats, Journal of Endocrinology, Vol: 221, Pages: 229-234, ISSN: 0022-0795

Obesity is a risk factor for sepsis morbidity and mortality, whereas the hypothalamic–pituitary–adrenal (HPA) axis plays a protective role in the body's defence against sepsis. Sepsis induces a profound systemic immune response and cytokines serve as excellent markers for sepsis as they act as mediators of the immune response. Evidence suggests that the adipokine leptin may play a pathogenic role in sepsis. Mouse endotoxaemic models present with elevated leptin levels and exogenously added leptin increased mortality whereas human septic patients have elevated circulating levels of the soluble leptin receptor (Ob-Re). Evidence suggests that leptin can inhibit the regulation of the HPA axis. Thus, leptin may suppress the HPA axis, impairing its protective role in sepsis. We hypothesised that leptin would attenuate the HPA axis response to sepsis. We investigated the direct effects of an i.p. injection of 2 mg/kg leptin on the HPA axis response to intraperitoneally injected 25 μg/kg lipopolysaccharide (LPS) in the male Wistar rat. We found that LPS potently activated the HPA axis, as shown by significantly increased plasma stress hormones, ACTH and corticosterone, and increased plasma interleukin 1β (IL1β) levels, 2 h after administration. Pre-treatment with leptin, 2 h before LPS administration, did not influence the HPA axis response to LPS. In turn, LPS did not affect plasma leptin levels. Our findings suggest that leptin does not influence HPA function or IL1β secretion in a rat model of LPS-induced sepsis, and thus that leptin is unlikely to be involved in the acute-phase endocrine response to bacterial infection in rats.

Journal article

McGowan BM, Minnion JS, Murphy KG, Roy D, Stanley SA, Dhillo WS, Gardiner JV, Ghatei MA, Bloom SRet al., 2014, Relaxin-3 stimulates the neuro-endocrine stress axis via corticotrophin-releasing hormone, JOURNAL OF ENDOCRINOLOGY, Vol: 221, Pages: 337-346, ISSN: 0022-0795

Journal article

Agahi A, Murphy KG, 2014, Models and Strategies in the Development of Antiobesity Drugs, VETERINARY PATHOLOGY, Vol: 51, Pages: 695-706, ISSN: 0300-9858

Journal article

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