Publications
2554 results found
Germain N, Galusca B, Caron-Dorval D, et al., 2014, Specific appetite, energetic and metabolomics responses to fat overfeeding in resistant-to-bodyweight-gain constitutional thinness, Nutrition & Diabetes, Vol: 4, ISSN: 2044-4052
Background: Contrasting with obesity, constitutional thinness (CT) is a rare condition of natural low bodyweight. CT exhibits preserved menstruation in females, no biological marker of undernutrition, no eating disorders but a bodyweight gain desire. Anorexigenic hormonal profile with high peptide tyrosine tyrosine (PYY) was shown in circadian profile. CT could be considered as the opposite of obesity, where some patients appear to resist diet-induced bodyweight loss.Objective: The objective of this study was to evaluate appetite regulatory hormones in CTs in an inverse paradigm of diet-induced weight loss.Methods: A 4-week fat overfeeding (2640 kJ excess) was performed to compare eight CT women (body mass index (BMI)<17.5 kg m−2) to eight female controls (BMI 18.5–25 kg m−2). Appetite regulatory hormones profile after test meal, food intake, bodyweight, body composition, energy expenditure and urine metabolomics profiles were monitored before and after overfeeding.Results: After overfeeding, fasting total and acylated ghrelin were significantly lower in CTs than in controls (P=0.01 and 0.03, respectively). After overfeeding, peptide tyrosine tyrosine (PYY) and glucagon-like-peptide 1 both presented earlier (T15 min vs T30 min) and higher post-meal responses (incremental area under the curve) in CTs compared with controls. CTs failed to increase bodyweight (+0.22±0.18 kg, P=0.26 vs baseline), contrasting with controls (+0.72±0.26 kg, P=0.03 vs baseline, P=0.01 vs CTs). Resting energy expenditure increased in CTs only (P=0.031 vs baseline). After overfeeding, a significant negative difference between total energy expenditure and food intake was noticed in CTs only (−2754±720 kJ, P=0.01).Conclusion: CTs showed specific adaptation to fat overfeeding: overall increase in anorexigenic hormonal profile, enhanced post prandial GLP-1 and PYY and inverse to controls change
Comninos AN, Jayasena CN, Stefanopoulou E, et al., 2014, The hypothalamic hormone neurokinin B: a novel therapeutic target for menopausal hot flushes, 30th Annual Meeting of the European-Society-of-Human-Reproduction-and-Embryology (ESHRE), Publisher: OXFORD UNIV PRESS, Pages: 105-105, ISSN: 0268-1161
Abbara A, Jayasena CN, Comninos AN, et al., 2014, Kisspeptin - a novel physiological trigger for oocyte maturation in IVF treatment, 30th Annual Meeting of the European-Society-of-Human-Reproduction-and-Embryology (ESHRE), Publisher: OXFORD UNIV PRESS, Pages: 50-50, ISSN: 0268-1161
Goldstone AP, Prechtl CG, Scholtz S, et al., 2014, Ghrelin mimics fasting to enhance human hedonic, orbitofrontal cortex, and hippocampal responses to food, AMERICAN JOURNAL OF CLINICAL NUTRITION, Vol: 99, Pages: 1319-1330, ISSN: 0002-9165
Jayasena CN, Abbara A, Veldhuis JD, et al., 2014, Increasing LH Pulsatility in Women With Hypothalamic Amenorrhoea Using Intravenous Infusion of Kisspeptin-54, Journal of Clinical Endocrinology and Metabolism, Vol: 99, Pages: E953-E961, ISSN: 0021-972X
Background:Hypothalamic amenorrhea (HA) is the one of the most common causes of period loss in women of reproductive age and is associated with deficient LH pulsatility. High-dose kisspeptin-54 acutely stimulates LH secretion in women with HA, but chronic administration causes desensitization. GnRH has paradoxical effects on reproductive activity; we therefore hypothesized that a dose-dependent therapeutic window exists within which kisspeptin treatment restores the GnRH/LH pulsatility in women with HA.Aim:The aim of the study was to determine whether constant iv infusion of kisspeptin-54 temporarily increases pulsatile LH secretion in women with HA.Methods:Five patients with HA each underwent six assessments of LH pulsatility. Single-blinded continuous iv infusion of vehicle or kisspeptin-54 (0.01, 0.03, 0.10, 0.30, or 1.00 nmol/kg/h) was administered. The LH pulses were detected using blinded deconvolution.Results:Kisspeptin increased LH pulsatility in all patients with HA, with peak responses observed at different doses in each patient. The mean peak number of pulses during infusion of kisspeptin-54 was 3-fold higher when compared with vehicle (number of LH pulses per 8 h: 1.6 ± 0.4, vehicle; 5.0 ± 0.5, kisspeptin-54, P < .01 vs vehicle). The mean peak LH pulse secretory mass during kisspeptin-54 was 6-fold higher when compared with vehicle (LH pulse secretory mass in international units per liter: 3.92 ± 2.31, vehicle; 23.44 ± 12.59, kisspeptin-54; P < .05 vs vehicle).Conclusions:Kisspeptin-54 infusion temporarily increases LH pulsatility in women with HA. Furthermore, we have determined the dose range within which kisspeptin-54 treatment increases basal and pulsatile LH secretion in women with HA. This work provides a basis for studying the potential of kisspeptin-based therapies to treat women with HA.
Brooks L, Cani P, Everard A, et al., 2014, Free Fatty Acid Receptor 2 (FFAR2) Is Important in Mediating the Effects of Fermentable Carbohydrate on Gut Inflammation but Not Intestinal Barrier Function in Obesity, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Alamshah A, Spreckley E, McGavigan AK, et al., 2014, L-Arginine Promotes Gut Hormone Release and Reduces Appetite in Rodents, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Comninos AN, Anastasovska J, Sahuri-Arisoylu M, et al., 2014, Kisspeptin Inhibits Neuronal Activity in the Amygdala of Male Mice, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Jayasena CN, Abbara A, Comninos AN, et al., 2014, Comparing the Effects of Pituitary Versus Hypothalamic Stimulation of the Human Reproductive Axis Using Equimolar Intravenous Infusions of Kisspeptin-10, Kisspeptin-54 and Gonadotrophin Releasing Hormone (GnRH) in Healthy Men, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Comninos AN, Jayasena CN, Stefanopoulou E, et al., 2014, Neurokinin B Administration Induces Menopausal-like Hot Flushes in Healthy Young Women, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Abbara A, Jayasena CN, Comninos AN, et al., 2014, Kisspeptin - a Novel Physiological Trigger for Oocyte Maturation in IVF Treatment, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Abbara A, Jayasena CN, Izzi-Engbeaya C, et al., 2014, Plasma Kisspeptin Measurement during Early Pregnancy Is a Highly Predictive Marker of Subsequent Miscarriage, Publisher: ENDOCRINE SOC, ISSN: 0163-769X
Kinsey-Jones JS, Beale KE, Cuenco J, et 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.
Vakilgilani T, Zac-Varghese S, Bloom SR, 2014, Gut peptides, Treatment of the Obese Patient, Pages: 37-55, ISBN: 9781493912025
Appetite and body weight are tightly regulated by appetite centres within the brainstem and hypothalamus. For weight to remain constant, energy intake and energy expenditure should be balanced. Information regarding energy intake is relayed to hypothalamic and brainstem nuclei via hormonal and neuronal signals from the gastrointestinal tract (GIT). Entero-endocrine cells throughout the GIT release gut hormones. These gut hormones exert diverse physiological functions including gut motility, acid secretion, appetite control and regulation of food intake. The release of gut hormones from entero-endocrine cells is stimulated by the presence of nutrients within the gut lumen and also by the enteric nervous system. We are recently beginning to understand how the diverse population of entero-endocrine cells function and signal to regulate appetite via both paracrine and endocrine means. Several gut hormones produced by the intestine and pancreas have been shown to inhibit food intake (anorexigenic) (Table 3.1). These include peptide tyrosine tyrosine 3-36 (PYY<inf>3-36</inf>), pancreatic polypeptide (PP), cholecystokinin (CCK), oxyntomodulin (OXM) and glucagon-like peptide-1 (GLP-1). Ghrelin produced in the stomach is the only gut hormone known to stimulate feeding (orexigenic). This chapter discusses the pathophysiological roles of orexigenic and anorexigenic gut hormones in the regulation of food intake.
Basharat S, Parker JA, Murphy KG, et 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.
Christakis IC, Minnion JM, Tan TT, et al., 2014, A surgical rat model for investigating pharmacokinetic parameters of drug compounds, Annual Meeting of the Society-of-Academic-and-Research-Surgery, Publisher: WILEY-BLACKWELL, Pages: 27-27, ISSN: 0007-1323
McGowan BM, Minnion JS, Murphy KG, et 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
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- Citations: 29
Saeed S, Bech PR, Hafeez T, et al., 2014, Changes in levels of peripheral hormones controlling appetite are inconsistent with hyperphagia in leptin-deficient subjects, ENDOCRINE, Vol: 45, Pages: 401-408, ISSN: 1355-008X
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- Citations: 14
Beale KE, Kinsey-Jones JS, Gardiner JV, et al., 2014, The Physiological Role of Arcuate Kisspeptin Neurons in the Control of Reproductive Function in Female Rats, ENDOCRINOLOGY, Vol: 155, Pages: 1091-1098, ISSN: 0013-7227
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- Citations: 36
Zac-Varghese S, Trapp S, Sayers S, et al., 2014, LKB1 restricts polyp development from entero-endocrine L cell precursors
Abbara A, Jayasena C, Comninos A, et al., 2014, Kisspeptin: a novel physiological trigger for oocyte maturation in in-vitro fertilisation treatment, LANCET, Vol: 383, Pages: 17-17, ISSN: 0140-6736
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- Citations: 7
Comninos A, Jayasena C, Nijher G, et al., 2014, The effects of kisspeptin administration on the menstrual cycle in healthy women, LANCET, Vol: 383, Pages: 37-37, ISSN: 0140-6736
Jayasena CN, Dhillo WS, Bloom SR, 2014, Does Kisspeptin signaling offer a new way to treat infertility?, Expert Review of Obstetrics & Gynecology, Vol: 4, Pages: 477-481, ISSN: 1747-4116
Jayasena CN, Nijher GMK, Narayanaswamy S, et al., 2014, Age-dependent elevations in plasma kisspeptin are observed in boys and girls when compared with adults, ANNALS OF CLINICAL BIOCHEMISTRY, Vol: 51, Pages: 89-96, ISSN: 0004-5632
Jayasena CN, Comninos AN, De Silva A, et al., 2014, Effects of Neurokinin B Administration on Reproductive Hormone Secretion in Healthy Men and Women, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 99, Pages: E19-E27, ISSN: 0021-972X
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- Citations: 30
Troke RC, Tan TM, Bloom SR, 2014, The future role of gut hormones in the treatment of obesity., Ther Adv Chronic Dis, Vol: 5, Pages: 4-14, ISSN: 2040-6223
The obesity pandemic presents a significant burden, both in terms of healthcare and economic outcomes, and current medical therapies are inadequate to deal with this challenge. Bariatric surgery is currently the only therapy available for obesity which results in long-term, sustained weight loss. The favourable effects of this surgery are thought, at least in part, to be mediated via the changes of gut hormones such as GLP-1, PYY, PP and oxyntomodulin seen following the procedure. These hormones have subsequently become attractive novel targets for the development of obesity therapies. Here, we review the development of these gut peptides as current and emerging therapies in the treatment of obesity.
Bech PR, Martin NM, Ramachandran R, et al., 2014, The biochemical utility of chromogranin A, chromogranin B and cocaine- and amphetamine-regulated transcript for neuroendocrine neoplasia, ANNALS OF CLINICAL BIOCHEMISTRY, Vol: 51, Pages: 8-21, ISSN: 0004-5632
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- Citations: 17
Chambers ES, Viardot A, Psichas A, et al., 2014, Targeted delivery of propionate to the human colon prevents body weight and intra-abdominal adipose tissue gain in overweight adults, PROCEEDINGS OF THE NUTRITION SOCIETY, Vol: 73, Pages: E22-E22, ISSN: 0029-6651
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- Citations: 1
Cegla J, Bloom SR, 2014, Gastrointestinal tract and appetite control, ADVANCED NUTRITION AND DIETETICS IN GASTROENTEROLOGY, Editors: Lomer, Publisher: WILEY-BLACKWELL, Pages: 48-54, ISBN: 978-0-470-67132-0
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- Citations: 1
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