Publications
2554 results found
Ma Y, Bloom SR, Gardiner JV, 2015, Arcuate nucleus glucokinase and dietary glucose intake, Oncotarget, Vol: 6, Pages: 19926-19927, ISSN: 1949-2553
Abbara A, Jayasena CN, Christopoulos G, et al., 2015, Efficacy of kisspeptin-54 to trigger oocyte maturation in women at high risk of OHSS during IVF therapy, Journal of Clinical Endocrinology and Metabolism, Vol: 100, Pages: 3322-3331, ISSN: 0368-1610
Context:In Vitro Fertilization (IVF) treatment is an effective therapy for infertility, but can result in the potentially life-threatening complication ‘ovarian hyperstimulation syndrome’ (OHSS).Objective:To investigate whether kisspeptin-54 can be used to effectively and safely trigger oocyte maturation in women undergoing IVF treatment at high risk of developing OHSS.Design:Phase 2 multi-dose open label randomized clinical trial carried out during 2013–2014.Setting:Hammersmith Hospital IVF unit, London, UK.Patients:Sixty women at high risk of developing OHSS Intervention:Following a standard recombinant FSH/GnRH antagonist protocol, patients were randomized to receive a single injection of kisspeptin-54 to trigger oocyte maturation using an adaptive design for dose allocation (3.2nmol/kg, n=5; 6.4nmol/kg, n=20; 9.6nmol/kg, n=15; 12.8nmol/kg, n=20). Oocytes were retrieved 36hrs after kisspeptin-54 administration, assessed for maturation, and fertilized by intra-cytoplasmic sperm injection (ICSI) with subsequent transfer of one or two embryos. Women were routinely screened for the development of OHSS.Main Outcome Measure:Oocyte maturation was measured by oocyte yield (percentage of mature oocytes retrieved from follicles ≥14mm on ultrasound). Secondary outcomes include rates of OHSS and pregancy. Results:Oocyte maturation occurred in 95% of women. Highest oocyte yield (121%) was observed following 12.8nmol/kg kisspeptin-54, which was +69% (CI -16%,+153%) greater than following 3.2nmol/kg. At all doses of kisspeptin-54, biochemical pregnancy, clinical pregnancy and live birth rates per transfer (n=51) were 63%, 53% and 45%, respectively. Highest pregnancy rates were observed following 9.6nmol/kg kisspeptin-54 (85%, 77% and 62%, respectively). No woman developed moderate, severe or critical OHSS.Conclusion:Kisspeptin-54 is a promising approach to effectively and safely trigger oocyte
Jayasena CN, Abbara A, Narayanaswamy S, et al., 2015, Direct comparison of the effects of intravenous kisspeptin-10, kisspeptin-54 and GnRH on gonadotrophin secretion in healthy men, Human Reproduction, Vol: 30, Pages: 1934-1941, ISSN: 1460-2350
study question: How potently does the novel hypothalamic stimulator of reproduction, kisspeptin, increase gonadotrophin secretionwhen compared with GnRH in healthy men?summaryanswer: At the doses tested, intravenous administration of either of two major kisspeptin isoforms, kisspeptin-10 and -54, wasassociated with similar levels of gonadotrophin secretion in healthy men; however, GnRH was more potent when compared with either kisspeptinisoform.what is known already: Kisspeptin-10 and -54 are naturally occurring hormones in the kisspeptin peptide family which potently stimulatesendogenous GnRH secretion from the hypothalamus, so have the potential to treat patients with reproductive disorders. Rodent studiessuggest that kisspeptin-54 is more potent when compared with kisspepitn-10; however, their effects have not previously been directly comparedin humans, or compared with direct pituitary stimulation of gonadotrophin secretion using GnRH.study design, size and duration: A single-blinded placebo controlled physiological study was performed from January to December2013. Local ethical approval was granted, and five participants were recruited to each dosing group.participants/materials, setting, methods: Healthy men were administered vehicle, kisspeptin-10, kisspeptin-54 andGnRH intravenously for 3 h on different study days. Each hormone was administered at 0.1, 0.3 and 1.0 nmol/kg/h doses (n ¼ 5 subjects pergroup). Regular blood sampling was conducted throughout the study to measure LH and FSH. Study visits were conducted at least a week apart.main results and the role of chance: Serum LH and FSH levels were 3-fold higher during GnRH infusion when comparedwith kisspeptin-10 and 2-fold higher when compared with kisspeptin-54 [mean area under the curve serum LH during infusion (in hours timesinternational units per litre, h.IU/l): 10.81+1.73, 1.0 nmol/kg/h kisspeptin-10; 14.43+1.27, 1.0 nmol/kg/h kisspeptin-54; 34.06+5.18,1.0 nmol/kg/h GnRH, P , 0.001 versus kis
Abbara A, Jayasena CN, Christopoulos G, et al., 2015, Kisspeptin-54 safely and effectively triggers oocyte maturation in women at high risk of the ovarian hyperstimulation syndrome (OHSS), 31st Annual Meeting of the European-Society-of-Human-Reproduction-and-Embryology (ESHRE), Publisher: OXFORD UNIV PRESS, Pages: 68-68, ISSN: 0268-1161
Jones BJ, Bloom SR, 2015, The new era of drug therapy for obesity: The evidence and the expectations, Drugs, Vol: 75, Pages: 935-945, ISSN: 1179-1950
There is an urgent need for effective pharmacological therapies to help tackle the growing obesity epidemic and the healthcare crisis it poses. The past 3 years have seen approval of a number of novel anti-obesity drugs. The majority of these influence hypothalamic appetite pathways via dopaminergic or serotoninergic signalling. Some are combination therapies, allowing lower doses to minimize the potential for off-target effects. An alternative approach is to mimic endogenous satiety signals using long-lasting forms of peripheral appetite-suppressing hormones. There is also considerable interest in targeting thermogenesis by brown adipose tissue to increase resting energy expenditure. Obesity pharmacotherapy has seen several false dawns, but improved understanding of the pathways regulating energy balance, and better-designed trials, give many greater confidence that recently approved agents will be both efficacious and safe. Nevertheless, a number of issues from preclinical and clinical development continue to attract debate, and additional large-scale trials are still required to address areas of uncertainty.
Jayasena CN, Comninos AN, Narayanaswamy S, et al., 2015, The identification of elevated urinary kisspeptin-immunoreactivity during pregnancy, ANNALS OF CLINICAL BIOCHEMISTRY, Vol: 52, Pages: 395-398, ISSN: 0004-5632
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- Citations: 9
Chambers ES, Viardot A, Psichas A, et al., 2015, Effects of elevating colonic propionate on liver fat content in overweight adults with non-alcoholic fatty liver disease: a pilot study, Proceedings of the Nutrition Society, Vol: 74, Pages: E30-E30, ISSN: 1475-2719
Hu MH, Li XF, McCausland B, et al., 2015, Relative importance of the arcuate and anteroventral periventricular kisspeptin neurons in control of puberty and reproductive function in female rats, Endocrinology, Vol: 156, Pages: 2619-2631, ISSN: 1945-7170
Chambers E, Viardot A, Psichas A, et al., 2015, Effects of Elevating Colonic Propionate on Liver Fat Content in Adults with Non-Alcoholic Fatty Liver Disease, FASEB JOURNAL, Vol: 29, ISSN: 0892-6638
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- Citations: 1
Comninos AN, Anastasovska J, Sahuri-Arisoylu M, et al., 2015, Kisspeptin signaling in the amygdala modulates reproductive hormone secretion, Brain Structure & Function, Vol: 221, Pages: 2035-2047, ISSN: 1863-2661
Kisspeptin (encoded by KISS1) is a crucial activator of reproductive function. The role of kisspeptin has been studied extensively within the hypothalamus but little is known about its significance in other areas of the brain. KISS1 and its cognate receptor are expressed in the amygdala, a key limbic brain structure with inhibitory projections to hypothalamic centers involved in gonadotropin secretion. We therefore hypothesized that kisspeptin has effects on neuronal activation and reproductive pathways beyond the hypothalamus and particularly within the amygdala. To test this, we mapped brain neuronal activity (using manganese-enhanced MRI) associated with peripheral kisspeptin administration in rodents. We also investigated functional relevance by measuring the gonadotropin response to direct intra-medial amygdala (MeA) administration of kisspeptin and kisspeptin antagonist. Peripheral kisspeptin administration resulted in a marked decrease in signal intensity in the amygdala compared to vehicle alone. This was associated with an increase in luteinizing hormone (LH) secretion. In addition, intra-MeA administration of kisspeptin resulted in increased LH secretion, while blocking endogenous kisspeptin signaling within the amygdala by administering intra-MeA kisspeptin antagonist decreased both LH secretion and LH pulse frequency. We provide evidence for the first time that neuronal activity within the amygdala is decreased by peripheral kisspeptin administration and that kisspeptin signaling within the amygdala contributes to the modulation of gonadotropin release and pulsatility. Our data suggest that kisspeptin is a ‘master regulator’ of reproductive physiology, integrating limbic circuits with the regulation of gonadotropin-releasing hormone neurons and reproductive hormone secretion.
Sam AH, Sleeth ML, Thomas EL, et al., 2015, Circulating pancreatic polypeptide concentrations predict visceral and liver fat content, Journal of Clinical Endocrinology and Metabolism, Vol: 100, Pages: 1048-1052, ISSN: 0021-972X
Context and objective:No current biomarker can reliably predict visceral and liver fat content, both of which are risk factors for cardiovascular disease. Vagal tone has been suggested to influence regional fat deposition. Pancreatic polypeptide (PP) is secreted from the endocrine pancreas under vagal control. We investigated the utility of PP in predicting visceral and liver fat.Patients and Methods:Fasting plasma PP concentrations were measured in 104 overweight and obese subjects (46 men and 58 women). In the same subjects, total and regional adipose tissue, including total visceral adipose tissue (VAT) and total subcutaneous adipose tissue (TSAT), were measured using whole-body magnetic resonance imaging. Intrahepatocellular lipid content (IHCL) was quantified by proton magnetic resonance spectroscopy.Results:Fasting plasma PP concentrations positively and significantly correlated with both VAT (r = 0.57, P < .001) and IHCL (r = 0.51, P < .001), but not with TSAT (r = 0.02, P = .88). Fasting PP concentrations independently predicted VAT after controlling for age and sex. Fasting PP concentrations independently predicted IHCL after controlling for age, sex, body mass index (BMI), waist-to-hip ratio, homeostatic model assessment 2-insulin resistance, (HOMA2-IR) and serum concentrations of triglyceride (TG), total cholesterol (TC), and alanine aminotransferase (ALT). Fasting PP concentrations were associated with serum ALT, TG, TC, low- and high-density lipoprotein cholesterol, and blood pressure (P < .05). These associations were mediated by IHCL and/or VAT. Fasting PP and HOMA2-IR were independently significantly associated with hepatic steatosis (P < .01).Conclusions:Pancreatic polypeptide is a novel predictor of visceral and liver fat content, and thus a potential biomarker for cardiovascular risk stratification and targeted treatment of patients with ectopic fat deposition.
McGavigan AK, O'Hara HC, Amin A, et al., 2015, L-cysteine suppresses ghrelin and reduces appetite in rodents and humans, INTERNATIONAL JOURNAL OF OBESITY, Vol: 39, Pages: 447-455, ISSN: 0307-0565
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- Citations: 28
Hill NE, Fallowfield JL, Delves SK, et al., 2015, Changes in Gut Hormones and Leptin in Military Personnel During Operational Deployment in Afghanistan, OBESITY, Vol: 23, Pages: 608-614, ISSN: 1930-7381
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- Citations: 8
Cegla J, Cuenco J, Minnion J, et al., 2015, Pharmacokinetics and pharmacodynamics of subcutaneously administered PYY<sub>3-36</sub> and its analogues in vivo, LANCET, Vol: 385, Pages: 28-28, ISSN: 0140-6736
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- Citations: 1
Jayasena CN, Comninos AN, Stefanopoulou E, et al., 2015, Neurokinin B Administration Induces Hot Flushes in Women, SCIENTIFIC REPORTS, Vol: 5, ISSN: 2045-2322
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- Citations: 70
Ramachandran R, Bech P, Murphy KG, et al., 2015, Comparison of the Utility of Cocaine- and Amphetamine-Regulated Transcript (CART), Chromogranin A, and Chromogranin B in Neuroendocrine Tumor Diagnosis and Assessment of Disease Progression, Journal of Clinical Endocrinology & Metabolism, Vol: 100, Pages: 1520-1528, ISSN: 1945-7197
Hussain S, Richardson E, Ma Y, et al., 2015, Glucokinase activity in the arcuate nucleus regulates glucose intake, Journal of Clinical Investigation, Vol: 125, Pages: 337-384, ISSN: 1558-8238
The brain relies on a constant supply of glucose, its primary fuel, for optimal function. A taste-independent mechanism within the CNS that promotes glucose delivery to the brain has been postulated to maintain glucose homeostasis; however, evidence for such a mechanism is lacking. Here, we determined that glucokinase activity within the hypothalamic arcuate nucleus is involved in regulation of dietary glucose intake. In fasted rats, glucokinase activity was specifically increased in the arcuate nucleus but not other regions of the hypothalamus. Moreover, pharmacologic and genetic activation of glucokinase in the arcuate nucleus of rodent models increased glucose ingestion, while decreased arcuate nucleus glucokinase activity reduced glucose intake. Pharmacologic targeting of potential downstream glucokinase effectors revealed that ATP-sensitive potassium channel and P/Q calcium channel activity are required for glucokinase-mediated glucose intake. Additionally, altered glucokinase activity affected release of the orexigenic neurotransmitter neuropeptide Y in response to glucose. Together, our results suggest that glucokinase activity in the arcuate nucleus specifically regulates glucose intake and that appetite for glucose is an important driver of overall food intake. Arcuate nucleus glucokinase activation may represent a CNS mechanism that underlies the oft-described phenomena of the “sweet tooth” and carbohydrate craving.
Christakis I, Georgiou P, Minnion J, et al., 2015, Learning curve of vessel cannulation in rats using cumulative sum analysis, JOURNAL OF SURGICAL RESEARCH, Vol: 193, Pages: 69-76, ISSN: 0022-4804
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- Citations: 4
Behary P, Cegla J, Tan TM, et al., 2015, Obesity: Lifestyle management, bariatric surgery, drugs, and the therapeutic exploitation of gut hormones, POSTGRADUATE MEDICINE, Vol: 127, Pages: 494-502, ISSN: 0032-5481
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- Citations: 13
Scott RV, Tan TM, Bloom SR, 2014, Can Bayliss and Starling gut hormones cure a worldwide pandemic?, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 592, Pages: 5153-5167, ISSN: 0022-3751
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- Citations: 4
Howard JW, Kay RG, Tan T, et al., 2014, Development of a high-throughput UHPLC-MS/MS (SRM) method for the quantitation of endogenous glucagon from human plasma, Bioanalysis, Vol: 6, Pages: 3295-3309, ISSN: 1757-6199
Jayasena CN, Abbara A, Izzi-Engbeaya C, et al., 2014, Reduced Levels of Plasma Kisspeptin During the Antenatal Booking Visit Are Associated With Increased Risk of Miscarriage, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 99, Pages: E2652-E2660, ISSN: 0021-972X
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- Citations: 48
Jayasena CN, Comninos AN, Narayanaswamy S, et al., 2014, Acute and chronic effects of kisspeptin-54 administration on GH, prolactin and TSH secretion in healthy women, Clinical Endocrinology, Vol: 81, Pages: 891-898, ISSN: 1365-2265
Cegla J, Troke RC, Jones B, et al., 2014, Coinfusion of low-dose GLP-1 and glucagon in man results in a reduction in food intake, Diabetes, Vol: 63, Pages: 3711-3720, ISSN: 0012-1797
Obesity is a growing epidemic, and current medical therapies have proven inadequate. Endogenous satiety hormones provide an attractive target for the development of drugs that aim to cause effective weight loss with minimal side effects. Both glucagon and GLP-1 reduce appetite and cause weight loss. Additionally, glucagon increases energy expenditure. We hypothesized that the combination of both peptides, administered at doses that are individually subanorectic, would reduce appetite, while GLP-1 would protect against the hyperglycemic effect of glucagon. In this double-blind crossover study, subanorectic doses of each peptide alone, both peptides in combination, or placebo was infused into 13 human volunteers for 120 min. An ad libitum meal was provided after 90 min, and calorie intake determined. Resting energy expenditure was measured by indirect calorimetry at baseline and during infusion. Glucagon or GLP-1, given individually at subanorectic doses, did not significantly reduce food intake. Coinfusion at the same doses led to a significant reduction in food intake of 13%. Furthermore, the addition of GLP-1 protected against glucagon-induced hyperglycemia, and an increase in energy expenditure of 53 kcal/day was seen on coinfusion. These observations support the concept of GLP-1 and glucagon dual agonism as a possible treatment for obesity and diabetes.
Tan TM, Salem V, Troke RC, et al., 2014, Combination of peptide YY3-36 with GLP-1(7-36) amide causes an increase in first-phase insulin secretion after IV glucose, Journal of Clinical Endocrinology and Metabolism, Vol: 99, Pages: E2317-E2324, ISSN: 0021-972X
Context: The combination of peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) has been proposed as a potential treatment for diabetes and obesity. However, the combined effects of these hormones, PYY3–36 and GLP-17–36 amide, on glucose homeostasis are unknown.Objective: This study sought to investigate the acute effects of PYY3–36 and GLP-17–36 amide, individually and in combination, on insulin secretion and sensitivity.Setting and Design: Using a frequently sampled iv glucose tolerance test (FSIVGTT) and minimal modeling, this study measured the effects of PYY3–36 alone, GLP-17–36 amide alone, and a combination of PYY3–36 and GLP-17–36 amide on acute insulin response to glucose (AIRg) and insulin sensitivity index (SI) in 14 overweight human volunteers, studied in a clinical research facility.Results: PYY3–36 alone caused a small but nonsignificant increase in AIRg. GLP-17–36 amide alone and the combination of PYY3–36 and GLP-17–36 amide did increase AIRg significantly. No significant differences in SI were observed with any intervention.Conclusions: PYY3–36 lacks any significant acute effects on first-phase insulin secretion or SI when tested using an FSIVGTT. Both GLP-17–36 amide alone and the combination of PYY3–36 and GLP-17–36 amide increase first-phase insulin secretion. There does not seem to be any additive or synergistic effect between PYY3–36 and GLP-17–36 amide on first-phase insulin secretion. Neither hormone alone nor the combination had any significant effects on SI.
Zac-Varghese S, Trapp S, Richards P, et al., 2014, The Peutz-Jeghers kinase LKB1 suppresses polyp growth from intestinal cells of a proglucagon-expressing lineage in mice, DISEASE MODELS & MECHANISMS, Vol: 7, Pages: 1275-1286, ISSN: 1754-8403
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- Citations: 10
Psichas A, Sleeth ML, Murphy KG, et al., 2014, The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents, International Journal of Obesity, Vol: 39, Pages: 424-429, ISSN: 1476-5497
Skrapits K, Borsay BA, Herczeg L, et al., 2014, Colocalization of Cocaine- and Amphetamine-Regulated Transcript with Kisspeptin and Neurokinin B in the Human Infundibular Region, PLoS ONE, Vol: 9, ISSN: 1932-6203
Kisspeptin (KP)- and neurokinin B (NKB)- synthesizing neurons of the hypothalamic arcuate nucleus play a pivotal role in the regulation of pulsatile gonadotropin-releasing hormone (GnRH) secretion. Unlike in rodents and sheep, the homologous KP and NKB neurons in the human infundibular region rarely express dynorphin- but often exhibit Substance P (SP) immunoreactivity, indicating remarkable species differences in the neurochemical phenotype of these neurons. In search for additional neuropeptides in human KP and NKB neurons, we carried out immunofluorescent studies on hypothalamic sections obtained from five postmenopausal women. Colocalization experiments provided evidence for the presence of cocaine- and amphetamine-regulated transcript (CART) in 47.9 ± 6.6% of KP-immunoreactive (IR) and 30.0 ± 4.9% of NKB-IR perikarya and in 17.0 ± 2.3% of KP-IR and 6.2 ± 2.0% of NKB-IR axon varicosities. All three neuropeptides were present in 33.3 ± 4.9% of KP-IR and 28.2 ± 4.6% of NKB-IR somata, respectively, whereas triple-labeling showed lower incidences in KP-IR (14.3 ± 1.8%) and NKB-IR (5.9 ± 2.0%) axon varicosities. CART-IR KP and NKB neurons established contacts with other peptidergic cells, including GnRH-IR neurons and also sent projections to the infundibular stalk. KP and NKB fibers with CART often contained SP as well, while being distinct from CART fibers co-containing the orexigenic peptide agouti-related protein. Presence of CART in human, but not rodent, KP and NKB neurons represents a new example of species differences in the neuropeptide repertoire of mediobasal hypothalamic KP and NKB neurons. Target cells, receptor sites and physiological significance of CART in the efferent communication of KP and NKB neurons in primates require clarification.
Jayasena CN, Abbara A, Comninos AN, et al., 2014, Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization, Journal of Clinical Investigation, Vol: 124, Pages: 3667-3677, ISSN: 0021-9738
BACKGROUND. Patients with mutations that inactivate kisspeptin signaling are infertile. Kisspeptin-54, the major circulating isoform of kisspeptin in humans, potently stimulates reproductive hormone secretion in humans. Animal studies suggest that kisspeptin is involved in generation of the luteinizing hormone surge, which is required for ovulation; therefore, we hypothesized that kisspeptin-54 could be used to trigger egg maturation in women undergoing in vitro fertilization therapy.METHODS. Following superovulation with recombinant follicle-stimulating hormone and administration of gonadotropin-releasing hormone antagonist to prevent premature ovulation, 53 women were administered a single subcutaneous injection of kisspeptin-54 (1.6 nmol/kg, n = 2; 3.2 nmol/kg, n = 3; 6.4 nmol/kg, n = 24; 12.8 nmol/kg, n = 24) to induce a luteinizing hormone surge and egg maturation. Eggs were retrieved transvaginally 36 hours after kisspeptin injection, assessed for maturation (primary outcome), and fertilized by intracytoplasmic sperm injection with subsequent transfer of one or two embryos.RESULTS. Egg maturation was observed in response to each tested dose of kisspeptin-54, and the mean number of mature eggs per patient generally increased in a dose-dependent manner. Fertilization of eggs and transfer of embryos to the uterus occurred in 92% (49/53) of kisspeptin-54–treated patients. Biochemical and clinical pregnancy rates were 40% (21/53) and 23% (12/53), respectively.CONCLUSION. This study demonstrates that a single injection of kisspeptin-54 can induce egg maturation in women with subfertility undergoing in vitro fertilization therapy. Subsequent fertilization of eggs matured following kisspeptin-54 administration and transfer of resulting embryos can lead to successful human pregnancy.TRIAL REGISTRATION. ClinicalTrials.gov NCT01667406.FUNDING. Medical Research Council, Wellcome Trust, and National Institute for Health Research.
Angelopoulos T, Kokkinos A, Liaskos C, et al., 2014, The effect of slow spaced eating on hunger and satiety in overweight and obese patients with type 2 diabetes mellitus., BMJ Open Diabetes Research and Care, Vol: 2, ISSN: 2052-4897
BACKGROUND: Slow spaced eating is associated with improved satiety and gut hormone responses in normal-weight participants. This crossover study compared the effect of slow and rapid eating patterns on hunger, fullness, glucose, insulin, and the appetite-related gut hormones peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and ghrelin in overweight and obese participants with type 2 diabetes mellitus (T2DM). METHODS: 20 overweight and obese participants with T2DM on metformin were recruited. A test meal of 300 mL ice-cream was consumed in random order in two different sessions by each participant; meal duration was 5 or 30 min. Fullness and hunger as assessed by visual analog scales (VAS), and glucose, insulin, PYY, GLP-1, and ghrelin were measured at baseline and at 30 min intervals after meal termination for 3 h. RESULTS: Fullness VAS ratings were significantly higher at the 90', 120', 150', and 180' time points and hunger ratings were lower at 90', 150', and 180' for the 30 min meal. The area under the curve (AUC) for fullness was higher after the 30 min meal than after the 5 min meal (11 943.7±541.2 vs 10 901.0±568.8 mm min, p=0.003) whereas the hunger AUC was lower (4442.9±328 vs 4966.7±347.5 mm min, p=0.012). There were no differences in glucose, insulin, PYY, GLP-1, and ghrelin responses. CONCLUSIONS: Slow spaced eating increased fullness and decreased hunger ratings in overweight and obese participants with T2DM, without the improvement in gut hormone responses found in normal-weight participants. Slow spaced eating may be a useful prevention strategy, but might also help curb food intake in those already suffering from obesity and diabetes.
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