NPY modulates PYY function in the regulation of energy balance and glucose homeostasis

Zhang, L.; Nguyen, Amy; Lee, I.-C. J.; Yulyaningsih, Ernie; Riepler, Sabrina J.; Stehrer, B; Enriquez, Ronaldo F.; Lin, Shu; Shi, Yan‐Chuan; Baldock, Paul A.; Sainsbury, Amanda; Herzog, Herbert

doi:10.1111/j.1463-1326.2012.01592.x

Cited by 30 publications

(29 citation statements)

References 50 publications

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“…13,16,24 Second, several of the novel endometrial carcinoma markers that we identified have been identified previously in other cancers (HS3ST2, 25 HTR1B, 26 MME 27 ) or involve important pathways in carcinogenesis such as Wnt signaling (ASCL2 28 ) and the Hedgehog pathway (ADCYAP1 29 ). In addition, NPY, one of our candidate markers, is proposed to function in energy balance and obesity, 30,31 which is notable because elevated body mass is strongly and consistently related to increased endometrial carcinoma risk. 32 Further studies are required to understand the role of these genes in endometrial carcinogenesis and to elucidate the etiologic heterogeneity of endometrial carcinomas reflected by the two groups of carcinomas with distinct methylation patterns observed in unsupervised hierarchical clustering.…”

Section: Discussionmentioning

confidence: 99%

Discovery and validation of methylation markers for endometrial cancer

et al. 2014

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The prognosis of endometrial cancer is strongly associated with stage at diagnosis, suggesting that early detection may reduce mortality. Women who are diagnosed with endometrial carcinoma often have a lengthy history of vaginal bleeding, which offers an opportunity for early diagnosis and curative treatment. We performed DNA methylation profiling on population-based endometrial cancers to identify early detection biomarkers and replicated top candidates in two independent studies. We compared DNA methylation values of 1500 probes representing 807 genes in 148 population-based endometrial carcinoma samples and 23 benign endometrial tissues. Markers were replicated in another set of 69 carcinomas and 40 benign tissues profiled on the same platform. Further replication was conducted in The Cancer Genome Atlas and in prospectively collected endometrial brushings from women with and without endometrial carcinomas. We identified 114 CpG sites showing methylation differences with p-values of ≤10−7 between endometrial carcinoma and normal endometrium. Eight genes (ADCYAP1, ASCL2, HS3ST2, HTR1B, MME, NPY, and SOX1) were selected for further replication. Age-adjusted odds ratios for endometrial cancer ranged from 3.44 (95%-CI: 1.33–8.91) for ASCL2 to 18.61 (95%-CI: 5.50–62.97) for HTR1B. An area under the curve (AUC) of 0.93 was achieved for discriminating carcinoma from benign endometrium. Replication in The Cancer Genome Atlas and in endometrial brushings from an independent study confirmed the candidate markers. This study demonstrates that methylation markers may be used to evaluate women with abnormal vaginal bleeding to distinguish women with endometrial carcinoma from the majority of women without malignancy.

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Section: Discussionmentioning

confidence: 99%

Discovery and validation of methylation markers for endometrial cancer

et al. 2014

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“…Combined deletion of PYY and NPY retards, however, the recovery from the hypophagic effect of BCG. To the contrary, hyperphagia provoked by food deprivation is enhanced in PYY−/− animals but left unchanged in NPY−/− as well as NPY−/−;PYY−/− mice (Zhang et al ., ), although another study holds that fasting‐induced hyperphagia is also enhanced in NPY−/− animals (Erickson et al ., ). These observations suggest that the reduction of food intake caused by fasting, on the one hand, and BCG, on the other hand, involves the NPY/PYY system to a different extent.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y and peptide YY protect from weight loss caused by Bacille Calmette–Guérin in mice

Painsipp

Köfer

Farzi

et al. 2013

British J Pharmacology

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Background and PurposeImmune challenge of mice with Bacille Calmette–Guérin (BCG) has been reported to cause transient weight loss and a behavioural sickness response. Although BCG-induced depression involves the kynurenine pathway, weight loss occurs independently of this factor. Because neuropeptide Y (NPY) and peptide YY (PYY) are involved in the regulation of food intake, we hypothesized that they play a role in the BCG-induced weight loss.Experimental ApproachMale wild-type, PYY knockout (PYY−/−), NPY knockout (NPY−/−) and NPY−/−;PYY−/− double knockout mice were injected with vehicle or BCG (approximately 108 colony-forming units per mouse), and their weight, locomotion, exploration and ingestion were recorded for 2 weeks post-treatment.Key ResultsDeletion of PYY and NPY aggravated the BCG-induced loss of body weight, which was most pronounced in NPY−/−;PYY−/− mice (maximum loss: 15%). The weight loss in NPY−/−;PYY−/− mice did not normalize during the 2 week observation period. BCG suppressed the circadian pattern of locomotion, exploration and food intake. However, these changes took a different time course than the prolonged weight loss caused by BCG in NPY−/−;PYY−/− mice. The effect of BCG to increase circulating IL-6 (measured 16 days post-treatment) remained unaltered by knockout of PYY, NPY or NPY plus PYY.Conclusions and ImplicationsThese data show that NPY and PYY are both required to protect from the action of BCG-evoked immune challenge to cause prolonged weight loss and disturb energy balance. The findings attest to an important role of NPY and PYY in orchestrating homeostatic reactions to infection and immune stimulation.

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“…Peptide YY consists of two forms, PYYa and PYYb (previously called PY) (Wahlestedt and Reis, 1993; Cerdá-Reverter and Larhammar, 2000; Sundström et al, 2013) and is a brain-gut peptide that acts as an anorexigenic signal in mammals (Blevins et al, 2008; Karra et al, 2009; Zhang et al, 2012). Interestingly, one of the first studies showing an effect of PYY on feeding in mammals used fish PYY (Balasubramaniam et al, 1992).…”

Section: Hormones Involved In Food Intakementioning

confidence: 99%

The Neuroendocrine Regulation of Food Intake in Fish: A Review of Current Knowledge

2016

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Fish are the most diversified group of vertebrates and, although progress has been made in the past years, only relatively few fish species have been examined to date, with regards to the endocrine regulation of feeding in fish. In fish, as in mammals, feeding behavior is ultimately regulated by central effectors within feeding centers of the brain, which receive and process information from endocrine signals from both brain and peripheral tissues. Although basic endocrine mechanisms regulating feeding appear to be conserved among vertebrates, major physiological differences between fish and mammals and the diversity of fish, in particular in regard to feeding habits, digestive tract anatomy and physiology, suggest the existence of fish- and species-specific regulating mechanisms. This review provides an overview of hormones known to regulate food intake in fish, emphasizing on major hormones and the main fish groups studied to date.

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NPY modulates PYY function in the regulation of energy balance and glucose homeostasis

Cited by 30 publications

References 50 publications

Discovery and validation of methylation markers for endometrial cancer

Discovery and validation of methylation markers for endometrial cancer

Neuropeptide Y and peptide YY protect from weight loss caused by Bacille Calmette–Guérin in mice

The Neuroendocrine Regulation of Food Intake in Fish: A Review of Current Knowledge

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