X Y Deng

Publications (4)48.44 Total impact

• Source

  Available from: Sylvia Ortmann

  Article: PYY3-36 as an anti-obesity drug target.

  M M Boggiano, P C Chandler, K D Oswald, R J Rodgers, J E Blundell, Y Ishii, A H Beattie, P Holch, D B Allison, M Schindler, [......], X Y Deng, D C Whitcomb, H Halem, J Taylor, J Dong, R Datta, M Culler, S Ortmann, T R Castañeda, M Tschöp
  [show abstract] [hide abstract]
  ABSTRACT: The neuropeptide Y (NPY)/peptide YY (PYY) system has been implicated in the physiology of obesity for several decades. More recently ignited enormous interest in PYY3-36, an endogenous Y2-receptor agonist, as a promising anti-obesity compound. Despite this interest, there have been remarkably few subsequent reports reproducing or extending the initial findings, while at the same time studies finding no anti-obesity effects have surfaced. Out of 41 different rodent studies conducted (in 16 independent labs worldwide), 33 (83%) were unable to reproduce the reported effects and obtained no change or sometimes increased food intake, despite use of the same experimental conditions (i.e. adaptation protocols, routes of drug administration and doses, rodent strains, diets, drug vendors, light cycles, room temperatures). Among studies by authors in the original study, procedural caveats are reported under which positive effects may be obtained. Currently, data speak against a sustained decrease in food intake, body fat, or body weight gain following PYY3-36 administration and make the previously suggested role of the hypothalamic melanocortin system unlikely as is the existence of PYY deficiency in human obesity. We review the studies that are in the public domain which support or challenge PYY3-36 as a potential anti-obesity target.
  Obesity Reviews 12/2005; 6(4):307-22. · 7.04 Impact Factor
• Article: Physiology: does gut hormone PYY3-36 decrease food intake in rodents?

  M Tschöp, T R Castañeda, H G Joost, C Thöne-Reineke, S Ortmann, S Klaus, M M Hagan, P C Chandler, K D Oswald, S C Benoit, [......], H Halem, J Taylor, J Dong, R Datta, M Culler, S Craney, D Flora, D Smiley, M L Heiman, D C Withcomb
  [show abstract] [hide abstract]
  ABSTRACT: Batterham et al. report that the gut peptide hormone PYY3-36 decreases food intake and body-weight gain in rodents, a discovery that has been heralded as potentially offering a new therapy for obesity. However, we have been unable to replicate their results. Although the reasons for this discrepancy remain undetermined, an effective anti-obesity drug ultimately must produce its effects across a range of situations. The fact that the findings of Batterham et al. cannot easily be replicated calls into question the potential value of an anti-obesity approach that is based on administration of PYY3-36.
  Nature 08/2004; 430(6996):1 p following 165; discussion 2 p following 165. · 36.28 Impact Factor
• Article: Chronic ethanol consumption induces gene expression of pancreatic monitor peptide, but not SPINK1/PSTI-56, in rats.

  H S Li, X Y Deng, B S Thompson, J Y Zhang, P G Wood, P K Eagon, D C Whitcomb
  [show abstract] [hide abstract]
  ABSTRACT: The primary factors that predispose humans to the development of alcoholic pancreatitis are unknown. One of the earliest observations in humans in whom this disease develops is pancreatic hypersecretion caused by unknown mechanisms. Messenger RNA (mRNA) differential display was performed in a rat model to investigate the molecular mechanisms associated with ethanol-induced pancreatic hypersecretion. Male Wistar rats were pair-fed Lieber-DeCarli diets with or without ethanol for 7 days or 4 weeks. Total RNA was extracted from the pancreas and its neurohormonal control sites. Differentially expressed complementary DNA (cDNA) tags were isolated, cloned, and sequenced. One 248-bp cDNA was consistently and strongly induced in the pancreata of rats fed ethanol for 4 weeks. The sequence was highly homologous to both rat pancreatic monitor peptide (MP) and pancreatic secretory trypsin inhibitor (PSTI-56), also known as serine protease inhibitor, Kazal type 1 (SPINK1). Confirmatory reverse-transcription-polymerase chain reaction showed that PSTI-56 expression remained unchanged, whereas MP mRNA levels were elevated more than four times in the pancreata of ethanol-fed rats. These results indicate that long-term ethanol ingestion increases MP mRNA levels in the rat pancreas. Because MP stimulates cholecystokinin release and cholecystokinin is an important stimulant of pancreatic secretion, the enhanced MP gene expression may contribute to pancreatic hypersecretion.
  Pancreas 09/2001; 23(2):117-24. · 2.39 Impact Factor
• Article: Rat mitochondrial ATP synthase ATP5G3: cloning and upregulation in pancreas after chronic ethanol feeding.

  H S Li, J Y Zhang, B S Thompson, X Y Deng, M E Ford, P G Wood, D B Stolz, P K Eagon, D C Whitcomb
  [show abstract] [hide abstract]
  ABSTRACT: Individuals with chronic excessive alcohol ingestion are put at the risk of acute and chronic pancreatitis. Underlying molecular mechanisms are unknown. Differential gene expression in the pancreas was profiled using mRNA differential display by comparison between control and ethanol-consuming rats. Male Wistar rats were fed with diets containing 6.7% (vol/vol) ethanol for 4 wk. A cDNA tag that was overexpressed in the pancreas of rats fed ethanol was isolated. A 723-bp cDNA was cloned from a rat pancreatic cDNA library, which encodes a novel rat mitochondrial ATP synthase subunit 9, isoform 3 (ATP5G3), which is homologous to a human ATP5G3 gene. Real-time PCR demonstrated that all three nuclear gene isoforms (ATP5G1, ATP5G2, and ATP5G3) were consistently upregulated in the pancreas of alcohol-consuming rats, parallel with mitochondrial injury. The cellular response to mitochondrial damage and metabolic stress may reflect an adaptive process for mitochondrial repair in pancreatic acinar cells during chronic ethanol ingestion.
  Physiological Genomics 08/2001; 6(2):91-8. · 2.73 Impact Factor