Abstract

The ineffective short-term control of feeding behavior compromises energy homeostasis and can lead to obesity. The gastrointestinal tract secretes several regulatory peptides. However, little is known about the stomach peptide contribution to the acute regulation of intake. In an attempt to identify new gastric signals, the serial analysis of gene expression (SAGE) method was used for the transcription profiling of stomach mucosa in 7 groups of mice: fasting and sacrificed 30 minutes, 1 hour, 3 hours after a low-fat (LF) or high-fat (HF) ad libitum meal. In total, 35 genes were differentially modulated by LF and HF meals compared to fasting, including 15 mRNAs coding for digestive enzymes/secretory proteins, and 10 novel transcripts. Although the basic expression profile did not undergo substantial variations, both LF and HF meals influenced the transcription. This study represents the first global analysis of stomach transcriptome as induced by different nutritional stimuli. Further studies including the characterization of novel genes may help to identify new targets for the therapy and prevention of obesity.

Highlights

  • Obesity epidemic continues its worrying global progression significant advances have been achieved in the knowledge of its causes and consequences

  • Food intake and daily overconsumption may have a predominant impact on body weight regulation, and this led large interest to focus on appetite/satiety balance as one of the key potential therapeutic targets [5]

  • In addition to mechanoreceptors and chemoreceptors, which are activated during a meal and signal to the brainstem through the vagal nerve [4], several gut-derived peptides and lipid mediators have a role in the regulation of food intake and energy homeostasis [7]

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Summary

Introduction

Obesity epidemic continues its worrying global progression significant advances have been achieved in the knowledge of its causes and consequences. This condition, in concert with glucose intolerance/type 2 diabetes, dyslipidemia, and metabolic syndrome, widely contributes to what has been recently defined as “prosperity’s plague” [1]. The stomach plays an essential mechanical role in the regulation of satiety perception and meal termination. It is, the first organ to receive the bolus of food. Gastric competence can be considered as the first limiting step of GI ingestive and digestive capacity and represents a relevant target for obesity

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