Abstract
The global burden of obesity and the challenges of prevention prompted researchers to investigate the mechanisms that control food intake. Food ingestion triggers several physiological responses in the digestive system, including the release of gastrointestinal hormones from enteroendocrine cells that are involved in appetite signalling. Disturbed regulation of gut hormone release may affect energy homeostasis and contribute to obesity. In this review, we summarize the changes that occur in the gut hormone balance during the pre- and postprandial state in obesity and the alterations in the diurnal dynamics of their plasma levels. We further discuss how obesity may affect nutrient sensors on enteroendocrine cells that sense the luminal content and provoke alterations in their secretory profile. Gastric bypass surgery elicits one of the most favorable metabolic outcomes in obese patients. We summarize the effect of different strategies to induce weight loss on gut enteroendocrine function. Although the mechanisms underlying obesity are not fully understood, restoring the gut hormone balance in obesity by targeting nutrient sensors or by combination therapy with gut peptide mimetics represents a novel strategy to ameliorate obesity.
Highlights
Obesity has increased dramatically over the past decades and reached epidemic proportions in adults and in children worldwide [1]
Obesity is defined by the World Health Organization as “abnormal or excessive fat accumulation that may impair health” and is classified by a body mass index (BMI) ≥ 30 kg/m2, which is a simple index of weight-for-height [2]
Ghrelin is a 28-amino acid peptide that is activated upon octanoylation of serine on the third N-terminal amino acid position, a posttranslational modification initiated by ghrelin O-acyl-transferase (GOAT) [59,60]
Summary
Obesity has increased dramatically over the past decades and reached epidemic proportions in adults and in children worldwide [1]. The rising prevalence and increased risk of developing chronic diseases exemplify the need for further research to improve understanding of the molecular mechanisms that are involved in the pathogenesis of obesity. Obesity is a multi-factorial disorder and arises from the complex interaction between genetic, environmental, behavioral and psychological factors [4]. Genetic research has led to the recognition of rare monogenic and more common polygenic forms of obesity with different genes, each contributing to the relative risk of developing obesity [5]. This genetic predisposition is associated with genes that control eating behavior and appetite [6,7]
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