The last decade has witnessed a marked increase in our understanding of the importance of gut hormones in the regulation of energy homeostasis. In particular, the discovery that the gut hormone peptide YY 3–36 (PYY3–36) reduced feeding in obese rodents and humans fuelled interest in the role of PYY3–36 in body weight regulation. Pharmacological and genetic approaches have revealed that the Y2-receptor mediates the anorectic effects of PYY3–36 whilst mechanistic studies in rodents identified the hypothalamus, vagus and brainstem regions as potential sites of action. More recently, using functional brain imaging techniques in humans, PYY3–36 was found to modulate neuronal activity within hypothalamic and brainstem, and brain regions involved in reward processing. Several lines of evidence suggest that low circulating PYY concentrations predispose towards the development and or maintenance of obesity. Subjects with reduced postprandial PYY release exhibit lower satiety and circulating PYY levels that correlate negatively with markers of adiposity. In addition, mice lacking PYY are hyperphagic and become obese. Conversely, chronic PYY3–36 administration to obese rodents reduces adiposity, and transgenic mice with increased circulating PYY are resistant to diet-induced obesity. Moreover, there is emerging evidence that PYY3–36 may partly mediate the reduced appetite and weight loss benefits observed post-gastric bypass surgery. Taken together these findings, coupled with the retained responsiveness of obese subjects to the effects of PYY3–36, suggest that targeting the PYY system may offer a therapeutic strategy to help treat obesity.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2008.164269

The role of peptide YY in appetite regulation and obesity

The endocannabinoid system (ECS) functions to adjust behavior and metabolism according to environmental changes in food availability. Its actions range from the regulation of sensory responses to the development of preference for the consumption of calorically-rich food and control of its metabolic handling. ECS activity is beneficial when access to food is scarce or unpredictable. However, when food is plentiful, the ECS favors obesity and metabolic disease. We review recent advances in understanding the roles of the ECS in energy balance, and discuss newly identified mechanisms of action that, after the withdrawal of first generation cannabinoid type 1 (CB1) receptor antagonists for the treatment of obesity, have made the ECS once again an attractive target for therapy.

https://www.cell.com/trends/endocrinology-metabolism/pdf/S1043-2760(15)00140-X.pdf

The Endocannabinoid System: Pivotal Orchestrator of Obesity and Metabolic Disease

Within the past 15 years, the endocannabinoid system (ECS) has emerged as a lipid signaling system critically involved in the regulation of energy balance, as it exerts a regulatory control on every aspect related to the search, the intake, the metabolism and the storage of calories. An overactive endocannabinoid cannabinoid type 1 (CB1) receptor signaling promotes the development of obesity, insulin resistance and dyslipidemia, representing a valuable pharmacotherapeutic target for obesity and metabolic disorders. However, because of the psychiatric side effects, the first generation of brain-penetrant CB1 receptor blockers developed as antiobesity treatment were removed from the European market in late 2008. Since then, recent studies have identified new mechanisms of action of the ECS in energy balance and metabolism, as well as novel ways of targeting the system that may be efficacious for the treatment of obesity and metabolic disorders. These aspects will be especially highlighted in this review.

New insights on the role of the endocannabinoid system in the regulation of energy balance

The obesity epidemic is a major health problem that is associated with increased morbidity and mortality Gastrointestinal hormones have been increasingly understood to be an important element in appetite regulation Several gastrointestinal hormones can contribute to obesity by modulating the activity of the gut-brain axis Bariatric surgery is currently the most effective therapy for significant and sustained weight loss in morbidly obese patients Understanding how gut hormones are altered by bariatric procedures has contributed to our understanding of the mechanisms of appetite In this review, we address several gastrointestinal hormones that are associated with obesity and consider how their levels are altered after bariatric surgery The review also addresses specific effects of different gut hormones on appetite, hunger, and energy balance

/pdf/mechanisms-of-weight-loss-after-gastric-bypass-and-gastric-4pob9c6alj.pdf

Mechanisms of weight loss after gastric bypass and gastric banding.

Since the discovery of leptin, great advances occurred in the characterization of hypothalamic mechanisms involved in the control of food intake and oxyntomodulin is currently recognized as a homeostasis energy regulator. This review discusses the most important interrelationships between the hormone oxyntomodulin and appetite, energy homeostasis and aspects of its role in nutritional biochemistry and physiology. Oxyntomodulin is an anorexigenic peptide produced by the L cells of the small intestine. Recent studies have shown that long-term use of oxyntomodulin in rats leads to reduced food intake and weight gain. Studies in humans have demonstrated that its administration reduces food intake by 25%. Therefore, oxyntomodulin represents a potent anti-obesity therapy. However, its mechanism of action is unknown. Current evidence suggests that it acts via the peptide receptor similar to glucagon 1. Moreover, the literature shows that together with the adoption of healthy habits and lifestyle changes, oxyntomodulin can reduce weight gain.

/pdf/oxintomodulina-e-obesidade-flcv0yjdrq.pdf

Oxintomodulina e obesidade

Background:  SR141716 has been shown to significantly inhibit food intake and reduce body weight by antagonizing CB1 receptors. The gut hormones peptide YY3–36 (PYY3–36) and oxyntomodulin (OXM) inhibit food intake through Y2 and Glucagon‐Like‐Peptide (GLP)‐1 receptors respectively.

Co-administration of SR141716 with peptide YY or oxyntomodulin has additive effects on food intake in mice

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Co-administration of SR141716 with peptide YY or oxyntomodulin has additive effects on food intake in mice