A Role for GLP-1 in Treating Hyperphagia and Obesity

Jun 10, 2020Endocrinology

GLP-1’s role in reducing excessive eating and obesity

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Abstract

Obesity prevalence has nearly tripled over the past 40 years, with significant impacts on health and quality of life.

Obesity is associated with increased risk of morbidity and mortality.
The global increase in food supply has led to greater access to energy-dense foods, contributing to obesity.
Hedonic foods and related nonfood cues activate brain circuits that drive increased food-seeking behavior and weight gain.
Behavioral therapies, such as diet and lifestyle modifications, often fail to achieve sustained weight loss, with weight regain common over time.
Biologically based treatments, including bariatric surgery and drug therapies targeting GLP-1R signaling, may offer new avenues for addressing obesity.
Bariatric surgery and GLP-1R agonist therapies can alter food reward processes and the motivation to overeat.

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Obesity is a chronic recurring disease whose prevalence has almost tripled over the past 40 years. In individuals with obesity, there is significant increased risk of morbidity and mortality, along with decreased quality of life. Increased obesity prevalence results, at least partly, from the increased global food supply that provides ubiquitous access to tasty, energy-dense foods. These hedonic foods and the nonfood cues that through association become reward predictive cues activate brain appetitive control circuits that drive hyperphagia and weight gain by enhancing food-seeking, motivation, and reward. Behavioral therapy (diet and lifestyle modifications) is the recommended initial treatment for obesity, yet it often fails to achieve meaningful weight loss. Furthermore, those who lose weight regain it over time through biological regulation. The need to effectively treat the pathophysiology of obesity thus centers on biologically based approaches such as bariatric surgery and more recently developed drug therapies. This review highlights neurobiological aspects relevant to obesity causation and treatment by emphasizing the common aspects of the feeding-inhibitory effects of multiple signals. We focus on glucagon like peptide-1 receptor (GLP-1R) signaling as a promising obesity treatment target by discussing the activation of intestinal- and brain-derived GLP-1 and GLP-1R expressing central nervous system circuits resulting from normal eating, bariatric surgery, and GLP-1R agonist drug therapy. Given the increased availability of energy-dense foods and frequent encounters with cues that drive hyperphagia, this review also describes how bariatric surgery and GLP-1R agonist therapies influence food reward and the motivational drive to overeat.

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A Role for GLP-1 in Treating Hyperphagia and Obesity

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