Fasting glucagon-like peptide 1 concentration is associated with lower carbohydrate intake and increases with overeating

Basolo, Alessio; Heinitz, Sascha; Stinson, Emma J.; Begaye, Brittany; Hohenadel, Maximilian; Piaggi, Paolo; Krakoff, Jonathan; Votruba, Susanne B.

doi:10.1007/s40618-018-0954-5

Cited by 13 publications

(9 citation statements)

References 45 publications

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“…Ghrelin may even contribute to genetic predispositions for sweet taste preference as in a Swedish population cohort, specific haplotypes for the pro-ghrelin gene are associated with an elevated consumption of sucrose, especially in men [ 72 ]. In contrast, fasting GLP-1 concentrations negatively predict intake of food rich in simple sugars in a vending machine paradigm [ 113 ], which the authors interpreted as evidence that GLP-1 plays a role in reward pathways regulating simple sugar intake. A number of studies also report altered food preferences following gastric bypass surgery, with a shift away from high sugar/fat preference [ 114 , 115 , 116 , 117 ].…”

Section: Nutrient Preferencementioning

confidence: 99%

Ghrelin and Glucagon-Like Peptide-1: A Gut-Brain Axis Battle for Food Reward

Décarie-Spain

Kanoski

2021

Nutrients

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Eating behaviors are influenced by the reinforcing properties of foods that can favor decisions driven by reward incentives over metabolic needs. These food reward-motivated behaviors are modulated by gut-derived peptides such as ghrelin and glucagon-like peptide-1 (GLP-1) that are well-established to promote or reduce energy intake, respectively. In this review we highlight the antagonizing actions of ghrelin and GLP-1 on various behavioral constructs related to food reward/reinforcement, including reactivity to food cues, conditioned meal anticipation, effort-based food-motivated behaviors, and flavor-nutrient preference and aversion learning. We integrate physiological and behavioral neuroscience studies conducted in both rodents and human to illustrate translational findings of interest for the treatment of obesity or metabolic impairments. Collectively, the literature discussed herein highlights a model where ghrelin and GLP-1 regulate food reward-motivated behaviors via both competing and independent neurobiological and behavioral mechanisms.

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Section: Nutrient Preferencementioning

confidence: 99%

Ghrelin and Glucagon-Like Peptide-1: A Gut-Brain Axis Battle for Food Reward

Décarie-Spain

Kanoski

2021

Nutrients

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“…Higher fasting plasma GLP-1 concentrations is associated with lower carbohydrate and simple sugar intake in humans (with a BMI = 30.3 [±9.5], without type 2 diabetes) (Basolo et al, 2019). Similarly, higher sugar intake is related to increased striatal response to food cues and decreased GLP-1 release following glucose intake in lean human volunteers (Dorton et al, 2017).…”

Section: Glp-1mentioning

confidence: 99%

Gut peptide regulation of food intake – evidence for the modulation of hedonic feeding

Woodward

Gribble

Reimann

et al. 2021

The Journal of Physiology

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The number of people living with obesity has tripled worldwide since 1975 with serious implications for public health, as having obesity is linked to a significantly higher chance of early death from associated comorbidities (metabolic syndrome, type 2 diabetes and cardiovascular disease). As obesity is a consequence of food intake exceeding the demands of energy expenditure, efforts are made to better understand the homeostatic and hedonic mechanisms governing food intake. Gastrointestinal peptides are secreted from enteroendocrine cells in response to nutrient and energy intake, and modulate food intake either via afferent nerves, including the vagus nerve, or directly within the central nervous system, predominantly gaining access at circumventricular organs. Enteroendocrine hormones modulate homeostatic control centres at hypothalamic nuclei and the dorso-vagal complex. Additional roles of these peptides in modulating hedonic food intake and/or preference via the neural systems of reward are starting to be elucidated, with both peripheral and central peptide sources potentially contributing to central receptor activation. Pharmacological interventions and gastric bypass surgery for the treatment of type 2 diabetes and obesity elevate enteroendocrine hormone levels and also alter food preference. Hence, understanding of the hedonic mechanisms mediated by gut peptide action could advance development of potential therapeutic strategies for the treatment of obesity and its comorbidities. Key points-Enteroendocrine cells produce a range of gut peptides that have key roles in the regulation of appetite and beneficial effects on body weight. -Gut peptides are secreted as feedback to nutrient and energy intake, communicating directly or indirectly with the brain. -These peptides, some of which are also expressed in the CNS, alter food intake and reward via their widely distributed receptors. -Understanding these interactions is one of the challenges for developing effective pharmacotherapies that reduce feeding without producing negative side effects (e.g. nausea).

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“…However, staggered meal intake resulted in higher GLP-1 levels and satiety, along with lower ghrelin and desire for food scores than non-staggered meal intake (Lemmens et al, 2011 ). Higher GLP-1 plasma levels before ad libitum food intake were associated with lower intake of carbohydrates and simple sugar but not total food intake (Basolo et al, 2019 ). When exposed to palatable food compared to non-palatable food, GLP-1 levels did not change significantly in obese patients (Rigamonti et al, 2015 ).…”

Section: Resultsmentioning

confidence: 99%

Can GLP-1 Be a Target for Reward System Related Disorders? A Qualitative Synthesis and Systematic Review Analysis of Studies on Palatable Food, Drugs of Abuse, and Alcohol

Eren-Yazicioglu

Yigit

Dogruoz

et al. 2021

Front. Behav. Neurosci.

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The role of glucagon-like peptide 1 (GLP-1) in insulin-dependent signaling is well-known; GLP-1 enhances glucose-dependent insulin secretion and lowers blood glucose in diabetes. GLP-1 receptors (GLP-1R) are also widely expressed in the brain, and in addition to its role in neuroprotection, it affects reward pathways. This systematic review aimed to analyze the studies on GLP-1 and reward pathways and its currently identified mechanisms.Methods: “Web of Science” and “Pubmed” were searched to identify relevant studies using GLP-1 as the keyword. Among the identified 26,539 studies, 30 clinical, and 71 preclinical studies were included. Data is presented by grouping rodent studies on palatable food intake, drugs of abuse, and studies on humans focusing on GLP-1 and reward systems.Results: GLP-1Rs are located in reward-related areas, and GLP-1, its agonists, and DPP-IV inhibitors are effective in decreasing palatable food intake, along with reducing cocaine, amphetamine, alcohol, and nicotine use in animals. GLP-1 modulates dopamine levels and glutamatergic neurotransmission, which results in observed behavioral changes. In humans, GLP-1 alters palatable food intake and improves activity deficits in the insula, hypothalamus, and orbitofrontal cortex (OFC). GLP-1 reduces food cravings partially by decreasing activity to the anticipation of food in the left insula of obese patients with diabetes and may inhibit overeating by increasing activity to the consumption of food in the right OFC of obese and left insula of obese with diabetes.Conclusion: Current preclinical studies support the view that GLP-1 can be a target for reward system related disorders. More translational research is needed to evaluate its efficacy on human reward system related disorders.

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Fasting glucagon-like peptide 1 concentration is associated with lower carbohydrate intake and increases with overeating

Cited by 13 publications

References 45 publications

Ghrelin and Glucagon-Like Peptide-1: A Gut-Brain Axis Battle for Food Reward

Ghrelin and Glucagon-Like Peptide-1: A Gut-Brain Axis Battle for Food Reward

Gut peptide regulation of food intake – evidence for the modulation of hedonic feeding

Can GLP-1 Be a Target for Reward System Related Disorders? A Qualitative Synthesis and Systematic Review Analysis of Studies on Palatable Food, Drugs of Abuse, and Alcohol

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