Brainstem GLP-1 signalling contributes to cancer anorexia-cachexia syndrome in the rat

Borner, Tito; Liberini, Claudia G.; Lutz, Thomas; Riediger, Thomas

doi:10.1016/j.neuropharm.2017.12.024

Cited by 25 publications

(16 citation statements)

References 57 publications

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“…In addition to not assessing CFA, these studies differ from the previous findings by usage of a shorter habituation period to the kaolin pellets [68] or lower dose of intra-NTS exendin-4 [67]. Consistent with a role for NTS GLP-1R signaling in mediating the nausea outcomes induced by this system, GLP-1R blockade attenuates anorexia and weight loss when infused into the NTS of tumor-bearing rats [153], and reduces pica induced by icv infusion in cisplatin-treated rats treated [154].…”

Section: Rodent Studiescontrasting

confidence: 54%

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: Rodent Studiescontrasting

confidence: 54%

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

Décarie-Spain

Kanoski

2021

Nutrients

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“…Selective ablation of NTS PPG neurons prevents stress-induced hyperphagia in mice but has no effect on long-term ad libitum food intake, body weight, or glucose tolerance [90]. These data suggest that NTS PPG neurons are not essential for long-term regulation of food intake but are required for the short-term hypophagia in response to stress [738,739].…”

Section: Glp-1 Effects On Food Intake and Body Weightmentioning

confidence: 99%

Glucagon-like peptide 1 (GLP-1)

Müller¹,

Finan²,

Bloom³

et al. 2019

Molecular Metabolism

1,141

861

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BackgroundThe glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential. Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. GLP-1 also has cardio- and neuroprotective effects, decreases inflammation and apoptosis, and has implications for learning and memory, reward behavior, and palatability. Biochemically modified for enhanced potency and sustained action, GLP-1 receptor agonists are successfully in clinical use for the treatment of type-2 diabetes, and several GLP-1-based pharmacotherapies are in clinical evaluation for the treatment of obesity.Scope of reviewIn this review, we provide a detailed overview on the multifaceted nature of GLP-1 and its pharmacology and discuss its therapeutic implications on various diseases.Major conclusionsSince its discovery, GLP-1 has emerged as a pleiotropic hormone with a myriad of metabolic functions that go well beyond its classical identification as an incretin hormone. The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders

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“…Indeed, the GLP‐1 agonist and insulin sensitizer exendin‐4 partially prevents cachexia in tumor‐bearing rats . Recent evidence further suggests that brainstem GLP‐1 signaling influences body weight loss and lean/fat mass in cachectic rodents . As for GIP, its plasma levels decrease in cachexia in rheumatoid arthritis patients .…”

Section: Absorption/malabsorption Of Energy Substratesmentioning

confidence: 99%

Energy metabolism in cachexia

et al. 2019

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Cachexia is a wasting disorder that accompanies many chronic diseases including cancer and results from an imbalance of energy requirements and energy uptake. In cancer cachexia, tumor‐secreted factors and/or tumor–host interactions cause this imbalance, leading to loss of adipose tissue and skeletal and cardiac muscle, which weakens the body. In this review, we discuss how energy enters the body and is utilized by the different organs, including the gut, liver, adipose tissue, and muscle, and how these organs contribute to the energy wasting observed in cachexia. We also discuss futile cycles both between the organs and within the cells, which are often used to fine‐tune energy supply under physiologic conditions. Ultimately, understanding the complex interplay of pathologic energy‐wasting circuits in cachexia can bring us closer to identifying effective treatment strategies for this devastating wasting disease.

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Brainstem GLP-1 signalling contributes to cancer anorexia-cachexia syndrome in the rat

Cited by 25 publications

References 57 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

Glucagon-like peptide 1 (GLP-1)

Energy metabolism in cachexia

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