Glucagon and GLP-1 inhibit food intake and increase c-fos expression in similar appetite regulating centres in the brainstem and amygdala

Parker, Jennifer; McCullough, Katherine; Field, Benjamin; Minnion, James; Martin, Niamh; Ghatei, Mohammad A.

doi:10.1038/ijo.2012.227

Cited by 84 publications

(71 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Peripheral as well as central administration of glucagon in rats reduced food intake and meal size in addition to reducing body weight gain (Geary et al 1993;Honda et al 2007). Combination of glucagon and GLP-1 agonists has been found to be benefi cial as a treatment of obesity rodents have been demonstrated (Pocai et al 2009) as GLP-1 prevented the hypoglycemia induced by glucagon (Parker et al 2013). …”

Section: Role Of the Gastrointestinal Tract Peptidesmentioning

confidence: 99%

See 1 more Smart Citation

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

View full text Add to dashboard Cite

Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

show abstract

Section: Role Of the Gastrointestinal Tract Peptidesmentioning

confidence: 99%

“…Circulating GLP-1 levels rise aft er a meal and fall in the fasted state. GLP-1 reduces food intake (Parker et al 2013), suppresses glucagon secretion (Hare 2010), and delays gastric emptying (Little et al 2006).…”

Section: Role Of the Gastrointestinal Tract Peptidesmentioning

confidence: 99%

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

View full text Add to dashboard Cite

show abstract

“…This growth factor has also been involved in the lipolytic action of glucagon in diabetic and non-diabetic animals and humans (11) . Additionally, peripherally administered glucagon inhibits food intake, presumably by the neural activation of appetite-regulating brain centres (199) . Thus, the combined activation of glucagon and GLP-1 receptors has been proved to be useful for the design of strategies against obesity and diabetes.…”

Section: Therapeutic Potential Of Modulating Glucagon Secretion and Amentioning

confidence: 99%

Nutrient regulation of glucagon secretion: involvement in metabolism and diabetes

et al. 2014

View full text Add to dashboard Cite

Glucose homeostasis is precisely regulated by glucagon and insulin, which are released by pancreatic a-and b-cells, respectively. While b-cells have been the focus of intense research, less is known about a-cell function and the actions of glucagon. In recent years, the study of this endocrine cell type has experienced a renewed drive. The present review contains a summary of established concepts as well as new information about the regulation of a-cells by glucose, amino acids, fatty acids and other nutrients, focusing especially on glucagon release, glucagon synthesis and a-cell survival. We have also discussed the role of glucagon in glucose homeostasis and in energy and lipid metabolism as well as its potential as a modulator of food intake and body weight. In addition to the well-established action on the liver, we discuss the effects of glucagon in other organs, where the glucagon receptor is expressed. These tissues include the heart, kidneys, adipose tissue, brain, small intestine and the gustatory epithelium. Alterations in a-cell function and abnormal glucagon concentrations are present in diabetes and are thought to aggravate the hyperglycaemic state of diabetic patients. In this respect, several experimental approaches in diabetic models have shown important beneficial results in improving hyperglycaemia after the modulation of glucagon secretion or action. Moreover, glucagon receptor agonism has also been used as a therapeutic strategy to treat obesity.

show abstract

“…Early studies have shown that administration of glucagon may reduce appetite in humans (32), but the physiological relevance of these findings has not been confirmed. However, combined administration of low doses of GLP-1 and glucagon inhibited food intake significantly and induced c-fos expression in the area postrema and amygdala in mice (33), and co-infusion of GLP-1 and glucagon has been shown to reduce food intake in humans (34).…”

Section: Introductionmentioning

confidence: 99%

Successful weight loss maintenance includes long-term increased meal responses of GLP-1 and PYY3–36

Iepsen

Lundgren

Holst

et al. 2016

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: The hormones glucagon-like peptide 1 (GLP-1), peptide YY ), ghrelin, glucose-dependent insulinotropic polypeptide (GIP) and glucagon have all been implicated in the pathogenesis of obesity. However, it is unknown whether they exhibit adaptive changes with respect to postprandial secretion to a sustained weight loss. Design: The study was designed as a longitudinal prospective intervention study with data obtained at baseline, after 8 weeks of weight loss and 1 year after weight loss. Methods: Twenty healthy obese individuals obtained a 13% weight loss by adhering to an 8-week very low-calorie diet (800 kcal/day). After weight loss, participants entered a 52-week weight maintenance protocol. Plasma levels of GLP-1, PYY 3-36 , ghrelin, GIP and glucagon during a 600-kcal meal were measured before weight loss, after weight loss and after 1 year of weight maintenance. Area under the curve (AUC) was calculated as total AUC (tAUC) and incremental AUC (iAUC). Results: Weight loss was successfully maintained for 52 weeks. iAUC for GLP-1 increased by 44% after weight loss (P < 0.04) and increased to 72% at week 52 (P = 0.0001). iAUC for PYY 3-36 increased by 74% after weight loss (P<0.0001) and by 36% at week 52 (P = 0.02). tAUC for ghrelin increased by 23% after weight loss (P<0.0001), but at week 52, the increase was reduced to 16% compared with before weight loss (P = 0.005). iAUC for GIP increased by 36% after weight loss (P = 0.001), but returned to before weight loss levels at week 52. Glucagon levels were unaffected by weight loss. Conclusions: Meal responses of GLP-1 and PYY 3-36 remained increased 1 year after weight maintenance, whereas ghrelin and GIP reverted toward before-weight loss values. Thus, an increase in appetite inhibitory mechanisms and a partly decrease in appetite-stimulating mechanisms appear to contribute to successful long-term weight loss maintenance.

show abstract

Glucagon and GLP-1 inhibit food intake and increase c-fos expression in similar appetite regulating centres in the brainstem and amygdala

Cited by 84 publications

References 32 publications

Central and peripheral control of food intake

Central and peripheral control of food intake

Nutrient regulation of glucagon secretion: involvement in metabolism and diabetes

Successful weight loss maintenance includes long-term increased meal responses of GLP-1 and PYY3–36

Contact Info

Product

Resources

About