Appetite

Appetite

Appetite regulation and the dysregulation of appetite hormones play a crucial role in the development and perpetuation of obesity. Hormones, including ghrelin, leptin, and glucagon-like peptide-1 (GLP-1), are key players in this process and as such, have been targeted by pharmaceutical companies. Dysregulation of these hormones can disrupt the balance between energy intake and expenditure, contributing to overeating and weight gain. 

Multiple hormonal signals influence appetite:

Hormones and the organ they originate from in the human body1

1. Ghrelin:

  • Role: Ghrelin is often referred to as the “hunger hormone” because it stimulates appetite. It is primarily produced in the stomach and plays a role in meal initiation.2
  • Dysregulation in Obesity: In obesity, there can be alterations in ghrelin levels and sensitivity. Some studies have shown that individuals with obesity may have reduced ghrelin suppression, leading to increased hunger and a greater propensity to consume more calories.3

2. Leptin:

  • Role: Leptin is produced by adipose tissue and is often referred to as the “satiety hormone.” It acts to suppress appetite and regulate energy expenditure by signalling to the brain information on the body’s energy stores.
  • Dysregulation in Obesity: Obesity is commonly associated with elevated levels of circulating leptin. However, many individuals with obesity develop a condition known as “leptin resistance.” In this state, the brain does not respond adequately to high leptin levels, resulting in a failure to effectively suppress appetite. This leads to increased food intake and contributes to further weight gain. 4, 5

3. GLP-1 (Glucagon-Like Peptide-1):

  • Role: GLP-1 is an incretin hormone produced in the small intestine in response to food intake. It plays a role in regulating blood sugar levels and appetite control. GLP-1 receptor agonists (such as semaglutide/Wegovy) are indicated for the treatment of type 2 diabetes and obesity and overweight due to their appetite-suppressing effects.
  • Therapeutic Use: GLP-1 receptor agonists, such as liraglutide and semaglutide, have been approved for the treatment of obesity in the US and UK. They reduce appetite, lead to weight loss, and may improve metabolic health in individuals with obesity or a BMI greater than 27. 6, 7

The regulation of appetite is highly complex and influenced by various factors, including genetics, lifestyle, and environmental factors, as previously discussed. The dysregulation of these appetite hormones is just one aspect of the multifaceted nature of obesity. Understanding how these appetite hormones work and how they are influenced by obesity is important to consider when developing your clinic’s weight management program.8 – 12

Secretion and expression of GLP-1 throughout the body

References:

  1. Woods et al. Int J Obes Relat Metab Disord 2002;26:S8–S10; Badman, Flier. Science 2005;307:1909–14
  2. Tschöp, M., Weyer, C., Tataranni, P. A., Devanarayan, V., Ravussin, E., & Heiman, M. L. (2001). Circulating ghrelin levels are decreased in human obesity. Diabetes, 50(4), 707-709.
  3. Nakazato, M., Murakami, N., Date, Y., Kojima, M., Matsuo, H., Kangawa, K., & Matsukura, S. (2001). A role for ghrelin in the central regulation of feeding. Nature, 409(6817), 194-198.
  4. Fruhbeck, G., Mendez-Gimenez, L., Fernandez-Formoso, J. A., & Fernandez Sánchez, A. (2014). New aspects of adipose tissue and its role in metabolic syndrome. Endocrinología y Nutrición (English Edition), 61(2), 88-94.
  5. Schwartz, M. W., & Porte, D. Jr. (2005). Diabetes, obesity, and the brain. Science, 307(5708), 375-379.
  6. Meier, J. J., & Nauck, M. A. (2015). Incretins and the development of type 2 diabetes. Current Diabetes Reports, 15(1), 86.
  7. Nuffer, W. A., Trujillo, J. M. (2019). Liraglutide: A new option for the treatment of obesity. Pharmacotherapy, 39(1), 110-125.
  8. Merchenthaler et al. J Comp Neurol 1999;403:261–80; Baggio,
  9. Drucker. Gastroenterology 2007;132:2131–57
  10. Ban et al. Circulation 2008;117:2340–50
  11. Vrang et al. Prog Neurobiol 2010;92:442–62
  12. Pyke et al. Endocrinology 2014;155:1280–90
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