Nowadays obesity rates have overtaken hunger rates globally with 39%, or 1.9 billion adults, being overweight and 13% obese. Being overweight is a major risk factor for cardiovascular disease, as well as cancers including breast, endometrial, prostate, liver, kidney and colon.2

Research on hunger, out of the University of California San Francisco and led by Lisa Beutler, has uncovered interesting dynamics between gut hormones and the brain.  Signals are sent between the brain and the gut, in-order-to maintain energy homeostasis.  There are two cell types that are studied most in hunger regulation. They are agouti-related protein (AgRP) and pro-opiomelanocortin (POMC) neurons. When food is detected, neurons send signals to inhibit AgRP via serotonin, cholecystokinin (CCK), and peptide YY (PYY).   Interestingly, even just sensory detection of food in mice triggered a quick and temporary inhibition. However, only the consumption of food caused sustained inhibition. The same effect was not seen in mice that were already satiated and found that the overall response was blood glucose independent.  While leptin is critical for regulation of hunger, they discovered that it had no acute in-vivo effect on food intake and was not required for the response of hunger and satiety neurons to sensory cues.  However, Leptin did activate POMC neurons and inhibit AgRP neurons on a timeline of hours, and only in food deprived animals.3   Additional research around Leptin is needed to better understand its role in obesity.        

For more information around obesity you can visit this link from the Mayo Clinic which covers symptoms, causes, diagnosis and treatment.

Agouti-Related Protein (Human, 86-132) AgRP



CCK products

Peptide YY

PYY products


Leptin Products


  1. World Health Organization. (2021, 9 June). Obesity and Overweight. Retrieved from
  2. World Health Organization. (2021, 9 June). Obesity and Overweight. Retrieved from
  3. R. Beutler, et al., Neuron, 96, 461 (2017). Retrieved from