Hormones of Hunger and Satiety | Part 10 Neurobiology of Food Intake | Macronutrients Lecture 46

The hunger hormone ghrelin and the satiety hormones GLP-1, PYY, CCK, and leptin coordinate satiety through signalling in the hindbrain and hypothalamus. Subscribe to Nourishable at    / nourishable  

This video is part 10 of the Neurobiology of Food Intake module within a lecture series on the nutrition science of macronutrients.


Neurobiology of Food Intake Lecture playlist:    • Neurobiology of Food Intake  

Macronutrients Lecture playlist:    • Macronutrients Lectures  

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The information in this video is not intended or implied to be a substitute for professional medical advice, diagnosis or treatment. All content, including text, graphics, images and information, contained on or available through this video is for general information purposes only.

References
Klockars, A. et al. Hypothalamic Integration of the Endocrine Signaling Related to Food Intake. Curr. Topics Behav. Neurosci. (2019) 43:239-270

Images
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Putting it all together - the hormones that regulate food intake! There are many factors regulating the short-term, meal to meal food intake. During the fasting state the hormone ghrelin will be secreted from the stomach. Ghrelin inhibits the vagus nerve which inhibits the nucleus tractus solitarius (NTS) of the hindbrain, in turn inhibiting satiety to induce hunger. Ghrelin stimulates the agouti-related peptide (AgRP) neurons to release the neurotransmitter NPY to inhibit activation of the paraventricular nucleus to increase food intake. This makes ghrelin an orexigenic hormone. GLP-1 binds to chemoreceptors on the vagus nerve to activate the vagus to send afferent signals to stimulate the nucleus tractus solitarius in the hindbrain to stimulate satiety. GLP slows gastric emptying which keeps the GI tract stretched and distended for longer - this activates the stretch-sensitive mechanoreceptors on the vagus to additionally stimulate the NTS. GLP-1 crosses the blood-brain-barrier of the hypothalamus to activate the POMC neurons in the arcuate nucleus. POMC neuron stimulation causes release of the neurotransmitter alpha MSH which stimulates the paraventricular hypothalamus to induce satiety. GLP-1 also inhibits the orexigenic AgRP neurons. GLP-1 is an anorexigenic, satiety-inducing hormone. PYY is a hormone secreted by L cells in the distal GI tract. It is secreted when digesting food in proportion to calories consumed. Protein intake additionally stimulates PYY secretion. PYY activates the vagus nerve to stimulate the nucleus tractus solitarius of the hindbrain to induce satiety. PYY also slows gastric motility which keeps the GI tract stretched and distended for longer - this stretch stimulates mechanoreceptors on the vagus as a further level of stimulation of the NTS to further induce satiety. Additionally, PYY acts at the level of the hypothalamus. PYY inhibits the orexigenic AgRP neurons in the arcuate nucleus. This inhibition of AgRP removes the inhibition on the paraventricular hypothalamus which in turn is activated to induced satiety. PYY is an anorexigenic, satiety-inducing hormone. Cholecystokinin, or CCK, is a hormone secreted by the I cells in the proximal intestine. It is secreted in response to fat and protein in the intestine. CCK stimulates the pancreas to release a cocktail of digestive enzymes required for digestion of carbohydrates, proteins, and fats. CCK also stimulates the gallbladder to release bile to enable emulsification of fats for efficient digestion. CCK stimulates chemoreceptors on the vagus which activates the nucleus tractus solitarius in the hindbrain to induce satiety. CCK also further stimulates PYY secretion from the distal intestine and inhibits secretion of the hunger hormone ghrelin from the stomach. CCK is an anorexigenic, satiety-inducing hormone. Leptin is a reflection of the energy stores in our body. Leptin is secreted by fat cells called adipocytes in proportion to adipose tissue mass. More adipose tissue mass, more leptin is secreted. Leptin crosses the blood-brain-barrier at the arcuate nucleus of the hypothalamus to stimulate the POMC neurons to release the neurotransmitter alpha MSH. Alpha MSH in turn stimulates the MC4R receptors of the paraventricular hypothalamus to induce satiety. Leptin also inhibits the orexigenic AgRP neurons.