Hormones That Regulate Hunger and Digestion

All too commonly, we suppress the normal physiology of a healthy digestive tract with our daily habits and medications. In doing so, we lose a precious opportunity to extract the greatest nutrition from our food, and we continue to suffer from common, but not normal, digestive complaints. How do we return to normal digestive physiology, and why is this an important pursuit?
Dr. Courtney Jackson is a naturopathic doctor who passionately promotes the healing power of whole foods to her patients and the public. She co-founded the Food as Medicine Institute at the National University of Natural Medicine in Portland, Oregon, where she continues to teach community-based cooking and nutrition workshops. Prior to medical school, Dr. Jackson earned her Bachelor of Science in Resource Ecology Management from the University of Michigan. She maintains a private practice at Grain Integrative Health where she offers comprehensive, patient-centered evaluations focusing on hormone, digestive, and cardiovascular health. Most recently, she co-authored the book Food as Medicine EverydayReclaim Your Health with Whole Foodswhich is a “highly accessible, thoroughly researched medical nutrition resource.”.
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In this video 5 hormones will be discussed that play important roles in the regulation of digestion in the Gastrointestinal tract..
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First we will shortly discuss some basic principles. With over thirty different hormones identified as being produced in the gastrointestinal tract, the gut has been described as ‘the largest endocrine organ in the body’. For the purpose of a correct definition: Hormones are chemical messengers secreted into blood that modify the physiology of target cells. So hormones are not secreted into the lumen of the gastrointestinal tract, but into the circulatory system, which will transport them to their destination. The definition of a target cell for a particular hormone is a cell that has receptors for that hormone and can thus respond to it..
The endocrine cells within the gastrointestinal tract are referred to collectively as the ‘enteric endocrine system’. Some of the best-studied enteric hormones are: Gastrin, Cholecystokinin, Secretin, Motilin and Gastric inhibitory polypeptide, which is also known as glucose dependent insulinotropic peptide. These are the 5 hormones that will be discussed in this video..
Another thing you must realize is the following: in contrast to endocrine glands like the anterior pituitary gland, in which essentially all cells produce hormones, the enteric endocrine system is diffuse. single hormone-secreting cells are scattered among other types of cells in the mucosa of the stomach and small intestine..
1. Gastrin.
The primary action of gastrin is: stimulation of gastric acid secretion..
Gastrin is secreted by “G” cells, these are located in the antrum of the stomach (and actually some in the duodenum as well)..
2. Cholecystokinin..
Cholecystokinin is the principle stimulus for delivery of bile and pancreatic enzymes into the small intestine, hereby stimulating the digestion of fat and proteins..
As mentioned previously, cholecystokinin and gastrin are highly similar peptides. Cholecystokinin (or CCK) is secreted by specialized gut endocrine cells called “I” cells in the mucosa of the duodenum and jejunum mainly in response to digestive products of fat, fatty acids, and monoglycerides in the intestinal contents. CCK mediates digestion in the small intestine various functions. It stimulates the acinar cells of the pancreas to release digestive enzymes and stimulates the secretion of a juice rich in pancreatic digestive enzymes..
3. Secretin..
Secretin functions as a type of fireman: in response to acid, it stimulates the pancreas and bile ducts to release a flood of bicarbonate base, which neutralizes the acid, and the secretion of secretin is turned off..
Secretin was the first gastrointestal hormone discovered and is secreted by specialized enteroendocrine cells called “S” cells in the mucosa of the duodenum in response to acidic gastric juice emptying into the duodenum from the pylorus of the stomach. Secretin has a mild effect on motility of the gastrointestinal tract and acts to promote pancreatic secretion of bicarbonate which in turn helps to neutralize the acid in the small intestine..
4. Motilin.
Motilin is released cyclially and stimulates waves of gastrointestinal motility called migrating motor complexes, which move through the stomach and small intestine every 90 minutes in a fasted person..
Motilin is secreted by endocrine “M” cells in the duodenum and jejunum during fasting, and the only known function of this hormone is to increase gastrointestinal motility..
5. Gastric Inhibitory Peptide..
It stimulates insulin secretion in a glucose dependent manner and inhibits gastric acid secretion and motor activity of the stomach.

This is a brief video detailing the main hormones in the GI tract, where they are localized, and their primary functions..
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ADDITIONAL TAGS:
HORMONE.
LOCALIZATION.
MAIN PHYSIOLOGIC ACTIONS.
Gastrin.
Gastric antrum, duodenum (G cells).
-stimulate secretion of gastric acid and intrinsic factor from parietal cells.
-stimulate secretion of pepsinogen from chief cells.
-promotes gastric and intestinal motility, mucosal growth.
Cholecystokinin (CCK).
Duodenum, jejunum (I cells).
-stimulate gallbladder contraction.
-stimulates release of pancreatic enzymes.
-relaxes sphincter of Oddi for release of bile and enzymes.
-role in inducing satiety.
Secretin.
Duodenum, jejunum (S cells).
-stimulate secretion of HCO3 from pancreas.
-inhibits gastrin and gastric acid secretion.
Vasoactive intestinal peptide (VIP).
Enteric nerves.
-increases water and electrolyte secretion from pancreas and gut.
-relaxes smooth muscles (via nitric oxide) of the gut.
Gastric inhibitory polypeptide (GIP).
Duodenum, jejunum (K cells).
-reduces gastric acid secretion and intestinal motility.
-stimulates insulin release.
Motilin.
Throughout the gut (Mo cells and ECL cells).
-increases small bowel motility (MMC during fasting) and gastric emptying.
Somatostatin.
Stomach, small intestine, and pancreas (D cells).
-inhibits secretion and action of many hormones, including all of the above.
Digestive hormones in the GI tract

The appetite pathway in the brain, leptin, and pathology of obesity. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/brain-and-nervous-system-videos/-/medias/c1a96592-f8fa-4a6b-9c27-bda67fa8f373-the-brain-s-hunger-satiety-pathways-and-obesity-narrated-anima.
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Food intake and energy expenditure must be balanced to maintain a healthy body weight. This balance is kept by the central nervous system, which controls feeding behavior and energy metabolism..
Several brain systems are involved, including the brainstem which receives neuronal inputs from the digestive tract, and the hypothalamus which picks up hormonal and nutritional signals from the circulation. They also interact with the reward and motivation pathways, which drive food-seeking behavior..
The arcuate nucleus, ARC, of the hypothalamus: two groups of neurons, with opposing functions, in the ARC: the appetite-stimulating neurons expressing NPY and AGRP peptides, and the appetite-suppressing neurons producing POMC peptide..
Neurons of the ARC project to other nuclei of the hypothalamus, of which the paraventricular nucleus, PVN, is most important. PVN neurons further process the information and project to other circuits outside the hypothalamus, thus coordinating a response that controls energy intake and expenditure..
Short-term regulation of feeding is based on how empty or how full the stomach is, and if there are nutrients in the intestine. In the fasting state, an empty stomach sends stretch information to the brainstem, signaling hunger. It produces a peptide called ghrelin, which acts on the arcuate nucleus to stimulate feeding. Ghrelin also acts directly on the PVN to reduce energy expenditure..
Upon food ingestion, distension of the stomach is perceived by the brainstem as satiety. Several other gut peptides are released from the intestine and act on the hypothalamus and other brain areas to suppress appetite and increase energy expenditure..
Long-term regulation takes cues from the amount of body fat: low body fat content encourages feeding and energy preservation, while high body fat suppresses appetite and promotes energy expenditure. Two hormones are involved: leptin and insulin..
Insulin is a hormone produced by the pancreas and is released into the bloodstream upon food ingestion, when blood glucose starts to rise. Leptin is a hormone secreted by adipose tissues in a process dependent on insulin. The amount of circulating leptin in the plasma is directly proportional to the body fat content. Increased leptin levels in the blood signal to the brain that the body has enough energy storage, and that it has to stop eating and burn more energy. Leptin and insulin seem to work together on hypothalamic nuclei, as well as other brain areas, to inhibit food intake and increase energy expenditure..
Obesity results from the dysregulation of feeding behaviors and energy metabolism. Obesity is associated with chronic low leptin activities, which trick the brain into thinking that the body is always starved. This leads to overeating and excessive energy storage as fats..
The major lifestyle factor is a high-fat, energy-rich diet. In an early stage of high-fat-diet–induced obesity, increased amounts of saturated fatty acids cross the blood brain barrier and provoke an inflammatory response in hypothalamic neurons. Inflammation induces stress in these neurons, blunting their response to leptin. This is known as leptin resistance. Leptin levels are high, but because the cells cannot react to leptin, the brain interprets it as low and triggers the starvation response..
Genetic factors include mutations in the leptin gene itself, or in one of the numerous downstream genes that are required for leptin action in various pathways. Leptin deficiency due to gene mutations is very rare. More common are mutations in the downstream genes, which render a certain pathway irresponsive to leptin..
A major risk factor for childhood obesity is maternal obesity and mother’s high-fat-diet during pregnancy and lactation. A maternal diet rich in saturated fats can cause inflammation in the infant’s hypothalamus. It may also prime the reward pathways in infants, influencing their food choice toward energy-rich foods.

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