Introduction
The primary purpose of the gastrointestinal tract is to deliver nutrients to our bodies through the processes of ingestion, motility, secretion, digestion, and absorption; this is accomplished through the intricate coordination of digestive processes controlled by the intrinsic nervous and endocrine systems. Although the nervous system affects many digestive processes, the GI tract is the largest endocrine organ in the body. It produces a variety of mediators that are crucial for controlling gastrointestinal (GI) tract functioning.
Depending on How the Molecule Is Supplied to the Target Cells, GI Hormones Can Be Classified As:
1. Endocrines.
2. Paracrine.
3. Neurocrine.
Enteroendocrine cells produce endocrine hormones directly into the bloodstream, which travel from the portal to the systemic circulation and then are transported to target cells with the hormone’s receptor-specificity.
The Five GI Hormones Considered Endocrines Are:
1. Gastrin.
2. Cholecystokinin (CCK).
3. Secretin.
4. Glucose-dependent insulinotropic peptide (GIP).
5. Motilin.
How do Gut Hormones Work Centrally and Peripherally to Affect Food Intake?
The hypothalamus is a key area for combining information from central and peripheral pathways and is important for controlling hunger. With the brainstem and upper cortical centers, there are also reciprocal connections. Two main neuronal populations in the arcuate nucleus of the hypothalamus regulate energy homeostasis and food intake.
The dorsal vagal complex in the brainstem is involved in receiving and relaying peripheral signals. Gut hormones influence digestion and nutrition absorption through a peripheral mechanism. They also function as neurotransmitters in the central nervous system to regulate eating. The hypothalamus and brainstem are involved in intricate homeostatic systems that closely regulate body weight by fusing peripherally derived signals of the body's nutritional and energy status with inputs from higher cortical centers.
Two distinct neuronal populations coexpress neuropeptide Y (NPY) and agouti-related peptide (AgRP)
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Which increases food intake, and proopiomelanocortin and cocaine- and amphetamine-regulated transcript, which inhibit food intake in the hypothalamic arectus nucleus.
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The dorsal vagal complex, which comprises the nucleus of the tractus solitaries, region postrema, and the dorsal motor nucleus of the vagus, plays a crucial part in transmitting peripheral signals, such as vagal afferents from the gut to the hypothalamus.
How Does the GI Tract Control Food Intake and Digestion?
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The gastrointestinal tract is the largest endocrine organ in the body since it contains more than 100 bioactive peptides and more than 30 gut hormone genes known to be expressed.
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Gut hormones and neurotransmitters are released from the gut in response to the meal's expectation and food's presence in the upper gastrointestinal system.
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These neurohumoral signals play a role in the beginning and continuation of food intake and the end of meals.
The upper GI tract plays a significant role in the negative feedback regulation of food intake. The transmission of the food-induced negative feedback signals, vital for deciding how much food to eat, is tightly linked to the vagus nerve. Increased meal size and duration result from sensory gut vagal fibers, but gastric preload-induced eating suppression is not prevented. This suggests vagal afferent signals play a role in fullness during spontaneous meals.
What Is Ileal Brake?
The ileal brake, a negative feedback mechanism, is activated when nutrients are perfused into the colon. This reduces upper gastrointestinal secretion, motility, and transit. Peptides may be mediators of this process. Fat is the most effective trigger of the ileal brake.
What Part Does Cholecystokinin (Gut Hormone) Play in Food Intake?
The first gut hormone discovered to influence food intake was cholecystokinin. Cholecystokinin has a brief plasma half-life of a few minutes and is released postprandially into circulation by the I cell of the small intestine. Within 15 minutes after meals, plasma cholecystokinin levels increase. Humans and rodents are said to consume less food after using cholecystokinin. cholecystokinin 1 and cholecystokinin 2 receptors, formerly known as cholecystokinin A and cholecystokinin B, are two subtypes of the cholecystokinin receptor. Cholecystokin 1 receptors on the vagal nerve play a major role in the anorectic action of cholecystokinin. The brainstem and hypothalamus are just two areas where cholecystokinin 1 and 2 receptors are found in abundance. In rats, intermittent prandial cholecystokinin infusion causes a reduction in meal size but also results in a compensatory increase in meal frequency.
What Part Does Pancreatic Polypeptide (PP) Play in Food Intake?
In the pancreatic islets of Langerhans, pancreatic polypeptide cells release pancreatic polypeptide. Through the Y4 receptor in the brainstem and hypothalamus, pancreatic polypeptide appears to decrease food intake directly. Rodent vagotomy completely reverses the anorectic effects of pancreatic polypeptide, indicating that pancreatic polypeptide may also work to decrease appetite by inhibiting the vagus nerve. The adaptor protein complex, neurotensin, dorsal vagus nucleus, ARC, and Paraventricular Hypothalamic Nucleus all express Y4 receptors. The brainstem is thought to be the primary site of action for pancreatic polypeptide, as evidenced by the discovery of saturable pancreatic polypeptide binding sites in the interpeduncular nucleus, adaptor protein complex, neurotensin, and dorsal vagus nucleus in an autoradiography investigation.
Depending on the delivery route, varied effects on food intake are seen after pancreatic polypeptide injection, similar to peptide-1 and peptide YY.
After a meal, circulating pancreatic polypeptide concentrations increase directly to the caloric load. Some investigations have shown significantly lower amounts in obese patients, despite contradicting reports about variations in circulation levels of pancreatic polypeptide between lean and obese adults. After a test meal, pancreatic polypeptide levels rise in anorexia. When compared to age- and weight-matched control participants, patients with Prader-Willi syndrome, have been shown to exhibit lower pancreatic polypeptide release both basally and postprandially.
What Part Does Glucago-Peptide-1 (GLP-1) Play in Food Intake?
In response to nutritional intake, L cells in the intestine consecrated glucagon-peptide-1 and peptide-1, and peptide YY. The glucagon-peptide-1 brief plasma half-life of 1-2 minutes is explained by the fast inactivation and removal of glucagon-peptide-1 from plasma circulation caused by an enzymatic DPPIV and renal clearance breakdown, respectively. The two physiologically active variants of glucagon-peptide-1 are glucagon-peptide-1 and glucagon-peptide-1 amide, the latter being the primary form in human circulation. Glucago-peptide-1 stimulates adenylyl cyclase activity and cAMP generation by acting on the glucagon-peptide-1R. Glucagon-peptide-1R is found throughout the body but is concentrated in the brain, GI tract, and pancreas. Following a meal, circulating glucagon-peptide-1 levels increase; during a fast, they decrease. Recent research indicates that levels increase before a meal. Glucago-peptide-1 decreases appetite, blocks glucagon secretion, and postpones stomach emptying.
What Part Does Ghrelin Play in Food Intake?
The hypothalamic arcuate nucleus also has lower ghrelin concentrations. The amount of circulating ghrelin rises before meals and drops quickly after that. Ghrelin can be administered centrally or peripherally, both of which cause rodents to eat more and gain weight while using their fat reserves less. There are inverse relationships between circulating ghrelin levels in humans and BMI (Body mass index). Both individuals with diet-induced weight loss and those with anorexia nervosa have high fasting plasma levels of ghrelin.
In contrast, obese individuals show a less pronounced decrease in plasma ghrelin following meal injection. Compared to non-cachectic patients with heart failure and control participants, plasma ghrelin levels are higher in cachectic patients with heart failure.
Conclusion
Multiple overlapping feeding systems demonstrate how important feeding behavior is for survival. However, in obese people subjected to high-calorie diets, these homeostatic feeding strategies can be seen as maladaptive. It is believed that several gut hormones contribute to long-term weight loss. To control food intake, gut hormones are essential for transmitting information about nutritional and energy status from the gut to the central nervous system. Oxyntomodulin, glucagon-like peptide-1, pancreatic polypeptide, peptide YY, and cholecystokinin decrease appetite through various yet complementary methods, whereas ghrelin increases food intake. Through all these mechanisms of action, gut hormones affect food intake.
