Introduction
Through influences on nutritional absorption and microbial composition, among other processes, gastrointestinal transit time may be a key regulator of glucose homeostasis and metabolic health. One of the processes driving the advantageous health effects of dietary fiber may be the modification of gastrointestinal transit. Two outcomes are improved glucose homeostasis and a lower chance of developing metabolic illnesses like obesity and type 2 diabetes mellitus. The regulation of gastrointestinal transit may be a possible mechanism by which dietary fiber intake has a beneficial metabolic impact on glucose homeostasis and metabolic health.
What Is Gastric Emptying and How Is It Controlled?
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Food is consumed and then travels via the esophagus and stomach to reach the stomach in seconds.
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After eating, the stomach's proximal region undergoes gastric accommodation, which increases the stomach's ability to store food.
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The distal antrum and pylorus are pushed toward one other by the patterns of contractile activity, which also stir gastric liquids.
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Solid foods can be broken down mechanically and chemically by the antrum, which repeatedly contracts and grinds food particles against the closed pylorus.
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The gastric emptying procedure allows the pylorus to open gradually to release chyme into the duodenum.
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The initial lag phase (T lag), which is the period between ingestion and the beginning of emptying, and the gastric emptying half-time (T1/2), which is the moment when half of the meal has been emptied, are common terms used to describe the gastric emptying rate.
The regulatory mechanisms coordinating the gastric emptying rate are complex and involve the central nervous system, enteric motor neurons, and gastric smooth muscle cells. Normal gastric emptying rate is stimulated by contractile activity of the stomach and small intestine, which is coordinated by the central nervous system, the vagus nerve, and neurohumoral peptides.
Many neurohumoral gut peptides, such as ghrelin, cholecystokinin, glucagon-like peptide-1 and -2, and peptide YY, are released during fasting and the postprandial state by enteroendocrine cells in the gastric and intestinal mucosa.
Consuming food reduces ghrelin secretion while increasing the secretion of cholecystokinin, peptide YY, and glucagon-like peptide-1. This modifies stomach and intestinal motility by activating receptors on sensory, vagal, and intrinsic afferent neurons. As a result, glucagon-like peptide-1, peptide YY, and cholecystokinin slow the gastric emptying rate and promote satiety. This negative feedback loop regulates the passage of food through the upper stomach absorption to enhance nutrient digestion.
How Can Gut Microorganisms Affect Metabolism?
The gut microbes are a new environmental component affecting the host's energy balance. Digestion, vitamin synthesis, and metabolism are the key physiological processes performed by gut bacteria. It improves the host's capacity to obtain energy from digested food and generates metabolites and microbial products such as short-chain fatty acids, secondary bile acids, and lipopolysaccharides. These metabolic and microbial byproducts function as signaling molecules that control hunger, gastrointestinal motility, energy absorption and storage, and energy expenditure. Numerous data imply that the gut microbiota may influence the emergence of obesity.
Microbial byproducts and metabolites can have an immediate impact on the physiology of the host. The host's immune system is matured by the microbiota, which also enhances the function of the intestinal barrier and prevents the colonization of dangerous bacteria. The commensal bacteria coexist with their host in symbiosis as a result. Commensal microorganisms can alter the host's energy homeostasis, contribute to obesity, and defend the host against pathogens.
According to research, the gut microbiota affects the composition of fatty acid tissues and increases the energy produced from meals. It also causes low-grade inflammation. The gut microbes and obesity may be related through several methods.
In humans and rats, metabolic disorders like obesity are linked to changes in gut microbiota composition. According to certain research, obese individuals and rodents have higher Firmicutes-to-Bacteroidetes ratios than lean controls.
How Gastric Emptying Controls Glucose Homeostasis?
The gastric emptying rate determines the rate at which glucose enters the duodenum, is absorbed, and appears elsewhere in the body. Gastric emptying rate accounted for almost 30 percent of the peak circulatory glucose concentration variation following an oral glucose load in healthy people and people with obesity and type 2 diabetes mellitus. The initial increase in postprandial glucose concentrations correlates with a larger initial gastric emptying rate.
Elevated postprandial blood glucose may eventually contribute to the emergence of insulin resistance and type 2 diabetes mellitus. According to reports, gastric emptying rates in overweight or obese people are either faster, similar, or delayed than in lean people.
However, a recent, extensive cross-sectional investigation found that obese and overweight persons had lower fasting plasma peptide YY concentrations than lean adults and that gastric emptying rates were faster, as determined by scintigraphy. It is, therefore, intriguing to hypothesize that faster gastric emptying in obesity may result in a quick rise in blood glucose, posing a persistent threat to postprandial glucose homeostasis.
How does the Gut-Brain Axis Modulate Gastrointestinal Metabolism?
To maintain the energy balance, the brain receives information from peripheral organs like the intestine. Known as the gut-brain axis, there is two-way communication between the gut and the brain. The brain communicates with the gut through efferent vagal signals and neuroendocrine pathways. When the bacteria recognize neurotransmitters such as catecholamines, 5-hydroxytryptamine (5-HT), and aminobutyric acid (GABA), the brain and gut microbes can communicate directly.
Alternatively, the brain and gut microbes can communicate indirectly through the influence of the intestinal microenvironment. Vagal efferent nerves govern intestinal processes like gut motility, acid, mucus secretion, intestinal barrier function, and mucosa immune response, all of which impact the gut microbes structure and functioning.
The stomach and gut microbiota can send signals directly to the brain via blood-borne chemicals and afferent spinal and vagal neurons. The production of hormones from intestinal enteroendocrine cells can be regulated by microbial products and metabolites generated by microbes. These hormones include peptide YY (PYY) and glucagon-like peptide-1 (GLP-1), both of which have receptors expressed in parts of the hypothalamus, a brain region that regulates energy balance.
Conclusion
Symbiotic gut microorganisms influence a variety of critical processes, including the regulation of energy balance. In addition to improving energy absorption, the gut microbiota also generates compounds and bacterial byproducts that bind to receptors in the intestine and other metabolically active organs to act as signaling molecules. These signals cause adjustments in hunger, digestive motility, energy absorption, storage, and expenditure, which leads to a net positive energy balance and weight gain. Gut bacteria transplantation reproduces the obesity phenotype in rats and humans with altered gut microbiota compositions that are less diverse than in lean controls. Modulation of GI transit may also alter the structure of the microorganisms.
Gut microbiota modulation has a Beneficial effect on the intestinal environment through microbial composition modification using probiotic, prebiotic, and postbiotic administration and fecal microbiota transplantation (FMT). All these approaches can be optimized by patient-tailored treatments to manage the individual’s physiology and pathology better. Live microorganisms that, when given in sufficient proportions, have a positive impact on host health are known as probiotics.
