L L-glutamate not only confers cognitive discrimination for umami taste in the oral cavity, but also conveys sensory information to vagal afferent fibers in the gastric mucosa. We used RT-PCR, western blotting, and immunohistochemistry to demonstrate that mGluR1 is located in glandular stomach. Double staining revealed that mGluR1 is found at the apical membrane of chief cells and possibly in parietal cells. Moreover, a diet with 1% L L-glutamate induced changes in the expression of pepsinogen C mRNA in stomach mucosa. These data suggest that mGluR1 is involved in the gastric phase regulation of protein digestion.
In the last 15 years, advancements in molecular biology have unraveled the proteins that function as taste receptors. There are at least five taste qualities that are consciously perceived, sweet, sour, salty, bitter, and umami. Of these five, sour and salty are mediated by ion channels, whereas the perception of sweet, umami, and bitter tastes is mediated by G protein-coupled receptors (GPCRs). These taste GPCRs belong to the TAS1R and TAS2R gene families. There are other nutrient-binding GPCRs whose taste function is still being studied such as CaSR, GPRC6A, GPR92, or GPR120. It has been suspected for more than a century that the gut can sense the chemical composition of foods. The description of multiple taste GPCRs in gastrointestinal (GI) cells suggests that there are nutrient-sensing mechanisms in the GI tract, oral, gastric, and intestinal mucosa. Oral sensing seems to mainly influence food discrimination and nutrient appetite, while post-oral chemosensors may relate to nutrient utilization and inhibition of appetite. The most common accepted view is that taste GPCRs are present in enteroendocrine cells among others also known as chemosensory cells. These cells express taste receptors and other taste-related genes. Although, functional cells of the GI mucosa that are not enteroendocrine or brush cells such as enterocytes or gastric cells may also hold receptive mechanisms that transduce the presence of certain nutrients in ingested foods and regulate gastric functions. This paper examines the importance of food chemical signals in their association with the neuroendocrine mechanisms they trigger, which are the core for metabolism and appetite regulation.
L‐glutamate is an abundant dietary amino acid, which can be free or bound to other amino acids within proteins. It plays an essential role in transdeamination and gluconeogenesis, and becomes a substrate for the synthesis of the antioxidant glutathione and the polyglutamated folic acid. The intestine extracts most of the dietary glutamate where acts as the main fuel for nutrient absorption. However, glutamate metabolism in the gastric mucosa is poorly understood. Recently, we found that dietary supplementation with monosodium glutamate can ameliorate the inflammation and the atrophy of pepsinogen‐secreting chief cells and acid secreting parietal cells caused by chronic infection with Helicobacter pylori. To uncover the protective mechanism of glutamate, we isolated chief cells from rat stomach by counterflow elutriation and density gradient. When cells became confluent, we exposed them to either buffer or 20 mM glutamate for 2 h. The molecular profile between both treatments was compared by GeneChip analysis, which suggested that L‐glutamate may detoxify ammonia through the synthesis of glutamine and signal cells through glutamate receptors and glutamate transporters.
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