Umami
Umami is one of the proposed five basic tastes sensed by specialized receptor cells present on the human tongue. The same taste is also known as xiānwèi (traditional Chinese: 鮮味; simplified Chinese: 鲜味) in Chinese cooking. Umami is a Japanese word meaning "savory" or "meaty" and thus applies to the sensation of savoriness—specifically, to the detection of glutamates, which are especially common in meats, cheese and other protein-heavy foods. The action of umami receptors explains why foods treated with monosodium glutamate (MSG) often taste "heartier".
Inasmuch as it describes the flavor common to savory products such as meat, cheese, duck, and mushrooms, umami is similar to Brillat-Savarin's concept of osmazome, an early attempt to describe the main flavoring component of meat as extracted in the process of making stock.
Umami was first identified as a taste in 1908 by Kikunae Ikeda of the Tokyo Imperial University while researching the strong flavor in seaweed broth. Ikeda isolated monosodium glutamate as the chemical responsible and, with the help of the Ajinomoto company, began commercial distribution of MSG products.
Umami, which has been known by Eastern civilizations for years, was recently brought to the forefront of Western awareness by Drs. Stephen Roper and Nirupa Chaudhari, researchers at the University of Miami, when they identified the actual taste receptor responsible for the sense of umami, a modified form of mGluR4, in which the end of the molecule is missing. Roper and Chaudhari named it "taste-mGluR4".
The negative effects of glutamate were first observed in 1954 by T. Hayashi, a Japanese scientist who noted that direct application of glutamate to the central nervous system caused seizure activity, though this report went unnoticed for several years. The toxicity of glutamate was then observed by D. R. Lucas and J. P. Newhouse in 1957 when the feeding of monosodium glutamate to newborn mice destroyed the neurons in the inner layers of the retina. Later, in 1969, John Olney discovered the phenomenon wasn't restricted to the retina but occurred throughout the brain and coined the term excitotoxicity. He also assessed that cell death was restricted to postsynaptic neurons, that glutamate agonists were as neurotoxic as their efficiency to activate glutamate receptors, and that glutamate antagonists could stop the neurotoxicity.
Inasmuch as it describes the flavor common to savory products such as meat, cheese, duck, and mushrooms, umami is similar to Brillat-Savarin's concept of osmazome, an early attempt to describe the main flavoring component of meat as extracted in the process of making stock.
Umami was first identified as a taste in 1908 by Kikunae Ikeda of the Tokyo Imperial University while researching the strong flavor in seaweed broth. Ikeda isolated monosodium glutamate as the chemical responsible and, with the help of the Ajinomoto company, began commercial distribution of MSG products.
Umami, which has been known by Eastern civilizations for years, was recently brought to the forefront of Western awareness by Drs. Stephen Roper and Nirupa Chaudhari, researchers at the University of Miami, when they identified the actual taste receptor responsible for the sense of umami, a modified form of mGluR4, in which the end of the molecule is missing. Roper and Chaudhari named it "taste-mGluR4".
The negative effects of glutamate were first observed in 1954 by T. Hayashi, a Japanese scientist who noted that direct application of glutamate to the central nervous system caused seizure activity, though this report went unnoticed for several years. The toxicity of glutamate was then observed by D. R. Lucas and J. P. Newhouse in 1957 when the feeding of monosodium glutamate to newborn mice destroyed the neurons in the inner layers of the retina. Later, in 1969, John Olney discovered the phenomenon wasn't restricted to the retina but occurred throughout the brain and coined the term excitotoxicity. He also assessed that cell death was restricted to postsynaptic neurons, that glutamate agonists were as neurotoxic as their efficiency to activate glutamate receptors, and that glutamate antagonists could stop the neurotoxicity.
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