Shalyndria
03-10-2004, 09:28 PM
Here's an article that's a little more in-depth than the average consumer reads. Just a blurb FYI.
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Focusing on the Brain
Researchers have zeroed in on the brain as they look for the primary defect in the counterregulatory system of people with diabetes. The brain is especially sensitive to changes in blood sugar levels, and some researchers think one particular area of the brain, the hypothalamus, may be the key.
Stephanie Amiel, M.D., of King's College in London is using an imaging method called positron emission tomography (PET) to track glucose as it travels through the brain. By labeling glucose with radioactive tracers, she can follow its path throughout the body. She wants to see where in the brain glucose accumulates, where it is metabolized, and how this changes in people with diabetes who are experiencing hypoglycemia. The findings of her JDRF-funded research may help determine where and how the brain seemingly "adapts" its ability to take up glucose.
At Yale University School of Medicine, Robert S. Sherwin, M.D., is conducting JDRF-funded research into the neurochemistry and function of the brain during hypoglycemia. He and his team will use a microdialysis technique to analyze the fluid between brain cells at various levels of hypoglycemia while the subjects undergo memory testing.
The Yale team will also use an imaging technique called noninvasive nuclear magnetic resonance spectroscopy to investigate what is happening in the brains of people while they are hypoglycemic. The researchers will be able to measure the rate of glucose metabolism and the action of neurotransmitters, the substances that transmit nerve impulses in the brain. A third phase of the project will use another type of imaging study, called functional MRI tests, to measure the effect of hypoglycemia on the changes that occur in various regions of the brain during cognitive tasks such as memorization.
Charles Mobbs, Ph.D., a JDRF researcher at Mount Sinai School of Medicine in New York City, is studying the glucose sensitivity of the neurons in the hypothalamus of people with diabetes, with the suspicion that their impaired responsiveness may be due to impaired action of the enzyme glucokinase. If this is the case, it may be possible to develop a drug to restore the glucokinase action to normal.
At the Veteran's Administration Puget Sound Health Care System in Seattle, Dianne Figlewitcz Lattermann, Ph.D., is conducting JDRF-funded research into specific nerve cells in the brain that she suspects may be responsible for the decreased response to hypoglycemia. So-called noradrenergic neurons, which help stimulate the brain during stress, may be impaired by hypoglycemia and consequently less able to function normally during subsequent episodes.
In addition, glucose transport across the blood-brain barrier—a mechanism that prevents many substances from leaving the blood and entering the brain—appears to be altered by hypoglycemia. In what may be a primitive protective response, the entrance of glucose into the brain increases during a hypoglycemic episode. If the brain "hoards" glucose this way, it may not recognize the next drop in blood sugar and may not initiate the counterregulatory response.
Stephen Davis, M.D., at Vanderbilt University in Nashville, Tennessee, suspects that the stress hormone cortisol may be at least one factor responsible for "blunting" the counterregulatory response. It is known that exercise can induce hypoglycemia, and also that exercise releases cortisol. Dr. Davis believes that the release of cortisol in response to physiologic stress—whether it be exercise or an episode of hypoglycemia—causes the brain to adapt and inhibit the counterregulatory release of glucagon and epinephrine.
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Shy
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Focusing on the Brain
Researchers have zeroed in on the brain as they look for the primary defect in the counterregulatory system of people with diabetes. The brain is especially sensitive to changes in blood sugar levels, and some researchers think one particular area of the brain, the hypothalamus, may be the key.
Stephanie Amiel, M.D., of King's College in London is using an imaging method called positron emission tomography (PET) to track glucose as it travels through the brain. By labeling glucose with radioactive tracers, she can follow its path throughout the body. She wants to see where in the brain glucose accumulates, where it is metabolized, and how this changes in people with diabetes who are experiencing hypoglycemia. The findings of her JDRF-funded research may help determine where and how the brain seemingly "adapts" its ability to take up glucose.
At Yale University School of Medicine, Robert S. Sherwin, M.D., is conducting JDRF-funded research into the neurochemistry and function of the brain during hypoglycemia. He and his team will use a microdialysis technique to analyze the fluid between brain cells at various levels of hypoglycemia while the subjects undergo memory testing.
The Yale team will also use an imaging technique called noninvasive nuclear magnetic resonance spectroscopy to investigate what is happening in the brains of people while they are hypoglycemic. The researchers will be able to measure the rate of glucose metabolism and the action of neurotransmitters, the substances that transmit nerve impulses in the brain. A third phase of the project will use another type of imaging study, called functional MRI tests, to measure the effect of hypoglycemia on the changes that occur in various regions of the brain during cognitive tasks such as memorization.
Charles Mobbs, Ph.D., a JDRF researcher at Mount Sinai School of Medicine in New York City, is studying the glucose sensitivity of the neurons in the hypothalamus of people with diabetes, with the suspicion that their impaired responsiveness may be due to impaired action of the enzyme glucokinase. If this is the case, it may be possible to develop a drug to restore the glucokinase action to normal.
At the Veteran's Administration Puget Sound Health Care System in Seattle, Dianne Figlewitcz Lattermann, Ph.D., is conducting JDRF-funded research into specific nerve cells in the brain that she suspects may be responsible for the decreased response to hypoglycemia. So-called noradrenergic neurons, which help stimulate the brain during stress, may be impaired by hypoglycemia and consequently less able to function normally during subsequent episodes.
In addition, glucose transport across the blood-brain barrier—a mechanism that prevents many substances from leaving the blood and entering the brain—appears to be altered by hypoglycemia. In what may be a primitive protective response, the entrance of glucose into the brain increases during a hypoglycemic episode. If the brain "hoards" glucose this way, it may not recognize the next drop in blood sugar and may not initiate the counterregulatory response.
Stephen Davis, M.D., at Vanderbilt University in Nashville, Tennessee, suspects that the stress hormone cortisol may be at least one factor responsible for "blunting" the counterregulatory response. It is known that exercise can induce hypoglycemia, and also that exercise releases cortisol. Dr. Davis believes that the release of cortisol in response to physiologic stress—whether it be exercise or an episode of hypoglycemia—causes the brain to adapt and inhibit the counterregulatory release of glucagon and epinephrine.
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Shy