He's a glucose hero, got stars in his eyes! 🎶
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A lil' #scienceGeek humor.
via Dept. of Science Jokes
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Let’s hear it for those unsung heroes.
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Your eyes make waste. Without it, you could go blind
One man’s trash is another man’s treasure, even at the level of the cell. That’s where—according to new research—a waste product of the retina fuels part of the eye that powers the rods and cones that help us sense light. Without this waste, that part of the eye “steals” glucose from the retina, leading to the death of retinal cells and likely vision loss. The finding could help explain why eyesight degenerates with age—and in diseases such as macular degeneration and diabetes.
“It’s almost a revolutionary concept” that there is such a tight coupling between the two parts of the eye, says Stephen Tsang, a retina specialist at Columbia University who was not involved in the work.
Rods and cones are very active, and they need a lot of energy to do their jobs. Exactly how they get this energy has long been a mystery. In previous studies, researchers showed that a layer of cells beneath the retina, the retinal pigment epithelium (RPE), ferries glucose from the blood to the retina. But it was unclear why the RPE didn’t keep the glucose for itself.
After a decade of study, biochemist James Hurley at the University of Washington in Seattle and his colleagues have now shown that the retina’s rods and cones burn the glucose, convert leftovers into a fuel called lactate, and then feed that back to the RPE. “There is a growing consensus that no cell exists on its own in complex tissues like the retina,” says Martin Friedlander, an ophthalmologist at The Scripps Research Institute in San Diego, California, who was not involved with the new work.
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Mom: if you're gonna eat that then I don't wanna hear about how your glucose is high later
Me, two hours later: *yelling from the next room over* I'M DYINGGGGGG
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And to think - plants can perform both processes!
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(Image caption: A region of the mouse brain known as the cNST (colored yellow at top) responded to the presence of sugar, even if it was infused directly into the gut. Credit: Tan et al./Nature 2020)
A Gut-to-Brain Circuit Drives Sugar Preference and May Explain Sugar Cravings
The sensation of sweetness starts on the tongue, but sugar molecules also trip sensors in the gut that directly signal the brain. This could explain why artificial sweeteners fail to satisfy the insatiable craving for sugar.
A little extra sugar can make us crave just about anything, from cookies to condiments to coffee smothered in whipped cream. But its sweetness doesn’t fully explain our desire. Instead, new research shows this magic molecule has a back channel to the brain.
Like other sweet-tasting things, sugar triggers specialized taste buds on the tongue. But it also switches on an entirely separate neurological pathway – one that begins in the gut, Howard Hughes Medical Institute Investigator Charles Zuker and colleagues report on April 15, 2020 in the journal Nature.
In the intestines, signals heralding sugar’s arrival travel to the brain, where they nurture an appetite for more, the team’s experiments with mice showed. This gut-to-brain pathway appears picky, responding only to sugar molecules – not artificial sweeteners.
Scientists already knew sugar exerted unique control over the brain. A 2008 study, for example, showed that mice without the ability to taste sweetness can still prefer sugar. Zuker’s team’s discovery of a sugar-sensing pathway helps explain why sugar is special – and points to ways we might quell our insatiable appetite for it.
“We need to separate the concepts of sweet and sugar,” says Zuker, a neuroscientist at Columbia University. “Sweet is liking, sugar is wanting. This new work reveals the neural basis for sugar preference.”
The term sugar is a catchall, encompassing a number of substances our bodies use as fuel. Eating sugar activates the brain’s reward system, making humans and mice alike feel good. However, in a world where refined sugar is plentiful, this deeply ingrained appetite can run amok. The average American’s annual sugar intake has skyrocketed from less than 10 pounds in the late 1800s to more than 100 pounds today. That increase has come at a cost: Studies have linked excess sugar consumption to numerous health problems, including obesity and type 2 diabetes.
Previously, Zuker’s work showed that sugar and artificial sweeteners switch on the same taste-sensing system. Once in the mouth, these molecules activate the sweet-taste receptors on taste buds, initiating signals that travel to the part of the brain that processes sweetness.
But sugar affects behavior in a way that artificial sweetener doesn’t. Zuker’s team ran a test pitting sugar against the sweetener Acesulfame K, which is used in diet soda, sweetening packets, and other products. Offered water with the sweetener or with sugar, mice at first drank both, but within two days switched almost exclusively to sugar water. “We reasoned this unquenchable motivation that the animal has for consuming sugar, rather than sweetness, might have a neural basis,” Zuker says.
By visualizing brain activity when the rodents consumed sugar versus artificial sweetener or water, the researchers for the first time identified the brain region that responds solely to sugar: the caudal nucleus of the solitary tract (cNST). Found in the brain stem, separate from where mice process taste, the cNST is a hub for information about the state of the body.
The path to the cNST, the team determined, begins in the lining of the intestine. There, sensor molecules spark a signal that travels via the vagus nerve, which provides a direct line of information from the intestines to the brain.
This gut-to-brain circuit favors one form of sugar: glucose and similar molecules. It ignores artificial sweeteners — perhaps explaining why these additives can’t seem to fully replicate sugar’s appeal. It also overlooks some other types of sugar, most notably fructose, which is found in fruit. Glucose is a source of energy for all living things. That could explain why the system’s specificity for the molecule evolved, say study lead authors Hwei Ee Tan and Alexander Sisti, who are graduate students in Zuker’s lab.
Previously, scientists speculated that sugar’s energy content, or calories, explained its appeal, since many artificial sweeteners lack calories. However, Zuker’s study showed this is not the case, since calorie-free, glucose-like molecules can also activate the gut-to-brain sugar-sensing pathway.
To better understand how the brain’s strong preference for sugar develops, his group is now studying the connections between this gut-brain sugar circuit and other brain systems, like those involved in reward, feeding, and emotions. Although his studies are in mice, Zuker believes that essentially the same glucose-sensing pathway exists in humans.
"Uncovering this circuit helps explain how sugar directly impacts our brain to drive consumption,” he says. “It also exposes new potential targets and opportunities for strategies to help curtail our insatiable appetite for sugar.”
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DIABETICS!! PLEASE READ!!!
Ugh. I just wanna put this out there for anybody who may need it.
I'm a type 2 diabetic, treating with low carb and high fiber diet and exercise. (Even though that kinda contradicts what I'm gonna say next)
I've been monitoring my blood sugar for a few months now and I've always used a Reli-On Prime meter because it's really easy to use and accurate.
Over vacation I had a situation where I needed to replace it and they didn't have the same one I was using, so I bought a brand called TrueMetrix Air.
I had eaten a large meal for the first time in a long time and I knew my glucose would be reasonably elevated. I used the TrueMetrix Air for the first time and it told me my reading was 86 mg/dL. EIGHTY SIX! After eating a huge carby sugary meal at Waffle House (which i knew i shouldnt have) I knew there was absolutely NO WAY my glucose was in the 80s.
So I used a different meter that was more accurate and realized that the TrueMetrix was no where near accurate. I read some reviews and have seen hundreds of examples when the TrueMetrix monitor reads as 80 mg/dL and isn't even close.
As many of you know, high and low glucose is very dangerous and need to be monitored as precise as possible. Someone had posted a review where their TrueMetrix has read 80 mg/dL when it was actually 250 mg/dL
This mistake could absolutely be life and death.
So, my point with this post is that if you or someone you know is diabetic or pre-diabetic, whether it be type 1 of type 2, DO NOT BUY THE TRUEMETRIX AIR!!! The reading grows more accurate if you test several times in a row but test strips are extremely expensive.
If you or your child or parent or whomever needs to buy a meter, let me say right now that sometimes it's better to spend the heavy money to get a good and accurate meters.
Today I went out and purchase the same Reli-On Prime which I had before (only 10 dollars, it's amazing) and also paid for a One Touch Verio. I highly recommend that if you have a TrueMetrix Air that you replace it immediately
(Sorry for tag reaching but it needs to be seen)
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*rings a bell* new oc everyone come get a load of this idiot
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Hey guys! For my first studyblr original post, I wanted to explain glycolysis. I found it way easier to learn it in terms of “energy-requiring” and “energy-releasing” phase, so here it is :) Hope you like it
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Fructose is generated in the human brain
Fructose, a form of sugar linked to obesity and diabetes, is converted in the human brain from glucose, according to a new Yale study. The finding raises questions about fructose’s effects on the brain and eating behavior.
The study was published on Feb. 23 by JCI Insight.
Fructose is a simple sugar found in fruits, vegetables, table sugar, and many processed foods. Excess consumption of fructose contributes to high blood sugar and chronic diseases like obesity. The Yale research team had demonstrated in a prior study that fructose and another simple sugar, glucose, had different effects on brain activity. But it was not known whether fructose was produced in the brain or crossed over from the bloodstream.
To investigate, the research team gave eight healthy, lean individuals infusions of glucose over a four-hour period. They measured sugar concentrations in the brains of the study participants using magnetic resonance spectroscopy, a noninvasive neuroimaging technique. Sugar concentrations in the blood were also assessed.
The researchers found cerebral fructose levels rose significantly in response to a glucose infusion, with minimal changes in fructose levels in the blood. They surmised that the high concentration of fructose in the brain was due to a metabolic pathway called the polyol pathway that converts glucose to fructose.
“In this study, we show for the first time that fructose can be produced in the human brain,” said first author Dr. Janice Hwang, assistant professor of medicine.
While the production of fructose in the brain had been seen in animals, it had not been demonstrated in humans, Hwang noted.
The finding raises several key research questions, which the research team plans to pursue. “By showing that fructose in the brain is not simply due to dietary consumption of fructose, we’ve shown fructose can be generated from any sugar you eat,” said Hwang. “It adds another dimension into understanding fructose’s effects on the brain.”
Glucose in the brain sends signals of fullness, but that is not the case with fructose, she said.
The conversion of glucose to fructose in the brain, known as the polyol pathway, also occurs in other parts of the body. “This pathway may be one other mechanism by which high blood sugar can exert its adverse effects,” Hwang added.
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'Exercise-in-a-pill' boosts athletic endurance by 70 percent
Salk Institute scientists, building on earlier work that identified a gene pathway triggered by running, have discovered how to fully activate that pathway in sedentary mice with a chemical compound, mimicking the beneficial effects of exercise, including increased fat burning and stamina. The study, which appears in Cell Metabolism on May 2, 2017, not only deepens our understanding of aerobic endurance, but also offers people with heart conditions, pulmonary disease, type 2 diabetes or other health limitations the hope of achieving those benefits pharmacologically.
Weiwei Fan, Wanda Waizenegger, Chun Shi Lin, Vincenzo Sorrentino, Ming-Xiao He, Christopher E. Wall, Hao Li, Christopher Liddle, Ruth T. Yu, Annette R. Atkins, Johan Auwerx, Michael Downes, Ronald M. Evans. PPARδ Promotes Running Endurance by Preserving Glucose. Cell Metabolism, 2017; 25 (5): 1186 DOI: 10.1016/j.cmet.2017.04.006
Salk scientists move one step closer to developing 'exercise-in-a-pill.' Partial view of a mouse calf muscle stained for different types of muscle fibers: oxidative slow-twitch (blue), oxidative fast-twitch (green), glycolytic fast-twitch (red). Credit: Salk Institute/Waitt Center
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Short Film Spotlight: Glucose by Jeron Braxton
Sugar was the engine of the slave trade that brought millions of Africans to America. Glucose is sweet, marketable, and easy to consume, but its surface satisfaction is a thin coating on the pain of many disenfranchised people.
Self-taught, Indianapolis-based animator Jeron Braxton took home the Short Film Jury Award for Animation at the 2018 Sundance Film Festival for what juror Chris Ware called “a mind-blowing and fresh language of imagery, avatar, and sound.” Check it out below.
>Film still courtesy of Glucose. photo: © 2018 Sundance Institute | Photo by Jemal Countess.
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Study reveals how a very low calorie diet can reverse type 2 diabetes
The research team investigated the effects of a very low calorie diet (VLCD), consisting of one-quarter the normal intake, on a rodent model of type 2 diabetes. Using a novel stable (naturally occurring) isotope approach, which they developed, the researchers tracked and calculated a number of metabolic processes that contribute to the increased glucose production by the liver. The method, known as PINTA, allowed the investigators to perform a comprehensive set of analyses of key metabolic fluxes within the liver that might contribute to insulin resistance and increased rates of glucose production by the liver — two key processes that cause increased blood-sugar concentrations in diabetes.
Using this approach the researchers pinpointed three major mechanisms responsible for the VLCD’s dramatic effect of rapidly lowering blood glucose concentrations in the diabetic animals. In the liver, the VLCD lowers glucose production by: 1) decreasing the conversion of lactate and amino acids into glucose; 2) decreasing the rate of liver glycogen conversion to glucose; and 3) decreasing fat content, which in turn improves the liver’s response to insulin. These positive effects of the VLCD were observed in just three days.
“Using this approach to comprehensively interrogate liver carbohydrate and fat metabolism, we showed that it is a combination of three mechanisms that is responsible for the rapid reverssal of hyperglycemia following a very low calorie diet,” said senior author Gerald I. Shulman, M.D., the George R. Cowgill Professor of Medicine and Cellular and Molecular Physiology and an investigator at the Howard Hughes Medical Institute.
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Study pinpoints brain cells that trigger sugar cravings and consumption
New research has identified the specific brain cells that control how much sugar you eat and how much you crave sweet tasting food.
Most people enjoy a sweet treat every now and then. But an unchecked “sweet tooth” can lead to overconsumption of sugary foods and chronic health issues like obesity and type 2 diabetes. Understanding the biological mechanisms that control sugar intake and preference for sweet taste could have important implications for managing and preventing these health problems.
The new study, led by Matthew Potthoff, PhD, associate professor of neuroscience and pharmacology in the University of Iowa Carver College of Medicine, and Matthew Gillum, PhD, at the University of Copenhagen in Denmark, focuses on actions of a hormone called fibroblast growth factor 21 (FGF21). This hormone is known to play a role in energy balance, body weight control, and insulin sensitivity.
“This is the first study that's really identified where this hormone is acting in the brain and that has provided some very cool insights to how it's regulating sugar intake,” says Potthoff, who also is a member of the Fraternal Order of Eagles Diabetes Research Center at the UI and the Iowa Neuroscience Institute.
Potthoff and his colleagues previously discovered that FGF21 is made in the liver in response to increased levels of sugar, and acts in the brain to suppress sugar intake and the preference for sweet taste.
Building on that finding, the team has now shown, for the first time, which brain cells respond to FGF21’s signals and how that interaction helps regulate sugar intake and sweet taste preference. The study, published in the journal Cell Metabolism, also reveals how the hormone mediates its effects.
Although it was known that FGF21 acted in the brain, identifying the exact cellular targets was complicated by the fact that the hormone’s receptor is expressed at very low levels and is therefore difficult to “see.” Using various techniques, the researchers were able to precisely identify which cells express the receptor for FGF21. By investigating these cells, the study shows that FGF21 targets glutamatergic neurons in the brain to lower sugar intake and sweet taste preference. The researchers also showed that FGF21’s action on specific neurons in the ventromedial hypothalamus reduce sugar intake by enhancing the neurons’ sensitivity to glucose.
Several drugs based on a modified form of FGF21 are already being tested as treatments for obesity and diabetes. The new findings could potentially lead to new drugs that more precisely target the different behaviors controlled by FGF21, which might help to control how much sugar a person eats.
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DISCLAIMER: after doing some research, I found that btz ISNT their nickname (it's 'Ballibo'), they won't be debuting on BTS' anniversary date (as some people were saying), and honestly they don't deserve the hate they've been receiving (as funny as some of the tweets are 😭). All joking aside, pls don't send hate to Ballistic Boyz!
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From Ancient Greek γλυκύς (sweet) and ῥάχις (spine, ridge); from Latin cerebrum (brain, skull), spīnālis (spinal, of the spine), fluidus (liquid, fluid, flowing, moist, soft) and from Ancient Greek γλυκύς (sweet)
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