Tag Archives: glucose

Hangry man.

Being hungry really does sour your mood, research reveals

That coworker who’ll lay into you if they skipped breakfast? New research suggests his metabolism is partly to blame.

Hangry man.

Image credits Olichel Adamovich.

Researchers from the University of Guelph have shown that a sudden drop in glucose — such as we experience when we’re hungry — can have a dramatic impact on our mood. The findings help explain why so many people bemoan getting “hangry“.

Food fight

“We found evidence that a change in glucose level can have a lasting effect on mood,” said coauthor Francesco Leri, a professor at the university’s Department of Psychology.

“I was skeptical when people would tell me that they get grouchy if they don’t eat, but now I believe it. Hypoglycemia is a strong physiological and psychological stressor.”

For the study, the team worked with a group of lab rats, following their emotional behavior after inducing hypoglycemia (low blood-sugar levels). The group was injected with a glucose metabolism blocker — which artificially induced hypoglycemia — and was placed in a special chamber. The same rats later received an injection of water and were placed in a different chamber.

At the end of the trials, the rats were allowed to enter one of the chambers — and actively avoided the one where they experienced hypoglycemia.

“This type of avoidance behaviour is an expression of stress and anxiety,” said Leri. “The animals are avoiding that chamber because they had a stressful experience there. They don’t want to experience it again.”

The team took blood samples of the rats at various stages during the experiment and report that rats showed higher blood levels of corticosterone, an indicator of physiological stress, following the first step of the trial. In other words, they were likely experiencing acute stress while their blood-sugar levels were artificially lowered to mimic skipping a meal or two.

The rats also appeared more sluggish when given the glucose metabolism blocker. While it may be argued that this effect stems from a lack of glucose in the rats’ systems — muscles use glucose as fuel — the team reports that this doesn’t seem to be the case. When the sluggish rats were given antidepressant medication, “the sluggish behavior was not observed. The animals moved around normally,” Leri explained.

“This is interesting because their muscles still weren’t getting the glucose, yet their behaviour changed.”

“This is interesting because their muscles still weren’t getting the glucose, yet their behaviour changed.”

Overall, the findings support the idea that animals (us humans included) experience anxiety and a sour mood when going hungry for too long. The results may help flesh out our understanding of the treatment dynamic for those who experience anxiety or depression. They may also shed some light on the (still poorly-understood) link between depression and diseases such as obesity, diabetes, and eating disorders.

“When people think about negative mood states and stress, they think about the psychological factors, not necessarily the metabolic factors,” said PhD student Thomas Horman, who led the study. “But we found poor eating behaviour can have an impact.”

“The factors that lead someone to develop depression and anxiety can be different from one person to the next. Knowing that nutrition is a factor, we can include eating habits into possible treatment.”

Next, the team plans to determine whether long-term hypoglycemia may be a risk factor for developing depression-like behavior. While a single missed meal may make us grumpy, doing so constantly may have a dramatic impact on our mood and quality of life:

“Poor mood and poor eating can become a vicious cycle in that if a person isn’t eating properly, they can experience a drop in mood, and this drop in mood can make them not want to eat,” Horman explains.

“If someone is constantly missing meals and constantly experiencing this stressor, the response could affect their emotional state on a more constant level.”

The paper “An exploration of the aversive properties of 2-deoxy-D-glucose in rats” has been published in the journal Psychopharmacology.

Researchers develop a pill that mimics the effects of exercising

Isn’t that great? If you’re as lazy as I am, this incredible news. Just imagine sitting on a couch all day and having rocking six-pack abs at the same time. Wow. But things aren’t that simple — well, not yet.

Via Pixabay/bosmanerwin

Scientists have been working on an “exercise pill” for quite some time. Studies conducted on mice show promising results, but FDA approval is still needed for the drug to be available to patients. Unfortunately, the FDA does not see the inability to exercise as a disease that requires treating.

Who really has the time now to exercise as much as the body needs? We’re constantly on the run, yes, but mostly metaphorically. We all know the tremendous benefits of working out on a regular basis, but let’s be honest: if we’re stuck in a stressful office environment, like a large part of the population is, where can we find the energy to work out at least half an hour each day? Or even the time? I’m not trying to make excuses for everyone. However, obesity rates are rising, and we should face the facts: our ancestors engaged in more physical activity than we do today. Our food is different as well — we mostly eat high-energy processed foods, not home cooked meals or fruits and vegetables from our own gardens.

Some would argue that lifestyle is a choice and that we are fully responsible for our health. I agree, but let’s take into the consideration that a healthy lifestyle is hard to maintain, with sugar addiction being one of our worst enemies.

Researcher Ronald Mark Evans, a biologist at the Salk Institute for Biological Studies in La Jolla, California, wanted to fight against obesity, so he and his team developed a drug that mimics the effects of exercise while eliminating the need to run a mile three times a week.

How does this pill work?

The compound, known as GW1516, or 516, essentially tricks the body to burn fat instead of glucose for energy; this typically takes longer for the body to do, as it prefers to use glucose first, then fat. The human body uses the same metabolic pathway when exercising: it preserves the sugar for the brain during periods of physical stress and signals the muscles to burn fat instead.


Ali Tavassoli, a professor at the University of Southampton, has also been studying similar effects using a drug known as compound 14.

Compound 14 changes the body’s metabolism by affecting the functionality of an enzyme called ATIC. By inhibiting this enzyme, researchers trigger a chain reaction that leads the cells’ central energy sensor to think it’s running out of sugar. In consequence, the cell’s metabolism and sugar uptake are fastened. Its developers think that if Compound 14 was successfully tested on humans, it could help substantially in the fight against obesity, which affects more than a third of the U.S.’s adult population.

“If you can bring them a small molecule that can convey the benefits of training, you can really help a lot of people,” Evans told Washington Post. 


Researchers aren’t only developing this drug for those who don’t have time to exercise; the drug’s main target is people physically incapable of working out. Helping people with muscle-wasting diseases and movement disorders, the frail, the very obese and post-surgical patients is the team’s principal priority.

Alas, FDA doesn’t recognize “the inability to exercise” as a condition. So Evans decided to make them listen: he targeted 516 young people with Duchenne muscular dystrophy. He thinks this approach has the best chance to get FDA approval.

“This [disease] afflicts kids who can’t exercise and ultimately die of muscle wasting, often at a relatively early age, at 15 or 16,” Evans says. “It’s a disease with a large unmet medical need.”

The drug is now undergoing a small human safety study. Evans says the compound has “a potentially wide application,” including for amyotrophic lateral sclerosis, Parkinson’s disease, and Huntington’s disease, and for “people in wheelchairs.”

He also believes it could be crucial for patients who develop acute kidney injury — a potentially fatal side effect of cardio-bypass surgery that is often associated with irreversible organ damage.

“The organ or tissue changes its metabolic properties and begins to burn sugar, and because it happens quickly, it’s very hard to stop,” Evans says. “Our drug helps to draw the tissue back to a more healthy state, returning it from a chronic inflammatory damaged state. It soaks up sugar. If you do this carefully and quickly, you can override the damage response.”

Scientists admit that some problems might appear if the drug becomes available to the general population. There will be no way to control abuse. Even professional athletes might be tempted to take it in order to boost their performances. The experimental 516 already is banned by the World Anti-Doping Agency, according to Evans, and “I’m sure any [future] version of it will be, too.”

Evans concludes: “I like exercising, and that’s good enough for me. People are designed to move. But if they can’t, it’s not healthy to be sedentary. That’s why we are developing this drug. We are trying to take science out of the laboratory and bring it into the clinic in a way that can change people’s lives. If we can do that, it would be a game-changer.”


Broccoli-derived compound could become a new treatment for type 2 diabetes

A concentrated extract obtained from broccoli has been found to reduce blood sugar levels by up to 10% in patients with type 2 diabetes, and could provide an unexpected but indispensable treatment for the condition.


The real bro when fighting type 2 diabetes.
Image credits Engin Akyurt.

Patients suffering from type 2 diabetes see their body’s production of and response to insulin — the hormone that regulates glucose levels in the blood — severely limited or dropping down to almost zero. Needless to say, this does not make for good news, and the condition is associated with a host of symptoms you don’t want — from increased thirst, kidney problems, increased chances of heart attacks and wounds which don’t heal to blindness and loss of limbs.

The go-to drug prescribed to keep the condition in check is metformin, which works by lowering glucose production and so its concentration in the blood. The caveat, however, is that metformin goes really hard on your kidneys, preventing roughly 15% of patients from using this drug as they risk irrevocable damage to the organs.

Eat your greens

While a diet rich in plants has been shown to help prevent diabetes, broccoli seems to be especially good at it. Some time ago, a chemical found in the sprouts called sulforaphane was found to reduce glucose levels in diabetic rats. A team of researchers led by Anders Rosengren of the University of Gothenburg in Sweden, now found that its effect also carries over to human patients.

The team gave 97 people with type 2 diabetes either a high concentration dose of sulforaphane daily over a three-months period or a placebo. All but three of the participants had prescriptions for metformin and continued to take the drug during the trial. Those three could control their condition relatively well without metformin. The dose of sulforaphane the team used was about one hundred times more concentrated than that in broccoli.

“It was the same as eating around five kilograms [11 pounds] of broccoli daily,” says Rosengren.

The team found that on average, participants who received sulforaphane had 10% lower blood glucose levels those in the control group (who received placebos). The largest drop was reported for obese participants with “dysregulated” diabetes, whose baseline glucose levels were the highest. While 10% might not sound like much, it’s enough to reduce the chances of complications developing in the eyes or kidneys, the team reports.

They also found that sulforaphane lowers blood glucose levels in a completely different way from metformin. The latter makes cells more responsive to insulin, making them clear more of the surplus sugar from the blood. Sulforaphane, by contrast, lowers the quantity of the sugar injected into the bloodstream in the first place by suppressing the activity of liver enzymes which drive glucose production.

Because they work on different ‘ends’ of the problem, the team is confident that the two drugs could be used to complement each other. Alternatively, sulforaphane can be used as a substitute for metformin in patients who can’t take the drug fearing kidney complications. Finally, as it lowers glucose production, sulforaphane could help pre-diabetic patients avoid the condition altogether. Coupled with other emerging treatments, we may be close to overcoming type 2 diabetes.

The team is now working with the Swedish Farmers’ Association to seek approval for the broccoli powder to be used as a drug.

The full paper “Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes” has been published in the journal Science Translational Medicine.

Fructose is actually produced in the brain, new study finds

A new Yale study has found that fructose is converted in the human brain from glucose, offering significant insight (but also raising questions) about our eating habits and cravings.

Fructose is found in fruits and veggies, but also in a lot of processed foods. It’s also been linked to obesity and cardiovascular issues. Image via Pixabay.

Fructose is a simple monosaccharide found in many fruits and vegetables, where it is often bonded to glucose. Pure, dry fructose is a very sweet, white, odorless, crystalline solid and is the most water-soluble of all the sugars. Because of its properties, it’s often added to processed and baked foods, to make them sweeter and tastier — but excess consumption contributes to high blood sugar and chronic diseases like obesity. A previous study had already shown that fructose and glucose have a significant effect on the brain, but it wasn’t clear if the fructose was produced in the brain or simply arrived there through the bloodstream.

To answer this question, researchers gave eight healthy participants infusions of fructose and glucose, while measuring sugar concentrations in their brains and bodies using a non-invasive technique called magnetic resonance spectroscopy. They found that when participants drank the glucose infusion, their fructose levels in the brain rose dramatically while levels in the brain remained relatively low.

“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.

“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,” Hwang added. “It adds another dimension into understanding fructose’s effects on the brain.”

This isn’t completely unexpected, as the same process had been observed in animals. However, it does bring a few interesting questions. It has been proven in rodents that fructose promotes feeding behavior while glucose doesn’t In other words, glucose makes you feel full, while fructose doesn’t. So what then is happening to our brain as it transforms glucose into fructose? Perhaps even more importantly, what does this mean for our health?

Dr. Kathleen Page, an endocrinologist and assistant professor of medicine at the University of Southern California Keck School of Medicine, who was not involved with the study, said that the findings are “intriguing” and, “if confirmed in future studies, could have important implications on the effects of sugar on brain function.”

Indeed, the study does come with a couple of limitations: for starters, there are only 8 participants, which is a pretty small sample size (though for the purpose, it seems relevant). Secondly, there’s only an indirect observation here, and the mechanism is still not properly understood. But we can still draw some conclusions.

The fact that fructose is increasingly used in the food industry is already worrying. Excess fructose consumption is already connected to insulin resistance, obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. The substance is also associated with a greater incidence of hypertension and risk of cardiac disease.

Journal Reference: Janice J. Hwang et al — The human brain produces fructose from glucose.  doi:10.1172/jci.insight.90508.

New enzyme could be used as an insulin alternative, to treat diabetes and obesity

University of Montreal Hospital Research Centre (CRCHUM) scientists have identified a new enzyme that could protect the body from toxic levels of intra-cell sugar. When there is too much sugar in the body it gets processed into glycerol-3-phosphate, a buildup of which can damage internal organs. The team behind the study proved that G3PP is able to extract excess sugar from cells.

Their discovery should lead to the development of therapeutics for obesity and type 2 diabetes.

Image via pixlr

“When glucose is abnormally elevated in the body, glucose-derived glycerol-3 phosphate reaches excessive levels in cells, and exaggerated glycerol 3 phosphate metabolism can damage various tissues,” said Marc Prentki, principal investigator at the CRCHUM and professor at the University of Montreal.

“We found that G3PP is able to breakdown a great proportion of this excess glycerol phosphate to glycerol and divert it outside the cell, thus protecting the insulin producing beta cells of pancreas and various organs from toxic effects of high glucose levels.”

Mammalian cells derive the bulk of their energy from oxidizing glucose and fatty acids. These substances govern many physiological processes, from insulin and glucose production, all the way to fat accumulation and nutrient metabolization. But a too large intake of glucose disrupts these processes and can lead to obesity, type 2 diabetes and cardiovascular diseases.

Beta cells in the pancreas respond to changes in blood sugar levels, cracking up or toning down on insulin — a hormone that controls glucose and fat utilization. Usually this keeps blood sugar levels stable and cells happy and well supplied with fuel. As glucose is being used in cells, glycerol-3-phosphate is formed, a molecule central to metabolism since it is needed for both energy production and fat formation.

But when these nutrients are found in excess, they can actually damage beta cells, inhibiting their function. Blood sugar levels remain unchecked, skyrocket, and damage the beta cells even further. This leads to a vicious circle, shutting down the body’s system of managing its fuel. G3PP however isn’t produced by beta cells, and the team hopes it can be used to regulate formation and storage of fat as well as production of glucose in the liver.

“By diverting glucose as glycerol, G3PP prevents excessive formation and storage of fat” says Dr Murthy Madiraju, a scientist at CRCHUM.

Dr Prentki added: ‘It is extremely rare since the 1960s that a novel enzyme is discovered at the heart of metabolism of nutrients in all mammalian tissues, and likely this enzyme will be incorporated in biochemistry textbooks.’

The research team is currently in the process of discovering ‘small molecule activators of G3PP’ to treat cardio-metabolic disorders. These drugs will form a new class of drugs, being unique in the way they operate inside the body.

The treatment will first have to be confirmed in several animal trials before drugs for human use can be developed.

“This is an interesting paper and to some extent unusual as new enzymes involved in metabolic control are rare,” said Professor Iain Broom, Director of the Centre for Obesity Research & Epidemiology, Robert Gordon University.

But we should take great care as we develop this class of drugs, he adds”

“Care should be taken, however, in reading too much into the possibilities for treatment of disease by focusing on such individual enzymes, especially as the evidence for this control mechanism comes from isolated cells.”

“This paper does have an important finding, however, and should not be dismissed lightly – but I would draw the line at statements of ‘guilt-free sugary treats’,” he said, referring to the media’s take on the story. ”

This is not an accurate by-line for this interesting piece of science.”

The paper can be found online in the journal Proceedings of the National Academy of Sciences.


artificial sweeteners

Artificial sweeteners lead to diabetes and weight gain, more so than sugar

artificial sweeteners

Image credits: Punching Judy, Flickr

If you’re trying to lose weight, then sugar is one of your main enemies. But everybody wants something sweet once in a while, so artificial sweeteners were invented, and in recent years, they’ve become quite popular. But now, a new study shows that artificial sweeteners are messing with our gut bacteria, also causing high sugar levels in our blood.

This seems pretty weird; our bodies can’t digest artificial sweeteners, so then how is it that they’re causing increased sugar levels? A team from the Weizmann Institute of Science in Israel found that artificial sweeteners are messing with our stomach’s “fauna” – the bacteria which inhabit our gut -, triggering glucose intolerance in the body – which is the first step towards metabolic syndrome and adult-onset diabetes.

“Our results suggest that in a subset of individuals, artificial sweeteners may affect the composition and function of the gut microbiome,” Eran Elinav, an immunologist and co-author of the study, explained at a press conference.

To understand exactly how this is happening, researchers analyzed three artificial sweeteners: aspartame, sucralose and sacchari; they found that all three of have an effect even stronger than sugar. The substances led to an increase in the bacterial fauna population, increasing the sugar levels.

Researchers then gave mice antibiotics, which interestingly enough wiped out the entire bacteria population, sending sugar levels back to normal values.

“This, in itself, was conclusive proof that changes to the gut bacteria are directly responsible for the harmful effects to their host’s metabolism. The group even found that incubating the microbiota outside the body, together with artificial sweeteners, was sufficient to induce glucose intolerance.”

After settling the issue on mice, they moved on to humans. Similar effects were observed – eating artificial sweeteners causes gut bacteria to thrive, raising the sugar levels in the blood, more than eating the same amount of sugar.

“Elinav believes that certain bacteria in the guts of those who developed glucose intolerance reacted to the chemical sweeteners by secreting substances that then provoked an inflammatory response similar to sugar overdose, promoting changes in the body’s ability to utilise sugar,” the press release explains.

So, while the exact underlying mechanisms remain to be figured out, and while researchers study why some bacteria are affected and some not, the takeaway message is really simple: avoid artificial sweeteners – they do more harm than sugar.

Mutant cockroaches learn to avoid sugar traps

Cockroaches, the blight of every urban apartment; they’re adaptable, they’re sturdy, and they reproduce really fast. The nasty, disease carrying bugs can eat pretty much anything they find around the house, from mold and rotten food to the thing they love the most – sugar.

cockroachWhen given the opportunity, cockroaches always go for the sugary treat – or at least they used to. According to a new study published in Science, some cockroaches have evolved to the point where they are actually refusing to eat sucrose, a form of sugar commonly found in plants.

“They now perceive glucose as bitter,” says Coby Schal, an entomologist at North Carolina State University and one of the report’s authors.

Why did this happen? Well, glucose is the main thing that attracts them in traps, and many of the little creatures have mutated so that they actually don’t like it anymore. They mutated so fast that it took everybody by surprise.

Back when prehistoric cockroaches lived in the wild, there’s a possibility that they didn’t gobble glucose as well, because many plants that contain it in the wild are poisonous – but that’s still debated.

However, as humans evolved and moved to caves, cockroaches were soon to follow. Away from the threat of poisonous plants, they started to develop a taste for sugars, because it is a highly nutritious source of energy, and it was to their advantage to consume it.

But the mutation remained in their gene, and when humans started putting sugar traps, we reactivated the old gene – so much that when we put sugar in front of (some groups of) cockroaches, they just “jump back as though you’ve given them an electric shock“.

Apparently cockroach researchers take their job pretty serios, and they want to dedicate the next decade or so to studying this adaptation.

“We have roaches in the freezer that date back to the 1930’s,” says Schal. “This is what’s going to be driving our research over the next five or ten years.”

But all hope of trapping these mutant critters not lost. Sucrose-averse roaches are still attracted to fructose, or fruit sugar, and maltose, which is found in beer (“they really love that stuff,” says Schal).


Brain power: harvesting power from the cerebrospinal fluid within the subarachnoid space. Inset at right: a micrograph of a prototype, showing the metal layers of the anode (central electrode) and cathode contact (outer ring) patterned on a silicon wafer. (Credit: Karolinska Institutet/Stanford University)

Brain glucose might power the future’s tiny medical implants

Brain power: harvesting power from the cerebrospinal fluid within the subarachnoid space. Inset at right: a micrograph of a prototype, showing the metal layers of the anode (central electrode) and cathode contact (outer ring) patterned on a silicon wafer. (Credit: Karolinska Institutet/Stanford University)

Brain power: harvesting power from the cerebrospinal fluid within the subarachnoid space. Inset at right: a micrograph of a prototype, showing the metal layers of the anode (central electrode) and cathode contact (outer ring) patterned on a silicon wafer. (Credit: Karolinska Institutet/Stanford University)

A team of researchers at MIT have successfully manage to fabric a fuel cell capable of running on glucose, which scientists envision will power highly efficient medical implants in the brain that can help paralyzed patients express motor functions again.  The outputted power is in the microwatt range, but despite its low range, scientists claim it’s just enough to fuel tiny devices.

A similar idea was expressed in the 1970s, when scientists demonstrated they could power a pacemaker which ran on a glucose powered fuel cell. The concept was soon abandoned in favor of the much more powerful lithium-ion batteries. These glucose fuel cells also used enzymes that proved to be impractical for long-term implantation in the body.

The MIT design uses a fuel cell on a silicon chip, the same technology used to make semiconductor electronic chips, with no biological components, allowing it to be integrated with other circuits that would be needed for a brain implant. The power conversion occurs due to  a clever platinum catalyst, a biocompatible material, which strips the electrons from glucose, mimicking enzyme activity that break down glucose to generate ATP – the energy of cells.  The researchers claim that the glucose fuel cell could get all the sugar it needs from the cerebrospinal fluid (CSF) that bathes the brain and protects it from banging into the skull.

Tests so far have shown that the fuel cell can generate power in the range of hundred of microwatts – quite enough to power ultra-low-power and clinically useful neural implant, according to the researchers. Scientists warrant, however, that we’re quite a few years from seeing this kind of technology applied in medical practice.

“It will be a few more years into the future before you see people with spinal-cord injuries receive such implantable systems in the context of standard medical care, but those are the sorts of devices you could envision powering from a glucose-based fuel cell,” says Benjamin Rapoport, a former graduate student in the Sarpeshkar lab and the first author on the new MIT study.

The findings were published in the journal PLoS ONE

via Kurzweil