Novel drug makes mice skinny even on sugary, fatty diet

Researchers from The University of Texas Health Science Center at San Antonio (UT Health San Antonio) have developed a small-molecule drug that prevents weight gain and adverse liver changes in mice fed a high-sugar, high-fat Western diet throughout life.

"When we give this drug to the mice for a short time, they start losing weight. They all become slim," said Madesh Muniswamy, PhD, professor of medicine in the health science center's Joe R. and Teresa Lozano Long School of Medicine.

Findings by the collaborators, also from the University of Pennsylvania and Cornell University, were published Feb. 27 in the high-impact journal Cell Reports. Muniswamy, director of the Center for Mitochondrial Medicine at UT Health San Antonio, is the senior author.

Fourth most common element

The research team discovered the drug by first exploring how magnesium impacts metabolism, which is the production and consumption of energy in cells. This energy, called ATP, fuels the body's processes.

Magnesium is the fourth most abundant element in the body after calcium, potassium and sodium, and plays many key roles in good health, including regulating blood sugar and blood pressure and building bones. But the researchers found that too much magnesium slows energy production in mitochondria, which are cells' power plants.

"It puts the brake on, it just slows down," said co-lead author Travis R. Madaris, doctoral student in the Muniswamy laboratory at UT Health San Antonio.

Deleting MRS2, a gene that promotes magnesium transport into the mitochondria, resulted in more efficient metabolism of sugar and fat in the power plants. The result: skinny, healthy mice.

Liver and adipose (fat) tissues in the rodents showed no evidence of fatty liver disease, a complication related to poor diet, obesity and type 2 diabetes.

Small-molecule agent

The drug, which the researchers call CPACC, accomplishes the same thing. It restricts the amount of magnesium transfer into the power plants. In experiments, the result was again: skinny, healthy mice. UT Health San Antonio has filed a patent application on the drug.

The mice served as a model system of long-term dietary stress precipitated by the calorie-rich, sugary and fatty Western diet. The familiar results of this stress are obesity, type 2 diabetes and cardiovascular complications.

"Lowering the mitochondrial magnesium mitigated the adverse effects of prolonged dietary stress," said co-lead author Manigandan Venkatesan, PhD, postdoctoral fellow in the Muniswamy lab.

Joseph A. Baur, PhD, of the University of Pennsylvania and Justin J. Wilson, PhD, of Cornell are among the collaborators. "We came up with the small molecule and Justin synthesized it," Madaris said.

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Ultra-processed foods may be linked to increased risk of cancer

Higher consumption of ultra-processed foods may be linked to an increased risk of developing and dying from cancer, an Imperial College London-led observational study suggests.

Researchers from Imperial’s School of Public Health have produced the most comprehensive assessment to date of the association between ultra-processed foods and the risk of developing cancers. Ultra-processed foods are food items which have been heavily processed during their production, such as fizzy drinks, mass-produced packaged breads, many ready meals and most breakfast cereals.

Ultra-processed foods are often relatively cheap, convenient, and heavily marketed, often as healthy options. But these foods are also generally higher in salt, fat, sugar, and contain artificial additives. It is now well documented that they are linked with a range of poor health outcomes including obesity, type 2 diabetes and cardiovascular disease.

The first UK study of its kind used UK Biobank records to collect information on the diets of 200,000 middle-aged adult participants. Researchers monitored participants’ health over a 10-year period, looking at the risk of developing any cancer overall as well as the specific risk of developing 34 types of cancer. They also looked at the risk of people dying from cancer.

The study found that higher consumption of ultra-processed foods was associated with a greater risk of developing cancer overall, and specifically with ovarian and brain cancers. It was also associated with an increased risk of dying from cancer, most notably with ovarian and breast cancers.

For every 10 per cent increase in ultra-processed food in a person’s diet, there was an increased incidence of 2 per cent for cancer overall, and a 19 per cent increase for ovarian cancer specifically.

Each 10 per cent increase in ultra-processed food consumption was also associated with increased mortality for cancer overall by 6 per cent, alongside a 16 per cent increase for breast cancer and a 30 per cent increase for ovarian cancer.

These links remained after adjusting for a range of socio-economic, behavioural and dietary factors, such as smoking status, physical activity and body mass index (BMI).

The Imperial team carried out the study, which is published in eClinicalMedicine, in collaboration with researchers from the International Agency for Research on Cancer (IARC), University of São Paulo, and NOVA University Lisbon.

Previous research from the team reported the levels of consumption of ultra-processed foods in the UK, which are the highest in Europe for both adults and children. The team also found that higher consumption of ultra-processed foods was associated with a greater risk of developing obesity and type 2 diabetes in UK adults, and a greater weight gain in UK children extending from childhood to young adulthood.

Dr Eszter Vamos, lead senior author for the study, from Imperial College London’s School of Public Health, said: “This study adds to the growing evidence that ultra-processed foods are likely to negatively impact our health including our risk for cancer. Given the high levels of consumption in UK adults and children, this has important implications for future health outcomes.

“Although our study cannot prove causation, other available evidence shows that reducing ultra-processed foods in our diet could provide important health benefits. Further research is needed to confirm these findings and understand the best public health strategies to reduce the widespread presence and harms of ultra-processed foods in our diet.”

Dr Kiara Chang, first author for the study, from Imperial College London’s School of Public Health, said: “The average person in the UK consumes more than half of their daily energy intake from ultra-processed foods. This is exceptionally high and concerning as ultra-processed foods are produced with industrially derived ingredients and often use food additives to adjust colour, flavour, consistency, texture, or extend shelf life.

“Our bodies may not react the same way to these ultra-processed ingredients and additives as they do to fresh and nutritious minimally processed foods. However, ultra-processed foods are everywhere and highly marketed with cheap price and attractive packaging to promote consumption. This shows our food environment needs urgent reform to protect the population from ultra-processed foods.”

The World Health Organisation and the United Nations’ Food and Agriculture Organisation has previously recommended restricting ultra-processed foods as part of a healthy sustainable diet.

There are ongoing efforts to reduce ultra-processed food consumption around the world, with countries such as Brazil, France and Canada updating their national dietary guidelines with recommendations to limit such foods. Brazil has also banned the marketing of ultra-processed foods in schools. There are currently no similar measures to tackle ultra-processed foods in the UK.

Dr Chang added: “We need clear front of pack warning labels for ultra-processed foods to aid consumer choices, and our sugar tax should be extended to cover ultra-processed fizzy drinks, fruit-based and milk-based drinks, as well as other ultra-processed products.

“Lower income households are particularly vulnerable to these cheap and unhealthy ultra-processed foods. Minimally processed and freshly prepared meals should be subsidised to ensure everyone has access to healthy, nutritious and affordable options.”

Read more at Science Daily

Sugar is processed differently in the brains of obesity-prone vs. obesity-resistant rats

On a diet? Perhaps you're avoiding sweets or carbs altogether or curbing late-night munchies. These are examples of behavior modifications and when it comes to food, avoiding those diet triggers can be pretty hard to do.

To understand what drives people to overeat, scientists are looking more closely at a brain structure involved in motivation, called the nucleus accumbens. This small region drives reward-seeking behaviors underlying the pursuit of sex, recreational drugs like nicotine and alcohol, and food.

"These brain motivation centers evolved to help us survive; finding food and having sex are essential to the survival of an individual and of a species," said Carrie Ferrario, Ph.D., associate professor in the Department of Pharmacology at U-M Medical School.

"What was advantageous when food was hard to find has become a disadvantage and unhealthy in the current food dense environment. This is compounded by the over-abundance of over-processed, low nutrition foods that may satisfy our taste but leave our bodies unnourished. People don't tend to find it difficult to turn down an extra serving of broccoli, but just one more french-fry or making room for a bit of chocolate dessert...that's a different story. The real challenge is overcoming these urges and changing our behavior when it comes to food," Ferrario added.

Given the immense toll obesity takes on virtually all body systems, Ferrario, Peter Vollbrecht, Ph.D., of Western Michigan University, and their colleagues are using rat models to understand potential brain differences between animals who are prone to over-eating and obesity and those who are not.

Previous research from Ferrario's lab pinpointed differences in the nucleus accumbens in obesity-prone and obesity-resistant rats. Their latest study, published in the Journal of Neurochemistry, tracked what was happening in real time in the brain when these animals were presented with glucose, a type of sugar, labeled with a tracer. The tracer allowed the researchers to measure this new sugar in the brain.

Sugar is the brain's main fuel source and once there, the molecule is broken down and used to create new molecules such as glutamine, glutamate, and GABA, each with an important role in influencing the activation of neurons in the brain and nervous system.

"Glucose that is consumed gets broken down and then its carbons get incorporated into neurotransmitters. We see those labelled carbons showing up in those molecules -- glutamate, glutamine, and GABA -- over time," explained Vollbrecht.

They found that glucose was taking longer to get into the nucleus accumbens of obesity-prone animals.

Furthermore, when measuring the concentration of the glutamate, glutamine, and GABA, they discovered excess levels of glutamate, an excitatory neurotransmitter. This, said the team, implied a defect in a neurotransmitter recycling process, typically maintained in the nervous system by star-shaped cells called astrocytes.

Normally, astrocytes will pull glutamate out of the space between neurons, called the synapse, convert it into glutamine, and then shuttle it back to cells that produce GABA or glutamate. This sequence is crucial for turning neurons off and on. "The findings suggest that we're getting too much glutamate and it's not being taken out of the synapse," said Vollbrecht.

Ferrario added, "The balance between glutamate and GABA (the main inhibitory transmitter) is really important for brain function and will influence activity of the neurons in the nucleus accumbens."

This balance, and therefore brain activity, is different in obesity-prone vs. obesity-resistant rats.

The fact that these rats are either prone to obesity or not is important for disentangling cause and effect, says Vollbrecht. "It allows us to remove diet as one of the variables."

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Sugar molecules as a target in cancer therapy

Cancer cells use sugar molecules on their surface to disable attacks by the body's immune system. Researchers at the University of Basel now report on how this mechanism can be neutralized.

The immune system is actually extremely well equipped to get rid of abnormal cells. As a safety mechanism, special features are built into healthy cells so that the immune system recognizes them, thus preventing a mistaken attack. However, cancer cells sneakily manipulate these safety mechanisms in such a way that the immune system leaves them alone.

Over the past few years, immunotherapies have revolutionized cancer treatment. These include therapies that prevent cancer cells from inhibiting the immune response. This involves blocking what are known as "immune checkpoints" using artificially produced proteins, which allows the immune cells to successfully attack the cancer cells.

"With many tumors, however, there have only been modest levels of success. That's why we're looking for new approaches to engage anti-tumor immune responses more efficiently," explains Professor Heinz Läubli from the Department of Biomedicine at the University of Basel and the University Hospital Basel. In the specialist journal Science Translational Medicine, his team, together with that of recent Nobel laureate Professor Carolyn Bertozzi from Stanford University, reports on a promising new approach. By altering sugar molecules on the surface of cancer cells in mice, the researchers were able to produce a significant increase in anti-tumor immune response.

How immune cells turn traitor

Their focus is on sugar molecules on the surface of the cancer cells, as well as on the cells in their immediate vicinity. These particular sugars, which contain sialic acid, also occur on healthy cells, and are important for cell-to-cell communication. However, tumors boost the proportion of these sugars on their surface.

Certain immune cells called macrophages recognize these sialic acid sugars and inadvertently turn traitor: they give other nearby immune cells the impression that all is well. The research team's experiments on mice have now been able to demonstrate that the sialic acid sugars can be removed, or at least very much reduced, with the help of an enzyme. This means that the macrophages no longer prevent the tumor coming under immunological attack.

A target structure for new therapies

More precise analyses have enabled the researchers to identify in mice exactly which receptor it is on the macrophages that recognizes the sialic acid sugars. If the equivalent receptor could be identified in humans, then that could be another interesting target in the bid to tackle cancer cells with the aid of the patient's own immune system.

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Non-nutritive sweeteners affect human microbiomes and can alter glycemic responses

Since the late 1800s non-nutritive sweeteners have promised to deliver all the sweetness of sugar with none of the calories. They have long been believed to have no effect on the human body, but researchers publishing in the journal Cell on August 19 challenge this notion by finding that these sugar substitutes are not inert, and, in fact, some can alter human consumers' microbiomes in a way that can change their blood sugar levels.

In 2014, senior author Eran Elinav an immunologist and microbiome researcher at the Weizmann Institute of Science and the German National Cancer Center (DKFZ) and his team found that non-nutritive sweeteners affected the microbiomes of mice in ways that could impact their glycemic responses. The team was interested in whether these results would also be found in humans.

To address this important question, the research team carefully screened over 1300 individuals for those who strictly avoid non-nutritive sweeteners in their day-to-day lives, and identified a cohort of 120 individuals. These participants were broken into six groups: two controls and four who ingested well below the FDA daily allowances of either aspartame, saccharin, stevia, or sucralose.

"In subjects consuming the non-nutritive sweeteners, we could identify very distinct changes in the composition and function of gut microbes, and the molecules they secret into peripheral blood. This seemed to suggest that gut microbes in the human body are rather responsive to each of these sweeteners," says Elinav. "When we looked at consumers of non-nutritive sweeteners as groups, we found that two of the non-nutritive sweeteners, saccharin and sucralose, significantly impacted glucose tolerance in healthy adults. Interestingly, changes in the microbes were highly correlated with the alterations noted in people's glycemic responses."

To establish causation, the researchers transferred microbial samples from the study subjects to germ-free mice -- mice that have been raised in completely sterile conditions and have no microbiome of their own.

"The results were quite striking," says Elinav. "In all of the non-nutritive sweetener groups, but in none of the controls, when we transferred into these sterile mice the microbiome of the top responder individuals collected at a time point in which they were consuming the respective non-nutritive sweeteners, the recipient mice developed glycemic alterations that very significantly mirrored those of the donor individuals. In contrast, the bottom responders' microbiomes were mostly unable to elicit such glycemic responses," he adds. "These results suggest that the microbiome changes in response to human consumption of non-nutritive sweetener may, at times, induce glycemic changes in consumers in a highly personalized manner."

Elinav says that he expects the effects of the sweeteners will vary person to person because of the incredibly unique composition of our microbiome. "We need to raise awareness of the fact that non-nutritive sweeteners are not inert to the human body as we originally believed. With that said, the clinical health implications of the changes they may elicit in humans remain unknown and merit future long-term studies."

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Your gut senses the difference between real sugar and artificial sweetener

Your taste buds may or may not be able to tell real sugar from a sugar substitute, but there are cells in your intestines that can and do distinguish between the two sweet solutions. And they can communicate the difference to your brain in milliseconds.

Not long after the sweet taste receptor was identified in the mouths of mice 20 years ago, scientists attempted to knock those taste buds out. But they were surprised to find that mice could still somehow discern and prefer natural sugar to artificial sweetener, even without a sense of taste.

The answer to this riddle lies much further down in the digestive tract, at the upper end of the gut just after the stomach, according to research led by Diego Bohórquez, an associate professor of medicine and neurobiology in the Duke University School of Medicine.

In a paper appearing Jan. 13 in Nature Neuroscience, "we've identified the cells that make us eat sugar, and they are in the gut," Bohórquez said. Infusing sugar directly into the lower intestine or colon does not have the same effect. The sensing cells are in the upper reaches of the gut, he said.

Having discovered a gut cell called the neuropod cell, Bohórquez with his research team has been pursuing this cell's critical role as a connection between what's inside the gut and its influence in the brain. The gut, he argues, talks directly to the brain, changing our eating behavior. And in the long run, these findings may lead to entirely new ways of treating diseases.

Originally termed enteroendrocrine cells because of their ability to secrete hormones, specialized neuropod cells can communicate with neurons via rapid synaptic connections and are distributed throughout the lining of the upper gut. In addition to producing relatively slow-acting hormone signals, the Bohórquez research team has shown that these cells also produce fast-acting neurotransmitter signals that reach the vagus nerve and then the brain within milliseconds.

Bohórquez said his group's latest findings further show that neuropods are sensory cells of the nervous system just like taste buds in the tongue or the retinal cone cells in the eye that help us see colors.

"These cells work just like the retinal cone cells that that are able to sense the wavelength of light," Bohórquez said. "They sense traces of sugar versus sweetener and then they release different neurotransmitters that go into different cells in the vagus nerve, and ultimately, the animal knows 'this is sugar' or 'this is sweetener.'"

Using lab-grown organoids from mouse and human cells to represent the small intestine and duodenum (upper gut), the researchers showed in a small experiment that real sugar stimulated individual neuropod cells to release glutamate as a neurotransmitter. Artificial sugar triggered the release of a different neurotransmitter, ATP.

Using a technique called optogenetics, the scientists were then able to turn the neuropod cells on and off in the gut of a living mouse to show whether the animal's preference for real sugar was being driven by signals from the gut. The key enabling technology for the optogenetic work was a new flexible waveguide fiber developed by MIT scientists. This flexible fiber delivers light throughout the gut in a living animal to trigger a genetic response that silenced the neuropod cells. With their neuropod cells switched off, the animal no longer showed a clear preference for real sugar.

"We trust our gut with the food we eat," Bohórquez said. "Sugar has both taste and nutritive value and the gut is able to identify both."

"Many people struggle with sugar cravings, and now we have a better understanding of how the gut senses sugars (and why artificial sweeteners don't curb those cravings)," said co-first author Kelly Buchanan, a former Duke University School of Medicine student who is now an Internal Medicine resident at Massachusetts General Hospital. "We hope to target this circuit to treat diseases we see every day in the clinic."

In future work, Bohórquez said he will be showing how these cells also recognize other macronutrients. "We always talk about 'a gut sense,' and say things like 'trust your gut,' well, there's something to this," Bohórquez said.

Read more at Science Daily

Blueprint reveals how plants build a sugar transport lane

A tiny region at the root tip has been found to be responsible for orchestrating the growth and development of the complex network of vascular tissues that transport sugars through plant roots.

In a paper published in Science today, an international team of scientists present a detailed blueprint of how plants construct phloem cells -- the tissue responsible for transporting and accumulating sugars and starch in the parts of the plant that we harvest (seeds, fruits and storage tubers) to feed much of the world.

This pivotal research reveals how global signals in root meristems coordinate distinct maturation phases of the phloem tissue.

Phloem is a highly specialised vascular tissue that forms an interconnected network of continuous strands throughout a plant's body. It transports sugars, nutrients and a range of signalling molecules between leaves, roots, flowers and fruits.

As a result, phloem is central to plant function. Understanding how the phloem network is initiated and develops is important for future applications in agriculture, forestry and biotechnology as it could reveal how to better transport this sugar energy to where it is needed.

How do plants build a sugar lane in a multi-lane highway?

Plant roots continue to grow throughout a plant's life. This phenomenon, known as indeterminate growth, means roots continually elongate as they add new tissues to the tip of the root -- like constructing a never-ending highway. A continuous file of specialised phloem cells running the length of roots (analogous to a lane on a highway) delivers the primary nutrient, sucrose, to the parts of the plant where it is needed for growth. To fulfil this vital role, phloem tissue must develop and mature rapidly so it can supply sugars to surrounding tissues -- akin to building a service lane that needs to be completed in the first stage of constructing a multi-lane highway.

The problem that has long puzzled plant scientists is how a single instructive gradient of proteins are able to stage the construction phases across all the different specialised cell files (highway lanes) that are present in roots. How does one cell type read the same gradient as its neighbours, but interprets it differently to stage its own specialised development is a question that plant scientists have been working to resolve.

Over the past 15 years, researchers in Yrjö Helariutta's teams at the University of Cambridge and University of Helsinkihave uncovered the central role of cell-to-cell communication and complex feedback-mechanisms involved in vascular patterning. This new research, undertaken with collaborators at New York University and North Carolina State University, reveals how this single lane of phloem cells is constructed independently of surrounding cells.

The Sainsbury/Helsinki group dissected each step in the construction of the phloem cell file (the sugar transport lane) in the model plant Arabidopsis thaliana using single-cell RNA-seq and live imaging. Their work showed how the proteins that control the broad maturation gradient of the root interact with the genetic machinery that specifically controls phloem development.

This is one mechanism that appears to help the phloem cell file to fast-track maturation using its own machinery to interpret the maturation cues. Dr Pawel Roszak, co-first-author of the study and researcher at the Sainsbury Laboratory Cambridge University (SLCU), explains: "We have shown how global signals in the root meristem interact with the cell type specific factors to determine distinct phases of phloem development at the cellular resolution. Using cell sorting followed by deep, high-resolution single-cell sequencing of the underlying gene regulatory network revealed a "seesaw" mechanism of reciprocal genetic repression that triggers rapid developmental transitions."

The group also showed how phloem development is staged over time, with early genetic programs inhibiting late genetic programs and vice versa -- just as the road asphalt-laying work crews' hand over construction to lane painters in the latter stages of highway construction. In addition, they showed how early phloem regulators instructed specific genes to split the phloem cells into two different subtypes -- like the construction of a fork in the road leading to two separate destinations.

Co-leader of the work, Professor Yrjö Helariutta, said his teams' reconstruction of the steps from birth to terminal differentiation of protophloem in the Arabidopsis root exposed the steps. Helariutta said: "Broad maturation gradients interfacing with cell-type specific transcriptional regulators to stage cellular differentiation is required for phloem development."

"By combining single-cell transcriptomics with live imaging, here we have mapped the cellular events from the birth of the phloem cell to its terminal differentiation into phloem sieve element cells. This allowed us to uncover genetic mechanisms that coordinate cellular maturation and connect the timing of the genetic cascade to broadly expressed master regulators of meristem maturation. The precise timing of developmental mechanisms was critical for proper phloem development, with apparent "fail safe" mechanisms to ensure transitions."

Read more at Science Daily

An easy relationship between a beetle and its yeast symbiont

Japanese lizard beetle larvae feed on yeast injected from their mothers' abdomens into the bamboo stems they are growing in. Now, scientists at Nagoya University have made a surprising discovery: the yeast can digest some complex sugars in the bamboo woody tissue, but it doesn't. Instead, it consumes much simpler and more available sugar sources.

"This was a real surprise," says Nagoya University bioagricultural researcher Wataru Toki. "While yeast can indeed decompose those indigestible components, our analysis shows the yeast actually grows on small molecule monosaccharides." The results are published in the journal Scientific Reports.

Female Japanese lizard beetles carry the yeast Wickerhamomyces anomalus in a specialised pocket-like organ. In spring, they dig holes in bamboo and insert their eggs and the yeast. W. anomalus grows into a sort of fungal garden that the very hungry beetle larvae munch on as soon as they hatch.

In other symbiotic relationships, fungi typically break down complex sugars into more digestible chunks that their host insects can feed on. Toki and his colleague, Dan Aoki, wanted to know whether this was also the case in the relationship between the Japanese lizard beetle and W. anomalus.

Their research suggests not. The scientists used a technique called ion exchange chromatography to analyse and compare the sugar content of fresh bamboo pith, and pith colonized by yeast alone or by yeast and beetle larvae. The comparison revealed that the yeast mostly ate the simple free sugars glucose and fructose.

This surprised the scientists because further tests showed that the yeast can actually digest some complex, indigestible sugars if necessary.

"Bamboo is not only a farm for the yeast but also a house for the larvae. So the larvae can live in a strong house safely because the house is not decomposed by the food," explains Toki.

Read more at Science Daily

Save the planet (and your health) by steering clear of sweets and pastries

Keen to do your bit for the environment? Cut back on sweets, pastries, fried foods and processed meat. According to a new study published this month, reducing these foods in our diet is not only better for our health but also the planet.

Australia and New Zealand households eat more discretionary and junk foods than recommended by dietary guidelines, contributing to food-related greenhouse gas emissions (GHGe) and other environmental impacts.

University of South Australia (UniSA) dietitian Sara Forbes, who led a review examining 20 studies on the environmental impacts of food consumption in both countries, says the findings highlight the need for more sustainable dietary choices.

According to a Federal Government report released in 2020, Australia emitted an estimated 510 metric tonnes of carbon dioxide, with food-related emissions accounting for 14.2 per cent of this total. The report found that the average Australian produces the equivalent of 19.7kg of carbon dioxide each day via their diets.

Another report from 2017 found that food waste comprises approximately six per cent of Australia's GHGe, considering the water, energy and pesticides used in food production and packaging that ends up in landfill, where it releases even more methane as it decomposes.

Unlike New Zealand, current Australian Dietary Guidelines (ADG) do not consider environmental impacts of food and need to be updated, researchers say.

The existing ADG recommends daily servings of 'core' foods every day: fruit and vegetables, grains, lean meats, fish, eggs, nuts, seeds, legumes, milk, cheese, yoghurt and alternatives.

These core foods are estimated to contribute between 67-73 per cent of total food-related GHGe in Australia, with meat, grains and dairy contributing the most emissions. Fruit and vegetables are two of the lowest contributors.

Non-core or 'discretionary' foods include sugar-sweetened drinks, alcohol, confectionary and processed meats, accounting for between 27-33 per cent of food-related GHGe. While the percentage is lower than core food emissions, the fact that Australians are consuming large amounts of avoidable energy-rich, nutrient-poor foods is not helping the environment.

In New Zealand, the highest greenhouse gas emitters are meat, seafood and eggs (35 per cent), followed by highly processed foods such as pastries and ice cream (34 per cent).

Other studies examined the environmental impacts of water use in food production.

Australian irrigators soak up eight million megalitres of water each year to grow crops, but the majority are exported, making it difficult to accurately reflect the nation's water footprint.

The researchers assessed 20 articles in their study, published in the past decade, with varying findings. Despite the differences, clear trends emerged.

"Discretionary foods have a higher cropland, water scarcity and Ecological Footprint. Meat also emits greenhouse gases, although its water scarcity footprint is lower compared to dairy products, cereals, grains, fruit and vegetables," Forbes says.

"It is time we better acknowledged the environmental impacts of the type and amount of food we eat, considering the planet as well as our health.

"By 2050, the world's population is projected to reach 10 billion people. There is no way we can feed that amount of people unless we change the way we eat and produce food."

Read more at Science Daily

Sugar not so nice for your child's brain development

 Sugar practically screams from the shelves of your grocery store, especially those products marketed to kids.

Children are the highest consumers of added sugar, even as high-sugar diets have been linked to health effects like obesity and heart disease and even impaired memory function.

However, less is known about how high sugar consumption during childhood affects the development of the brain, specifically a region known to be critically important for learning and memory called the hippocampus.

New research led by a University of Georgia faculty member in collaboration with a University of Southern California research group has shown in a rodent model that daily consumption of sugar-sweetened beverages during adolescence impairs performance on a learning and memory task during adulthood. The group further showed that changes in the bacteria in the gut may be the key to the sugar-induced memory impairment.

Supporting this possibility, they found that similar memory deficits were observed even when the bacteria, called Parabacteroides, were experimentally enriched in the guts of animals that had never consumed sugar.

"Early life sugar increased Parabacteroides levels, and the higher the levels of Parabacteroides, the worse the animals did in the task," said Emily Noble, assistant professor in the UGA College of Family and Consumer Sciences who served as first author on the paper. "We found that the bacteria alone was sufficient to impair memory in the same way as sugar, but it also impaired other types of memory functions as well."

Guidelines recommend limiting sugar

The Dietary Guidelines for Americans, a joint publication of the U.S. Departments of Agriculture and of Health and Human Services, recommends limiting added sugars to less than 10 percent of calories per day.

Data from the Centers for Disease Control and Prevention show Americans between the ages 9-18 exceed that recommendation, the bulk of the calories coming from sugar-sweetened beverages.

Considering the role the hippocampus plays in a variety of cognitive functions and the fact the area is still developing into late adolescence, researchers sought to understand more about its vulnerability to a high-sugar diet via gut microbiota.

Juvenile rats were given their normal chow and an 11% sugar solution, which is comparable to commercially available sugar-sweetened beverages.

Researchers then had the rats perform a hippocampus-dependent memory task designed to measure episodic contextual memory, or remembering the context where they had seen a familiar object before.

"We found that rats that consumed sugar in early life had an impaired capacity to discriminate that an object was novel to a specific context, a task the rats that were not given sugar were able to do," Noble said.

A second memory task measured basic recognition memory, a hippocampal-independent memory function that involves the animals' ability to recognize something they had seen previously.

In this task, sugar had no effect on the animals' recognition memory.

"Early life sugar consumption seems to selectively impair their hippocampal learning and memory," Noble said.

Additional analyses determined that high sugar consumption led to elevated levels of Parabacteroides in the gut microbiome, the more than 100 trillion microorganisms in the gastrointestinal tract that play a role in human health and disease.

To better identify the mechanism by which the bacteria impacted memory and learning, researchers experimentally increased levels of Parabacteroides in the microbiome of rats that had never consumed sugar. Those animals showed impairments in both hippocampal dependent and hippocampal-independent memory tasks.

"(The bacteria) induced some cognitive deficits on its own," Noble said.

Noble said future research is needed to better identify specific pathways by which this gut-brain signaling operates.

Read more at Science Daily

Sweet taste reduces appetite?

 The sweet taste of sugar is very popular worldwide. In Austria and Germany, the yearly intake per person adds up to about 33 and 34 kilograms, respectively. Thus, sugar plays an increasingly role in the nutrition and health of the population, especially with regard to body weight. However, little is known about the molecular (taste) mechanisms of sugar that influence dietary intake, independently of its caloric load.

Taste receptor and satiety regulation

"We therefore investigated the role of sweet taste receptor activation in the regulation of satiety," says Veronika Somoza, deputy head of the Department of Physiological Chemistry at the University of Vienna and director of the Leibniz Institute for Food Systems Biology at the Technical University of Munich.

For this purpose, the scientists conducted a blinded, cross-over intervention study with glucose and sucrose. A total of 27 healthy, male persons, between 18 and 45 years of age, received either a 10 percent glucose or sucrose solution (weight percent) or one of the sugar solutions supplemented with 60 ppm lactisole. Lactisole is a substance that binds to a subunit of the sweet receptor and reduces the perception of sweet taste. Despite different types of sugar, all solutions with or without lactisole had the same energy content.

Two hours after drinking each of the test solutions, the participants were allowed to have as much as breakfast they wanted. Shortly before and during the 120-min waiting period, the researchers took blood samples in regular intervals and measured their body temperature.

Additional 100 kilocalories on average

After the consumption of the lactisole-containing sucrose solution, the test persons had an increased energy intake from breakfast of about 13 percent, about 100 kilocalories more, than after drinking the sucrose solution without lactisole. In addition, the subjects of this group showed lower body temperature and reduced plasma serotonin concentrations. Serotonin is a neurotransmitter and tissue hormone which, among other things, has an appetite-suppressing effect. In contrast, the researchers observed no differences after administration of the lactisole-containing glucose solution and the pure glucose solution.

"This result suggests that sucrose, regardless of its energy content, modulates the regulation of satiety and energy intake via the sweet taste receptor," says Barbara Lieder, head of Christian Doppler Laboratory for Taste Research and also deputy head of the Department of Physiological Chemistry of the Faculty of Chemistry at University of Vienna.

The first study author of the study, Kerstin Schweiger, University of Vienna adds: "We do not know yet why we could not observe the lactisole effect with glucose. However, we suspect it is because glucose and sucrose activate the sweet receptor in different ways. We also assume that mechanisms independent of the sweet receptor play a role."

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Prebiotic chemistry: In the beginning, there was sugar

 Organic molecules formed the basis for the evolution of life. But how could inorganic precursors have given rise to them? Ludwig-Maximilians-Universitaet (LMU) in Munich chemist Oliver Trapp now reports a reaction pathway in which minerals catalyze the formation of sugars in the absence of water.

More than 4 billion years ago, the Earth was very far from being the Blue Planet it would later become. At that point it had just begun to cool and, in the course of that process, the concentric structural zones that lie ever deeper beneath our feet were formed. The early Earth was dominated by volcanism, and the atmosphere was made up of carbon dioxide, nitrogen, methane, ammonia, hydrogen sulfide and water vapor. In this decidedly inhospitable environment the building blocks of life were formed. How then might this have come about?

Researchers have puzzled over the question for decades. The first breakthrough was made in 1953 by two chemists, named Stanley Miller and Harold C. Urey, at the University of Chicago. In their experiments, they simulated the atmosphere of the primordial Earth in a closed reaction system that contained the gases mentioned above. A miniature 'ocean' was heated to provide water vapor, and electrical discharges were passed through the system to mimic the effects of lightning. When they analyzed the chemicals produced under these conditions, Miller and Urey detected amino acids -- the basic constituents of proteins -- as well as a number of other organic acids.

It is now known that the conditions employed in these experiments did not reflect those that prevailed on the early Earth. Nevertheless, the Miller-Urey experiment initiated the field of prebiotic chemical evolution. However, it not throw much light on how other classes of molecules found in all biological cells -- such as sugars, fats and nucleic acids -- might have been generated. These compounds are however indispensable ingredients of the process that led to the first bacteria and subsequently to photosynthetic cyanobacteria that produced oxygen. This is why Oliver Trapp, Professor of Organic Chemistry at LMU, decided to focus his research on the prebiotic synthesis of these substances.

From formaldehyde to sugar

The story of synthetic routes from smaller precursors to sugars goes back almost a century prior to the Miller-Urey experiment. In 1861, the Russian chemist Alexander Butlerov showed that formaldehyde could give rise to various sugars via what became known as the formose reaction. Miller und Urey in fact found formic acid in their experiments, and it can be readily reduced to yield formaldehyde. Butlerov also discovered that the formose reaction is promoted by a number of metal oxides and hydroxides, including those of calcium, barium, thallium and lead. Notably calcium is abundantly available on and below the Earth's surface.

However, the hypothesis that sugars could have been produced via the formose reaction runs into two difficulties. The 'classical' formose reaction produces a diverse mixture of compounds, and it takes place only in aqueous media. These requirements are at odds with the fact that sugars have been detected in meteorites.

Together with colleagues at LMU and the Max Planck Institute for Astronomy in Heidelberg, Trapp therefore decided to explore whether formaldehyde could give rise to sugars in a solid-phase system. With a view to simulating the kinds of mechanical forces to which solid minerals would have been subjected, all the reaction components were combined in a ball mill -- in the absence of solvents, but adding enough formaldehyde to saturate the powdered solids

And indeed, the formose reaction was observed and several different minerals were found to catalyze it. The formaldehyde was adsorbed onto the solid particles, and the interaction resulted in the formation of the formaldehyde dimer (glycolaldehyde) -- and ribose, the 5-carbon sugar that is an essential constituent of ribonucleic acid (RNA). RNA is thought to have merged prior to DNA, and it serves as the repository of genetic information in many viruses, as well as providing the templates for protein synthesis in all cellular organisms. More complex sugars were also obtained in the experiments, together with a few byproducts, such as lactic acid and methanol.

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Bone Loss: Perforated bone tissue from too little sugar

 Could something as simple as a certain type of sugar water be medicine for perforated bones, and even bone marrow cancer itself?

Inside our bodies are some jellyfish-like cells that actually eat away at our bones. Every year, they eat about ten per cent of the bone mass in our body. Fortunately, other cells usually follow and build up new bone.

We undergo a kind of continuous remodelling and repair that enables most of us to traipse around with steel in our legs and arms.

In people with bone marrow cancer, the bone-eating cells run amok. They become too numerous and eat too much. The bone-building gang doesn't have time to rebuild the bone mass, despite overtime and long shifts. Bone tissue gets gobbled up.

Many people with bone marrow cancer often end up with perforated bones, a condition that is very painful to live with. They sometimes experience collapsed vertebrae or suffer broken bones just by turning in bed.

For decades, scientists around the world have been scratching their heads and wondering what the cause could be. Various theories have been launched, but researchers have not reached a consensus on the main cause.

Bone marrow cancer remains an incurable disease so far. Available treatments can prolong life, but not cure the disease.

Now Standal and her research group at the Centre of Molecular Inflammation Research (CEMIR) at the Norwegian University of Science and Technology (NTNU) have discovered a piece of the puzzle that looks very promising.

They have come to the conclusion that the cause of the bone destruction is too little sugar. We're not talking about the sugar we eat in our cakes and biscuits, but sugar that resides in a substance that is important for the immune system.

To get to the bottom of how sugar is related to bone loss, we need to get into the bone marrow. This is the soft cavity that inside all our bones.

Within the bones are plasma cells. When bacteria or viruses enter the body, the plasma cells begin their job of getting rid of the invaders. Antibodies are produced which are sent via the blood, ready to do battle.

So far so good, but in people with bone marrow cancer, far too much of one type of antibody is produced. It's going amok here, too. The antibody that the cancer makes is also completely useless. It doesn't knock out either the cold or the flu but just takes up too much space and displaces other types of antibodies.

"I thought simply. If people with bone marrow cancer have too much of the antibody and too many bone-eating cells, then they must be connected," Standal says.

The search for an answer gobbled a lot of her working hours for almost five years. The hard work was fortunately not in vain, and has led to a completely new and fundamental understanding.

This is how Standal arrived at the answer:

The vast majority of patients with bone marrow cancer develop perforated bones, but not all. Standal asked nicely, and received samples from patients with bone loss. She also took samples from patients without this kind of bone loss.

The researchers extracted antibodies from the samples and cultured bone-eating cells in the laboratory.

When Standal placed the bone-eating cells into the antibody of the patients with bone perforations, she discovered that the number of bone-eating cells increased.

When she put the bone-eating cells into the antibody of the patients without bone perforations, she discovered that the number of bone-eating cells did not increase.

"Why that was the case became the next interesting thing to figure out," Standal says.

The antibody carries a type of sugar that "decorates" it, in a way. The sugar has an effect on how the antibody works. Standal found her way to Manfred Wuhrer at the Center for Proteomics and Metabolomics of the Leiden University Medical Center in the Netherlands. He is a specialist in this type of sugar, and Standal sent the samples to him.

He found that individuals with bone loss were missing two sugar molecules at the end of a long chain inside the antibody.

"There was too little sugar," says Standal.

But this answer wasn't sufficient, either.

Although a difference was detected between the two groups, the researchers could not confirm that the missing sugar molecules were the reason patients developed more bone-eating cells. Several further experiments had to be conducted.

The research team went to the lab and put more sugar on the antibody. This did not lead to more bone-eating cells. Standal also did the opposite, removing sugar from the antibody. This did lead to more bone-eating cells.

The researchers then had sufficient test results to show that too little sugar can be decisive for the number of bone-eating cells. But this is not enough in medical research -- at least not if the goal is to use the knowledge to make medicine for humans.

The next step involved animal experiments with mice that have bone marrow cancer. The mice were divided into two groups and were given two different types of sugar water. In theory, one type of sugar water would lead to more sugar on the antibody.

"The theory actually worked. The mice that received this type of sugar water had smaller perforations in their bone tissue. They also developed less cancer," says Standal.

Now she has to carry out more animal experiments to move forward on the path towards a treatment that can give patients with bone marrow cancer a better life.

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Scientists discover how malaria parasites import sugar

The consumption of sugar is a fundamental source of fuel in most living organisms. In the malaria parasite Plasmodium falciparum, the uptake of glucose is essential to its life cycle. Like in other cells, sugar is transported into the parasite by a transport protein -- a door designed for sugar to pass through the cell membrane. The details in how this door works has now been revealed.

"By elucidating the atomic structure of the sugar-transporting-protein PfHT1, we can better understand how glucose is transported into the parasite," says David Drew, Wallenberg Scholar at the Department of Biochemistry and Biophysics and leading the study at Stockholm University.

The main goal of the research is basic understanding of this important biological process, but with the potential for development of new antimalarial drugs. Malaria kills almost half a million persons each year, according to the WHO. By blocking the door for sugar, it has been shown that one can stop the growth of the malaria parasites.

"It's a long process from a compound with antimalarial activity to a drug that can be taken in the clinic. However, with this knowledge one can improve known antimalarial compounds so that they are more specific to the malarial transporter, so they do not have the side-effect of stopping sugar transport into our own cells. As such, this knowledge increases the likelihood that more specific compounds can be developed into a successful drug," says David Drew.

Despite million's years of evolution between parasites and humans the research show that glucose is surprisingly captured by the sugar transporting protein in malaria parasites in a similar manner as by transporters in the human brain.

"This conservation reflects the fundamental importance of sugar uptake -- basically, nature hit on a winning concept and stuck with it," says David Drew.

However, the malaria parasite is more flexible. Other sugars, such as fructose, can also be imported. This flexibility could give a selective advantage to the malaria parasite so that it can survive under conditions when its preferred energy source glucose is unavailable.

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