Tag Archives: #sugar

Having A Sweet Tooth May Be A Good Thing—If You’re A Songbird (Biology)

Study finds songbirds CAN taste sugar

Contrary to conventional thought, songbirds can taste sugar—even though songbirds are the descendants of meat-eating dinosaurs and are missing a key protein that allows humans and many other animals to taste sweetness. An international team investigated how many bird species can taste sweet and how far back that ability evolved. Their work was published today in the journal Science.

The researchers offered two species of songbirds a choice between sugar water and plain water—nectar-taking honeyeaters, as well as canaries, a grain-eating bird not known for consuming sweet foods. They also examined taste receptor responses sampled from a variety of other species. Regardless of whether their main diet consisted of seeds, grains, or insects, songbird taste receptors responded to sugars.

New Holland Honeyeater
New Holland Honeyeater by Gerald Allen, Macaulay Library at the Cornell Lab of Ornithology. © MPIO

“This was a clear hint that we should concentrate on a range of songbirds, not only the nectar-specialized ones, when searching for the origins of avian sweet taste,” explains senior author Maude Baldwin at the Max Planck Institute for Ornithology in Germany. Baldwin led this study with Yasuka Toda from Meiji University in Japan.

Sugar is a vital carbohydrate providing lots of energy and may have had far-reaching effects on songbird evolution. Though it is thought that most bird lineages can’t taste sweetness at all, the scientists now believe that songbirds, which account for more than 40% of the world’s bird species, can actually taste sweet, and that sugary food sources may have contributed to their success.

Baldwin and Toda dug down to the molecular level to understand the modifications to the “umami” taste receptor that enabled sweet perception among songbirds.

“Because sugar detection is complex, we needed to analyze more than one hundred receptor variants to reveal the molecular mechanisms underlying the sugar responses,” says Toda. These exact changes coincide only slightly with those seen in the distantly-related hummingbirds, even though similar areas of the receptor are modified.

Though songbirds evolved similar workarounds to taste sweetness, they did so at different times, in different places, and in slightly different ways—an example of “convergent evolution.” Some songbirds, such as honeyeaters, sunbirds, honeycreepers, and flowerpiercers are now just as dependent on nectar as the hummingbirds.

“This study fundamentally changes the way we think about the sensory perceptions of nearly half the world’s birds,” says study co-author Eliot Miller at the Cornell Lab of Ornithology. “It demonstrates that most songbirds definitely can taste sweet and got there by following nearly the same evolutionary path that hummingbirds did—it’s a neat story about how convergence happens.”

This model shows the convergent evolution of sweet perception. Songbirds and hummingbirds independently evolved to taste sweetness using the savory (umami) taste receptor. This makes up for their lack of the T1R2 protein that allows humans and many other mammals to taste sweetness. Yasuka Toda et. al, Early origin of sweet perception in the songbird radiation. Science. July 9, 2021

Exploring the songbird family tree, the researchers conclude that songbirds evolved to sense sweetness approximately 30 million years ago, before the early ancestors of songbirds left Australia, where all songbirds originated. Even after songbirds radiated across the world, they kept their ability to taste sugar.

Researchers in Japan, Germany, the United States, Hong Kong, and Australia participated in this study. Future studies will explore how sweet perception has coevolved with other physiological traits, such as changes in digestion and metabolism, across bird evolution.

Featured image: New Holland Honeyeater by Gerald Allen, Macaulay Library at the Cornell Lab of Ornithology © MPIO

Yasuka Toda, Meng-Ching Ko, Qiaoyi Liang, Eliot T. Miller, Alejandro Rico-Guevara, Tomoya Nakagita, Ayano Sakakibara, Kana Uemura, Timothy Sackton, Takashi Hayakawa, Simon Yung Wa Sin, Yoshiro Ishimaru, Takumi Misaka, Pablo Oteiza, James Crall, Scott V. Edwards, William Buttemer, Shuichi Matsumura and Maude W. Baldwin (2021). Early origin of sweet perception in the songbird radiation. Science. July 9, 2021.
DOI: 10.1126/science.abf6505

Provided by MPIO

Low Levels of A Simple Sugar – A New Biomarker for Severe MS? (Medicine)

Researchers from the ECRC in Berlin, together with scientists from the United States and Canada, have discovered a sugar molecule whose levels are reduced in the blood of patients with particularly severe multiple sclerosis. Their discovery could pave the way for a new therapeutic approach, the team reports in medical journal JAMA Neurology.

Multiple sclerosis, or MS for short, manifests itself slightly differently in each person – which is why some call it “the disease of a thousand faces.” Arguably the worst manifestation of MS is its chronic progressive form. Unlike the more common relapsing-remitting variant (RRMS), in which sufferers are often symptom-free for months or even years, patients with the primary progressive form of the disease (PPMS) see their condition steadily deteriorate with no remissions.

Poorly insulated neurons die off

“We were able to show that, in this particularly severe form of the disease, there are significantly lower concentrations of N-acetylglucosamine in the blood serum than there are in healthy people or patients with relapsing-remitting MS.”

— Dr. Alexander Brandt, First author of the study

Today’s therapeutic approaches are based on the assumption that the immune system is making a mistake and waging an inappropriate attack on the layer of myelin that surrounds and insulates the nerve cells’ long, cable-like branches called axons. “In progressive MS, neurodegenerative processes steadily multiply and cause more and more neurons in the brain and spinal cord to die,” explains Dr. Alexander Brandt, lead author of the study that has now been published in the journal JAMA Neurology. “However, we still do not know what exactly causes this disease variant.” 

Together with Professor Friedemann Paul from the Experimental and Clinical Research Center (ECRC ), a joint institution of Charité – Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), as well as eleven colleagues from Berlin, Irvine and Toronto, Brandt now hopes he has shed some more light on the subject. As the team reports in their study, it appears that the simple sugar N-acetylglucosamine, or GlcNAc for short, could play an important role in the development of progressive MS. Inside an organism, GlcNAc and other sugar molecules attach to proteins on the cell surface in the form of chains. This mechanism, which is known as glycosylation, controls various cell functions by forming branched structures from these sugar chains.

The sugar molecule could serve as a biomarker

“We studied 120 subjects from Irvine and were able to show that, in this particularly severe form of the disease, there are significantly lower concentrations of N-acetylglucosamine in the blood serum than there are in healthy people or patients with relapsing-remitting MS,” reports Brandt. At the time of this study, the physician was head of the Translational Neuroimaging laboratory in Paul’s Clinical Neuroimmunology group at Charité. Brandt has since moved to the School of Medicine at the University of California, Irvine (UCI) as an associate professor of neurology, but remains a guest researcher at Charité.

“In another study of 180 patients from Berlin with relapsing-remitting or progressive MS, we also found that low serum levels of GlcNAc are associated with the development of the progressive form of the disease, clinical disability and neurodegeneration,” adds the study’s corresponding author, Professor Michael Demetriou of UC Irvine. “This opens up potential new avenues for identifying, at an early stage, which patients are at higher risk of progressive MS and adjusting their treatment accordingly.”

Human treatment studies now in the pipeline

Our study opens up potential new avenues for identifying, at an early stage, which patients are at higher risk of progressive MS and adjusting their treatment accordingly.

— Dr. Michael Demetriou, corresponding author of the study

Back in autumn 2020, Brandt, Demetriou and other researchers working with the then lead author Dr. Michael Sy from UC Irvine published a study in the Journal of Biological Chemistry. They had administered GlcNAc to lactating mice and found that the animals passed on this simple sugar, which incidentally is also contained in human breast milk, to their offspring. This stimulated primary myelination of the neuronal axons in the young animals. “We also observed in the mouse experiments that N-acetylglucosamine activates myelin progenitor cells, thus promoting both primary myelination and the repair of damaged myelin,” says Brandt.

The researchers therefore hope that GlcNAc not only has potential as a suitable biomarker for progressive MS, but could also pave the way for new therapeutic strategies. “Our hope is that we can use GlcNAc and the associated glycosylation mechanism to promote myelin repair and thus reduce neurodegeneration,” summarizes Brandt. An initial, as-yet-unpublished phase I trial has just been completed with around 30 subjects, where the scientists investigated the safety of taking GlcNAc in certain doses. If it is shown to be safe, the scientists hope to be able to conduct further studies into this simple sugar’s possible efficacy as an MS therapy.

This study was funded in part by a grant from the National Institute of Allergy and Infectious Disease and the National Center for Complimentary and Integrative Health as well as the German Excellence Cluster NeuroCure.


Alexander Brandt et. al. (2021): „Association of a Marker of N-Acetylglucosamine With Progressive Multiple Sclerosis and Neurodegeneration“, JAMA Neurology, DOI:10.1001/jamaneurol.2021.1116

Provided by MDC Berlin

Less Sugar, Please! New Studies Show Low Glucose Levels Might Assist Muscle Repair (Biology)

Skeletal muscle satellite cells found to grow better with less glucose in vitro

Researchers from Tokyo Metropolitan University have shown that skeletal muscle satellite cells, key players in muscle repair, proliferate better in low glucose environments. This is contrary to conventional wisdom that says mammalian cells fare better when there is more sugar to fuel their activities. Because ultra-low glucose environments do not allow other cell types to proliferate, the team could produce pure cultures of satellite cells, potentially a significant boost for biomedical research.

Healthy muscles are an important part of a healthy life. With the wear and tear of everyday use, our muscles continuously repair themselves to keep them in top condition. In recent years, scientists have begun to understand how muscle repair works at the cellular level. Skeletal muscle satellite cells have been found to be particularly important, a special type of stem cell that resides between the two layers of sheathing, the sarcolemma and basal lamina, that envelopes myofiber cells in individual muscle fibers. When myofiber cells get damaged, the satellite cells go into overdrive, multiplying and finally fusing with myofiber cells. This not only helps repair damage, but also maintains muscle mass. To understand how we lose muscles due to illness, inactivity, or age, getting to grips with the specific mechanisms involved is a key challenge for medical science.

A team of scientists from Tokyo Metropolitan University led by Assistant Professor Yasuro Furuichi, Associate Professor Yasuko Manabe and Professor Nobuharu L Fujii have been studying how skeletal muscle satellite cells multiply outside the body. Looking at cells multiplying in petri dishes in a growth medium, they noticed that higher levels of glucose had an adverse effect on the rate at which they grew. This is counterintuitive; glucose is considered to be essential for cellular growth. It is converted into ATP, the fuel that drives a lot of cellular activity. Yet, the team confirmed that lower glucose media led to a larger number of cells, with all the biochemical markers expected for greater degrees of cell proliferation.

They also confirmed that this doesn’t apply to all cells, something they successfully managed to use to their advantage. In experiments in high glucose media, cultures of satellite cells always ended up as a mixture, simply due to other cell types in the original sample also multiplying. By keeping the glucose levels low, they were able to create a situation where satellite cells could proliferate, but other cell types could not, giving a very pure culture of skeletal muscle satellite cells. This is a key prerequisite for studying these cells in a variety of settings, including regenerative medicine. So, was the amount of glucose in their original experiment somehow “just right”? The team added glucose oxidase, a glucose digesting enzyme, to get to even lower levels of glucose, and grew the satellite cells in this glucose-depleted medium. Shockingly, the cells seemed to fare just fine, and proliferated normally. The conclusion is that these particular stem cells seem to derive their energy from a completely different source. Work is ongoing to try to pin down what this is.

The team notes that the sugar levels used in previous experiments matched those found in diabetics. This might explain why loss of muscle mass is seen in diabetic patients, and may have significant implications for how we might keep our muscles healthier for longer.

This work was supported by JSPS KAKENHI Grants-in-Aid of Scientific Research (18K19751, 20H04079, 17H02159, 18H04086), Sumitomo Dainippon Pharma Co., Ltd., and the Uehara Memorial Foundation.

Featured image: Reducing glucose concentration enhances cell proliferation of muscle stem cells, suggesting that excess glucose impedes cell proliferation capacity. © Tokyo Metropolitan University

Reference: Yasuro Furuichi, “Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions”, Front. Cell Dev. Biol., 01 March 2021 | https://doi.org/10.3389/fcell.2021.640399

Provided by Tokyo Metropolitan University

Sugar Not So Nice For Your Child’s Brain Development (Food)

New research shows how high consumption affects learning, memory

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.

Emily Noble in her lab. (Photo by Cal Powell)

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.

“The question now is how do these populations of bacteria in the gut alter the development of the brain?” Noble said. “Identifying how the bacteria in the gut are impacting brain development will tell us about what sort of internal environment the brain needs in order to grow in a healthy way.”

The article, “Gut microbial taxa elevated by dietary sugar disrupt memory function,” appears in Translational Psychiatry. Scott Kanoski, associate professor in USC Dornsife College of Letters, Arts and Science, is corresponding author on the paper.

Additional authors on the paper are Elizabeth Davis, Linda Tsan, Clarissa Liu, Andrea Suarez and Roshonda B. Jones from the University of Southern California; Christine Olson, Yen-Wei Chen, Xia Yang and Elaine Y. Hsiao from the University of California-Los Angeles; and Claire de La Serre and Ruth Schade from UGA.

Provided by University of Georgia

Circadian Clock Gene Rev-erb Linked to Dawn Phenomenon in Type 2 Diabetes (Medicine)

Researchers at Baylor College of Medicine may have found an explanation for dawn phenomenon, an abnormal increase of blood sugar only in the morning, observed in many patients with type 2 diabetes.

Researchers at Baylor College of Medicine, Shandong University in China and other institutions may have found an explanation for dawn phenomenon, an abnormal increase of blood sugar only in the morning, observed in many patients with type 2 diabetes. They report in the journal Nature that mice lacking the circadian clock gene called Rev-erb in the brain show characteristics similar to those of dawn phenomenon.

The researchers then looked at Rev-erb gene expression in patients with type 2 diabetes comparing a group with dawn phenomenon to a group without it and found that the gene’s expression followed a different temporal pattern between these two groups. The findings support the idea that an altered daily rhythm of expression of the Rev-erb gene may underlie dawn phenomenon. Future investigations may lead to therapies.

“We began this study to investigate what was the function of Rev-erb in the brain,” said co-corresponding author Dr. Zheng Sun, associate professor of medicine-endocrinology, diabetes and metabolism at Baylor. “We are interested in this gene because it is a ‘druggable’ component of the circadian clock with potential applications in the clinic. Rev-erb is expressed only during the day but not at night. When we started, we did not know where this was going to lead us.”

The researchers first developed a mouse model by knocking out the Rev-erb gene in GABA neurons. They chose this approach because the gene’s expression is highly enriched in a particular brain area called the suprachiasmatic nucleus that is mainly composed of GABA neurons.

An unexpected finding

“We observed something very interesting in these mice,” Sun said. “They were glucose intolerant – that is they had high glucose levels – only in the evening. Mice are nocturnal, meaning that they become active in the evening as people do in the morning.”

When the body awakes and takes in food, insulin is secreted from the pancreas to signal the body to lower blood sugar. Insulin is more effective in doing this job upon waking than at other times of the day. This high insulin sensitivity is probably because the body is anticipating feeding behaviors upon waking up. In mice, high insulin sensitivity occurs in the evening, while in people it occurs in the morning.

Sun and his colleagues found that the abnormal higher glucose levels observed in the evening in Rev-erb knockout mice resulted from an insufficient suppression of liver glucose production by insulin. Their data demonstrate an essential role of neural Rev-erb in regulating the hepatic insulin sensitivity rhythm independent of eating behaviors or basal hepatic glucose production.

Next, the researchers looked to understand how defects in Rev-erb gene expression in the brain can result in changes in the ability of the liver to respond to insulin. They discovered that the suprachiasmatic nucleus GABA neurons in Rev-erb knockout mice had a higher firing activity than those neurons of normal mice when the animals woke up, and that this neuronal hyperactivity was sufficient and necessary to cause glucose intolerance in the evening. In normal mice, these GABA neurons drop their firing activity in the evening, lowering sugar blood levels. Interestingly, by re-expressing Rev-erb back in the knockout mice, the researchers found that Rev-erb expression is only needed during the day, but not needed at night, which is in line with the highly oscillatory expression pattern of endogenous Rev-erb in normal condition.

Connecting with dawn phenomenon

Mice having higher glucose levels in the evening reminded Sun and his colleagues of dawn phenomenon observed in people with type 2 diabetes. “Given the similarities of the phenomenon in mice and people, we thought that maybe this gene that we are studying could be linked to the biology of dawn phenomena in diabetic patients,” said Sun, a member of Baylor’s Dan L Duncan Comprehensive Cancer Center and the Huffington Center on Aging.

In collaboration with Qilu Hospital of Shandong University in China, the researchers followed 27 type2 diabetes patients with continuous glucose monitoring. They found that, although the patients had diabetes with similar severity in terms of their basal glucose levels, obesity and other parameters, about half of the patients had dawn phenomenon while the other half did not.

“We collected the patients’ blood at different times of the day and determined the expression of the Rev-erb gene in white blood cells, which has been reported to correlate well with the central clock in the brain,” Sun said. “Interestingly, we found that the gene’s expression followed a temporal pattern that was different between those with dawn phenomenon and those without,” Sun said. “We propose that the altered temporal pattern of expression of this gene may explain dawn phenomena in people. It is possible that, in the future, a drug might be used to regulate this gene to treat the condition. But that’s a long shot.”

See the publication for a complete list of the contributors to this work and the financial sources of support.

Reference: Ding, G., Li, X., Hou, X. et al. REV-ERB in GABAergic neurons controls diurnal hepatic insulin sensitivity. Nature (2021). https://doi.org/10.1038/s41586-021-03358-w

Provided by Baylor College of Medicine

How SARS-CoV-2’s Sugar-Coated Shield Helps Activate the Virus? (Biology)

SARS-CoV-2, the virus that causes COVID-19, is coated with sugars called glycans, which help it evade the immune system. New research shows precisely how those sugars help the virus become activated and infectious and could help with vaccine and drug discovery.

One thing that makes SARS-CoV-2, the virus that causes COVID-19, elusive to the immune system is that it is covered in sugars called glycans. Once SARS-CoV-2 infects someone’s body, it becomes covered in that person’s unique glycans, making it difficult for the immune system to recognize the virus as something it needs to fight. Those glycans also play an important role in activating the virus. Terra Sztain-Pedone, a graduate student, and colleagues in the labs of Rommie Amaro at the University of California, San Diego and Lillian Chong at the University of Pittsburgh, studied exactly how the glycans activate SARS-CoV-2. Sztain-Pedone will present the research on Thursday, February 25 at the 65th Annual Meeting of the Biophysical Society.

For SARS-CoV-2 to become activated and infectious, the spike proteins on the outside of the virus need to change shape so it can stick to our cells. Scientists knew that the glycans that coat these spikes help SARS-CoV-2 evade the immune system, but it was not known what role they played in the activation process. Studying these molecules is tricky because they are so small and have many parts that move in subtle ways. “There are half a million atoms in just one of these spike protein simulations,” Sztain-Pedone explained.

Using advanced High Performance Computing algorithms that run many simulations in parallel, the research team examined how the positions of each of those atoms changes as the SARS-CoV-2 spike becomes activated. “Most computers wouldn’t be able to do this with half a million atoms,” Sztain-Pedone says.

The team was able to identify the glycans and molecules that are responsible for activating the spike protein. “Surprisingly, one glycan seems to be responsible for initiating the entire opening,” Sztain-Pedone says. Other glycans are involved in subsequent steps. To validate their findings, the team is currently working with Jason McLellan, a professor at the University of Texas, Austin, and colleagues who are performing experiments with spike proteins in the lab.

There is potential to use the simulations developed by Sztain-Pedone and colleagues to identify treatments that will block or prevent SARS-CoV-2 activation. “Because we have all these structures, we can do small molecule screening with computational algorithms,” Sztain-Pedone explained. They can also study new virus mutations, such as the B.1.1.7 variant that is currently spreading, to “look at how that might affect the spike protein activation,” Sztain-Pedone says.

Featured image: Image of the SARS-CoV-2 spike in the active position. Dark blue glycans shield the spike from the immune system, participate in activation, and stabilize the active form. The receptor binding domain changes shape in order to bind human cells is shown in cyan. Image credit: Lorenzo Casalino, Amaro Lab, UCSD.

Provided by Biophysical Society

The Regulatory Network of Sugar and Organic Acid in Watermelon Fruit is Revealed (Botany / Agriculture)

Recently, the innovation project watermelon and melon cultivation and physiology team of Zhengzhou Fruit Research Institute has made new progress in the metabolism regulation of sugar and organic acid in watermelon fruit. The changes of sugar and organic acid during the fruit development were analyzed and the key gene networks controlling the metabolism of sugar and organic acid during the fruit development were identified. These results provided a theoretical basis for watermelon quality breeding, which had important scientific significance for the development of watermelon industry and the improvement of watermelon breeding level in China. The related research results were published in the journals of Horticulture Research and Scientia Horticulturae.

Figure 1 Gene networks and key candidate genes involved in sugar and organic acid regulation during watermelon fruit development © Zhengzhou Fruit Research Institute

The sensory quality of watermelon fruit is determined by the content of sugar and organic acid, which determines the taste of watermelon during the development and maturation of watermelon fruit. The sweet watermelon ‘203Z’ and sour watermelon ‘SrW’ of its isogenic line were used as materials, the genes and gene networks co-expressed with glycolic acid metabolism were searched through WGCNA analysis of transcriptional and metabolite data. Three gene expression networks were identified, including 2443 genes that were highly correlated with sugar and organic acid metabolism in watermelon fruits. Seven key genes involved in sugar and organic acid metabolism of watermelon fruits were screened by significance and qRT-PCR analysis. Among them, Cla97C01G000640, Cla97C05G087120 and Cla97C01G018840 were sugar transporters. Cla97C03G064990 was a sucrose synthase. Cla97C07G128420, Cla97C03G068240 and Cla97C01G008870 were highly correlated with malic acid and citric acid, which were the transporters and regulators of malic acid and citric acid. These genes were verified in the natural population, and the results showed that the expressions of these 7 genes were significantly positively correlated with the contents of sugar and organic acid in watermelon fruit.

These researches were funded by the Agricultural Science and Technology Innovation Program (CAAS-ASTIP-2016-ZFRI-07), National Key R&D Program of China (2018YFD0100704), the China Agriculture Research System (CARS-25-03) and the National Nature Science Foundation of China (31672178 and 31471893).

Reference: Umer, M.J., Bin Safdar, L., Gebremeskel, H. et al. Identification of key gene networks controlling organic acid and sugar metabolism during watermelon fruit development by integrating metabolic phenotypes and gene expression profiles. Hortic Res 7, 193 (2020). https://www.nature.com/articles/s41438-020-00416-8 https://doi.org/10.1038/s41438-020-00416-8

Provided by Nanjing Agriculture University the Academy of Sciences

Sugars Influence Cell-to-surface Adhesion (Biology)

Biotechnologists measure the forces with which algae cells adhere to surfaces and move on them.

How can cells adhere to surfaces and move on them? This is a question which was investigated by an international team of researchers headed by Prof. Michael Hippler from the University of Münster and Prof. Kaiyao Huang from the Institute of Hydrobiology (Chinese Academy of Sciences, Wuhan, China). The researchers used the green alga Chlamydomonas reinhardtii as their model organism. They manipulated the alga by altering the sugar modifications in proteins on the cell surface. As a result, they were able to alter the cellular surface adhesion, also known as adhesion force. The results have now been published in the open access scientific journal “eLife”.

Using TIRF microscopy, Flagella-mediated adhesion can be visualized and analysed.
© Lara Hoepfner

Background and methodology

In order to move, the green alga has two thread-like flagella on its cell surface. The alga actually uses these flagella for swimming, but it can also use them to adhere to surfaces and glide along them. The researchers now wanted to find out how movement and adhesion on the part of the alga can be manipulated. “We discovered that proteins on cell surfaces that are involved in this process are modified by certain sugars. If these sugar chains on the proteins are altered, this enables their properties to be altered,” explains Michael Hippler from the Institute of the Biology and Biotechnology of Plants at Münster University. Experts then describe such proteins as being N-glycosylated – a modification in which carbohydrates are docked onto amino groups. Alterations to these sugar modifications by genetically manipulating the algae showed that the adhesion force of the algae and, as a result, any adhesion to surfaces were reduced. At the same time, there was no change in the cells gliding on the surface. The much-reduced force with which the mutants adhere to surfaces is therefore still sufficient, under laboratory conditions, to enable gliding to take place.

Flagella-mediated adhesion and gliding by Chlamydomonas reinhardtii (green alga) on a solid surface (top). Using TIRF microscopy, these dynamics can be visualized and analysed (bottom). © Lara Hoepfner

In order to study these processes, the researchers first used so-called insertional mutagenesis and the CRISPR/Cas9 method to deactivate genes which encode enzymes relevant to the N-glycosylation process. “The next step was to analyse the sugar modifications of these genetically altered algae strains using mass spectrometry methods,” says Michael Hippler, explaining the team’s approach. In order to visualise the cell-gliding, the researchers used a special method of optical microscopy – total internal reflection fluorescence microscopy (TIRF). This method is frequently used to carry out examinations of structures which are located very close to a surface. For this purpose, a fluorescent protein was expressed in the flagella of the algae in order to make the flagella and the cell-gliding visible.

In order to measure how much force was used in adhering the individual cells to the surface, atomic force microscopy was used and micropipette adhesion measurements were undertaken in collaboration with groups at the University of Liverpool (UK) and the Max Planck Institute of Dynamics and Self-Organization in Göttingen. “This enabled us to verify that adhesion forces in the nanometre range are reduced by altering the protein sugar modifications,” adds Kaiyao Huang.

The two flagella on the green alga resemble for example not only the flagella of sperm but also other movable flagella. These are usually called ‘cilia’ and are also found in the human body – for example in the respiratory tracts. “If we transfer our findings to human cells, sugar-modified proteins could be used to change the interaction of sperm or cilia with all sorts of surfaces,” say Kaiyao Huang and Michael Hippler.

Research participants

Besides researchers from the University of Münster, scientists from Berlin’s Humboldt University, the Universities of Wuhan (China) and Liverpool (England) and the Max Planck Institute of Dynamics and Self-Organization in Göttingen contributed to the study.


The study received financial support from the German Research Foundation (DFG) and the National Nature Science Foundation of China, as well as from the Royal Society and the Biotechnology and Biological Sciences Research Council in the UK.

References: Nannan Xu, Anne Oltmanns, Longsheng Zhao, Antoine Girot, Marzieh Karimi, Lara Hoepfner, Simon Kelterborn, Martin Scholz, Julia Beißel, Peter Hegemann, Oliver Bäumchen, Lu-Ning Liu, Kaiyao Huang, Michael Hippler (2020). Altered N-glycan composition impacts flagella mediated adhesion in Chlamydomonas reinhardtii. eLife. DOI: 10.1101/2020.05.18.102624 https://elifesciences.org/articles/58805

Provided by WMU Munster

Sweet Taste Reduces Appetite? (Food)

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.”

“So there is still a lot of research needed to clarify the complex relationships between sugar consumption, taste receptors and satiety regulation on the molecular level,” says Veronika Somoza. In particular, as sweet receptors are also found in the digestive tract and little is known about their function there. The first steps have nevertheless been taken.

References : Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects: Schweiger K et al., Nutrients 2020, 12(10), 3133; https://www.mdpi.com/2072-6643/12/10/3133

Provided by University of Vienna