Saccharin and acesulfame K are detected by two types of bitter taste receptors from the taste receptor type 2 (TAS2R) family: TAS2R31 and TAS2R43. When investigators measured the inhibitory effects of various compounds against TAS2R31, they found that menthols reduced the responses of TAS2R31-expressing cells to saccharin. Additionally, another compound called (R)-(-)-carvone (which gives spearmint leaves their sweetish minty smell) showed a strong inhibitory effect on TAS2R31 and TAS2R43 after the use of saccharin and acesulfame K.

Unlike menthol, (R)-(-)-carvone did not have a notable cooling sensation. As cooling sensation is often not desirable in food flavoring, (R)-(-)-carvone is a promising candidate for lessening the unpleasant aftertaste of artificial sweeteners.

"The bitter taste inhibitors identified in this study have potential applications in food products, suggesting their utility in enhancing the palatability of foods containing artificial sweeteners," said corresponding author Takumi Misaka, PhD, of the University of Tokyo.

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Researchers at the University of British Columbia have shown that our gut bacteria can feed on these large molecules -- something thought to not be possible -- thanks to enzymes that normally help us break down dietary fiber.

"Researchers assumed that these thickening agents, which are artificial derivatives of natural cellulose, just pass right through the digestive system unaltered," says Dr. Deepesh Panwar, a postdoctoral fellow at the Michael Smith Laboratories and lead author of the study published in the Journal of Bacteriology. "But our study provides a first glimpse at how these food additives are actually digested by our gut bacteria thanks to natural polysaccharides in our diets."

The complex structure of these cellulose derivatives is what makes them valuable as thickening agents in popular products like ketchup, salad dressing and even toothpaste. This structure is also why gut bacteria have a harder time breaking them down -- and why in higher concentrations, they're even used as laxatives.

This new in vitro study, however, shows that if our gut bacteria are 'primed' with natural polysaccharides -- long chains of sugars found in fruits, vegetables and cereals -- the cellulose derivatives can be digested. This is because the natural polysaccharides activate enzymes that are produced on bacteria cell surfaces that can also break down artificial cellulose molecules.

The findings don't challenge the fact that these compounds are safe to consume, proven by years of testing and history of use. However, the new research suggests that more work should be done to explore the physical, chemical and biological effects of the digestion of cellulose derivatives by gut bacteria.

One reason researchers may not have seen this before is because bacteria in the lab are often exposed to polysaccharides, including cellulose derivatives, in isolation, instead of in combinations that mimic our diet. On their own, these cellulose derivatives can't activate the same enzymes, preventing their digestion.

"It was really unexpected for us to see that these cellulose derivatives are in fact used as a source of sugar for bacterial growth," says Dr. Harry Brumer, a professor in the Michael Smith Laboratories and Department of Chemistry. "It is always a surprise when a new finding goes against the conventional wisdom, in this case showing that these common additives are not just inactive thickeners."

Dr. Brumer also notes that the next steps in this research will be to look for this ability in a wider range of human gut bacteria, and eventually explore potential effects on nutrition in people.

So, next time you pair a green salad with a sweet dressing, know that your gut bacteria are hard at work helping to break down all parts of your meal.

However, less attention has been paid to its role in day-to-day situations.

In a study published in Molecular Metabolism, University of Michigan researchers have shown that a specific population of neurons in the hypothalamus help the brain maintain blood glucose levels under routine circumstances.

Over the past five decades, researchers have shown that dysfunction of the nervous system can lead to fluctuations in blood glucose levels, especially in patients with diabetes.

Some of these neurons are in the ventromedial nucleus of the hypothalamus, a region of the brain that controls hunger, fear, temperature regulation and sexual activity.

"Most studies have shown that this region is involved in raising blood sugar during emergencies," said Alison Affinati, M.D., Ph.D., assistant professor of internal medicine and member of Caswell Diabetes Institute.

"We wanted to understand whether it is also important in controlling blood sugar during day-to-day activities because that's when diabetes develops."

The group focused on VMH^Cckbr neurons, which contain a protein called the cholecystokinin b receptor.

They used mouse models in which these neurons were inactivated.

By monitoring the blood glucose levels, the researchers found that VMH^Cckbr neurons play an important role in maintaining glucose during normal activities, including the early part of the fasting period between the last meal of the day and waking up in the morning.

"In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don't become hypoglycemic overnight," Affinati said.

To do so, the neurons direct the body to burn fat through a process called lipolysis.

"In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don't become hypoglycemic overnight."

-Alison Affinati, M.D., Ph.D.

The fats are broken down to produce glycerol, which is used to make sugar.

When the group activated the VMH^Cckbr neurons in mice, the animals had increased glycerol levels in their bodies.

These findings could explain what happens in patients with prediabetes, since they show an increase in lipolysis during the night.

The researchers believe that in these patients, the VMH^Cckbr neurons could be overactive, contributing to higher blood sugar.

These nerve cells, however, only controlled lipolysis, which raises the possibility that other cells might be controlling glucose levels through different mechanisms.

"Our studies show that the control of glucose is not an on-or-off switch as previously thought," Affinati said.

"Different populations of neurons work together, and everything gets turned on in an emergency. However, under routine conditions, it allows for subtle changes."

The team is working to understand how all the neurons in the ventromedial nucleus co-ordinate their functions to regulate sugar levels during different conditions, including fasting, feeding and stress.

They are also interested in understanding how the brain and nervous system together affect the body's control of sugar, especially in the liver and pancreas.

The work was carried out by a team of U-M researchers at the Caswell Diabetes Institute who focus on the neuronal control of metabolism -- the roles played by the brain and nervous system in metabolic control and disease.

Additional authors: Jiaao Su, Abdullah Hashsham, Nandan Kodur, Carla Burton, Amanda Mancuso, Anjan Singer, Jennifer Wloszek, Abigail J. Tomlinson, Warren T. Yacawych, Jonathan N. Flak, Kenneth T. Lewis, Lily R. Oles, Hiroyuki Mori, Nadejda Bozadjieva-Kramer, Adina F. Turcu, Ormond A. MacDougald and Martin G. Myers.

Funding/disclosures: Research support was provided by the Michigan Diabetes Research Center (NIH grant P30 DK020572), the Mouse Metabolic Phenotyping Center -- Live (U2CDK135066) Physiology Phenotyping Core, the Michigan Nutrition and Obesity Center Adipose Tissue Core (P30 DK089503); Department of Veterans Affairs (IK2BX005715); the Warren Alpert Foundation; Endocrine Fellows Foundation; Marilyn H. Vincent Foundation and Novo Nordisk. This work was also supported in part by NIH grant K08 DK1297226.