Diet-induced Alteration of Intestinal Stem Cell Function (in mice)

“The first thing we noticed was that the small intestine increases greatly in size on the high-calorie diet,” says study leader Anika Böttcher. “Together with Fabian Theis’ team of computational biologists at Helmholtz Munich, we then profiled 27,000 intestinal cells from control diet and high fat/high sugar diet-fed mice. Using new machine learning techniques, we thus found that intestinal stem cells divide and differentiate significantly faster in the mice on an unhealthy diet.” The researchers hypothesize that this is due to an upregulation of the relevant signaling pathways, which is associated with an acceleration of tumor growth in many cancers. “This could be an important link: Diet influences metabolic signaling, which leads to excessive growth of intestinal stem cells and ultimately to an increased risk of gastrointestinal cancer,” says Böttcher.

Helmholtz Zentrum München – German Research Center for Environmental Health. “New link between diet, intestinal stem cells and disease discovered.” ScienceDaily. http://www.sciencedaily.com/releases/2021/11/211119155604.htm (accessed November 27, 2021).

I wonder what Dr. Lustig would say about this study?

Dr. Robert Lustig – The Sugar Pandemic – 2012 Presentation at Yale University and Dr. Robert Lustig on Sugar.

SARS-CoV-2 Variants – (in mice)

Pre-print therefore not peer reviewed. No, I don’t hang out on Twitter all day long. Yes, the study is somewhat geeky. BUT here’s the money sentence:

This abrogation of the species barrier raises the possibility of wild rodent secondary reservoirs and provides new experimental models to study disease pathophysiology and countermeasures.

The B1.351 and P.1 variants extend SARS-CoV-2 host range to mice — https://www.biorxiv.org/content/10.1101/2021.03.18.436013v1

Now I can’t stop thinking about “secondary reservoirs”.

ACE2-interacting domain of SARS-CoV-2

In a study published in the Journal of Neuroimmune Pharmacology, mouse models with COVID-19 showed positive results when a small peptide was introduced nasally. The peptide proved effective in reducing fever, protecting the lungs, improving heart function and reversing cytokine storm — a condition in which an infection triggers the immune system to flood the bloodstream with inflammatory proteins. The researchers also report success in preventing the disease from progression.

Rush University Medical Center. “Potential COVID-19 drug is successful in lab study: Peptide reduced COVID-19 symptoms in mice.” ScienceDaily. http://www.sciencedaily.com/releases/2021/01/210119194322.htm (accessed January 20, 2021).

Journal Reference – Ramesh K. Paidi, Malabendu Jana, Rama K. Mishra, Debashis Dutta, Sumita Raha, Kalipada Pahan. ACE-2-interacting Domain of SARS-CoV-2 (AIDS) Peptide Suppresses Inflammation to Reduce Fever and Protect Lungs and Heart in Mice: Implications for COVID-19 Therapy. Journal of Neuroimmune Pharmacology, 2021; DOI: 10.1007/s11481-020-09979-8

Our neighbor Dr. Arlan Richardson at https://nathanshockcenters.org/oklahoma part of the University of Oklahoma Health Sciences Center knows a lot about mice. I’ll have to ask him what he thinks of the potential of this peptide for human use.

N501Y mutation in SARS-CoV-2 virus causes increased infectivity, disease severity in mice — Science Chronicle

Chinese researchers found N501Y mutation in a mouse-adapted SARS-CoV-2 virus strain. In the mouse model, the N501Y mutation was found to increase the binding affinity of the virus with the mouse ACE2 receptor. The mutation in the mouse-adapted strain also caused increased virulence. In a preliminary report posted on December 19, Dr. Andrew Rambaut from […]

N501Y mutation in SARS-CoV-2 virus causes increased infectivity, disease severity in mice — Science Chronicle

Interesting article and the last paragraphs must be emphasized.

Dr. Gagandeep Kang, Professor of Microbiology at CMC Vellore, however, cautions that emergence of N501Y mutation has been seen on other occasions. According to her, the N501Y mutation in a strain that has been adapted to infect a mouse model cannot be compared with the N501Y mutation seen in the new variant infecting humans. And the severity of diseases caused by the mutation in the mouse model has no relevance to humans, she says.

“At this time, one can only say the mutation increases binding affinity in humans and hence increased transmissibility. Nothing can be said about disease severity,” says Dr. Kang.  

Visceral fat delivers signal to the brain that hurts cognition

“We have identified a specific signal that is generated in visceral fat, released into the blood that gets through the blood brain barrier and into the brain where it activates microglia and impairs cognition.”

Visceral fat delivers signal to the brain that hurts cognition

Quote and article link presented without the usual sarcasm.

Molecule found in oranges could reduce obesity and prevent heart disease and diabetes

In mice, so don’t start gorging on oranges.

Sorry, sarcasm restriction didn’t last long.

Early studies on the diet suggested red wine was a major contributor to the health benefits of the Mediterranean diet because it contains a compound called resveratrol, which activated a certain pathway in cells known to increase lifespan and prevent aging-related diseases. However, work in Mashek’s lab suggests that it is the fat in olive oil, another component of the Mediterranean diet, that is actually activating this pathway.

Olive oil in the diet may also help mitigate aging-related diseases

 

High-protein diets boost artery-clogging plaque

High-protein diets boost artery-clogging plaque, mouse study shows

In mice.

The mice on the high-fat, high-protein diet developed worse atherosclerosis — about 30% more plaque in the arteries — than mice on the high-fat, normal-protein diet, despite the fact that the mice eating more protein did not gain weight, unlike the mice on the high-fat, normal-protein diet.

“This study is not the first to show a telltale increase in plaque with high-protein diets, but it offers a deeper understanding of the impact of high protein with the detailed analysis of the plaques,” Razani said. “In other words, our study shows how and why dietary protein leads to the development of unstable plaques.”

Scientists uncover how high-fat diet drives colorectal cancer growth

In mice.

The research, conducted in a mouse model, suggests how lifestyle and genetics converge. The researchers found that animals with an APC mutation, the most common genetic mutation found in humans with colorectal cancer, developed cancer faster when fed a high-fat diet.

The mice with APC mutations developed benign growths called adenomas. In humans, adenomas are common in the intestine and are routinely removed during colonoscopies. These growths normally take decades to turn into malignant adenocarcinomas. Yet the adenomas in these mice quickly turned cancerous when given high-fat diets.

Longer daily fasting times improve health and longevity (in mice)

The scientists randomly divided 292 male mice into two diet groups. One group received a naturally sourced diet that was lower in purified sugars and fat, and higher in protein and fiber than the other diet. The mice in each diet group were then divided into three sub-groups based on how often they had access to food. The first group of mice had access to food around the clock. A second group of mice was fed 30 percent less calories per day than the first group. The third group was meal fed, getting a single meal that added up to the exact number of calories as the round-the-clock group. Both the meal-fed and calorie-restricted mice learned to eat quickly when food was available, resulting in longer daily fasting periods for both groups.

The scientists tracked the mice’s metabolic health through their lifespans until their natural deaths and examined them post-mortem. Meal-fed and calorie-restricted mice showed improvements in overall health, as evidenced by delays in common age-related damage to the liver and other organs, and extended longevity. The calorie-restricted mice also showed significant improvement in fasting glucose and insulin levels compared to the other groups. Interestingly, the researchers found that diet composition had no significant impact on lifespan in the meal fed and calorie restricted groups.

Source article here.

One of my neighbors is a mouse researcher.  I bet he’s really excited this weekend.

The NIH webpage on caloric restriction and fasting diets is here.

Social Isolation Transforms the Brain

In mice.

Confirming and extending previous observations, the researchers showed that prolonged social isolation leads to a broad array of behavioral changes in mice. These include increased aggressiveness towards unfamiliar mice, persistent fear, and hypersensitivity to threatening stimuli. For example, when encountering a threatening stimulus, mice that have been socially isolated remain frozen in place long after the threat has passed, whereas normal mice stop freezing soon after the threat is removed. These effects are seen when mice are subjected to two weeks of social isolation, but not to short-term social isolation — 24 hours — suggesting that the observed changes in aggression and fear responses require chronic isolation.

Though the work was done in mice, it has potential implications for understanding how chronic stress affects humans.

Get out of the house.  Socialize with friends and family.  Leave the cell phone at home.

Social media is not social.  It’s a serious public health problem for the brainwashed masses with addictive behaviors.

Read the source article here.