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Category: food

A fresh approach to peppermint: 250 new variants could boost flavor and fight disease

The genomics of peppermint are not as fresh as their flavor but scientists from the University of California, Davis, have found a way to breathe new genetic variation into the species. The findings, published in the Proceedings of the National Academy of Sciences, could help the mint industry develop new varieties of peppermint and provide a roadmap for improving clonal crops more generally.

Similar to strawberries, potatoes and many fruit trees, peppermint plants (Mentha × piperita) are reproduced asexually by a process called clonal propagation. In the case of peppermint, this means that their genomes have remained unaltered for more than 200 years. This lack of genetic variation leaves them susceptible to disease and means that properties such as yield and flavor have remained stagnant.

UC Davis plant biologists used radiation to induce mutations in the leading peppermint clone grown in the United States, resulting in more than 250 new and genetically distinct variants. Altogether, they introduced 1,406 large genetic mutations, which can now be used to identify key genes for breeding or selecting new and superior peppermint varieties.

A neuropeptide regulates cell non-autonomous protein homeostasis

FLP-17’s role in stress resistance aligns with its established functions. FLP-17 belongs to an evolutionarily conserved class, FMRF-amide/RF-amide neuropeptides, that plays important roles in energy balance and reproduction across phyla.34,35 In C. elegans, FLP-17 is secreted from a pair of sensory neurons (BAG) in response to low oxygen and high carbon dioxide, which can be caused by unfavorable food conditions or pathogens.36,37 FLP-17 then acts through specific neurons to inhibit egg laying and initiate an aversion behavior until the animal has reached more favorable conditions.30,36 Interestingly, unfavorable food conditions and pathogens also threaten organismal protein homeostasis.33,38 Therefore, we speculate that FLP-17 evolved to simultaneously protect the animal from proteotoxic stress while facilitating a behavioral program to help the animal navigate to more favorable conditions.

To coordinate adaptive behavioral and metabolic responses, FLP-17 primarily signals through the GPCR EGL-6 in specific neurons.30,31 Therefore, we tested whether EGL-6 also mediates FLP-17’s role in UPRER activation and found that FLP-17-induced activation of the UPRER and ER stress resistance is partially dependent on EGL-6. Egl-6 expression is predominantly neuronal, evidenced by transcriptional reporters and single-cell RNA-seq datasets.30,39 However, low levels of egl-6 expression were detected in intestine-specific translation of ribosome-affinity purification, which may better reflect protein levels.40 This suggests that FLP-17 may signal either through an intermediate cell type (such as a neuron) or directly to the intestine to activate UPRER.30,39 Furthermore, the partial dependence, combined with persistent stress gene activation in egl-6 (lof) backgrounds (Figure 5 E), indicates that additional unidentified receptors and mechanisms likely contribute to FLP-17 phenotypes.

Although FLP-17 was sufficient to activate the UPRER, it was not required for cell non-autonomous activation of the UPRER by glial:: xbp-1s, as flp-17 null mutants did not suppress glial:: xbp-1s phenotypes. This likely reflects neuropeptide network redundancy. Supporting this hypothesis, flp-17 (lof)) resulted in modest upregulation of stress response genes (Figure S3G) and a slight increase in hsp-4p::GFP in the glial:: xbp-1s animals (Figure 2D), suggesting compensatory activation of stress signaling pathways when FLP-17 is absent. This compensation could occur through multiple mechanisms. First, glial:: xbp-1s may induce multiple neuropeptides that provide functionally redundant UPRER activation. While no other candidate from our neuropeptidomics screen was individually sufficient to induce UPRER, we cannot exclude compensation by peptides not detected in our analysis, such as insulin-like peptides.

How Intestinal Aging Encourages Harmful Bacteria

In Aging Cell, researchers have elucidated the relationship between intestinal aging and age-related changes to the gut microbiome.

Two interdependent biologies

The human gut works through the interaction of two entirely different sets of cells. The first is the body’s actual cells, including the intestinal barrier between the gut and the rest of the body, various types of ordinary immune cells, and Peyer’s patches with follicle-associated epithelium (FAE) areas that contain microfold cells (M cells), which perform crucial immunoregulatory tasks [1]. The second is the gut microbiome, the various types of bacteria that help us digest food.

Scientists Say This Simple Supplement May Actually Reverse Heart Disease

Scientists in Japan say a common supplement may actually help “unclog” certain diseased heart arteries from the inside out.

A simple food supplement sold in Japan may have helped reverse a dangerous form of heart disease that often resists standard treatment, according to researchers at Osaka University. The findings, originally published in the European Heart Journal, continue to attract attention because they describe something rarely seen in cardiology: clogged heart arteries becoming noticeably clearer after a nutritional intervention rather than conventional cholesterol lowering alone.

Scientists target a hidden form of heart disease.

Digital therapy outperforms referrals to campus clinics among college students

College students with anxiety, depression and eating disorders may be more likely to start and to respond more positively to therapy offered via a digital app compared to referrals to in-person campus clinics, according to a study led by Penn State researchers and published in the journal Nature Human Behaviour.

Globally, an estimated 40% to 60% of college students experience a mental health disorder at some point, and the need for campus counseling services has increased faster than institutions’ capacity to provide these services, according to the researchers.

The research team wanted to see if a proactive intervention using a digital therapy app could effectively treat anxiety disorders, depression and eating disorders, as well as address the increased need for psychological services.

Harmless viruses trap Salmonella on flexible polymer in portable microfluidic sensor

Researchers at Worcester Polytechnic Institute (WPI) have developed a solid polymer coated with harmless viruses to detect the bacteria Salmonella enterica (S. enterica), an advance that could lead to new ways of finding contamination in the food supply. The work is published in the journal ACS Applied Bio Materials.

The group, led by Yuxiang “Shawn” Liu, an associate professor in the Department of Mechanical and Materials Engineering, reports that the technology can rapidly capture and visualize foodborne bacterial contaminants in tiny fluid samples. With no need for incubation or complicated equipment in research centers, the technology has the potential to be used as a rapid biosensor in field applications and in areas with few resources.

“We have a solid surface that can be used anywhere in the food supply chain, from farm to fridge, to detect foodborne bacteria with minimum human intervention,” Liu says.

FDA Approves Novel Weekly Basal Insulin for T2D

The FDA has approved once-weekly insulin icodec-abae (Awiqli; Novo Nordisk) for use in adults with type 2 diabetes (T2D), with a current projected launch in the second half of 20,261 for the 700-units/mL dose. This novel treatment option is a first-in-its-class therapeutic, freeing patients living with T2D from their strict schedule of daily basal insulin injections and reducing total injections from 7 to 1 for each 7-day period.

Its indication is as an adjunct to diet and exercise for improved glycemic control, as well as for patients also taking mealtime insulin or another common oral antidiabetic agent and/or a glucagon-like peptide-1 receptor agonist. A prescription is required, and administration is with or without food via a prefilled FlexTouch device on the same day each week.

Data from 4 of the trials in the phase 3a ONWARDS program and 2,680 adult patients with uncontrolled T2D support this approval; their primary end point of interest was reduction in hemoglobin A1c. Overall, the ONWARDS program encompasses 6 phase 3a trials and more than 4,000 adults with type 1 diabetes (T1D) or T2D.

Insulin icodec-abae (Awiqli; Novo Nordisk) is now approved for use in the US, Canada, European Union, Switzerland, and 12 other countries.

A brain reward circuit inhibited by next-generation weight-loss drugs in mice

New research using humanized mouse models has finally pulled back the curtain on how these small-molecule drugs work in the brain, revealing that they don’t just tell the body it’s full—they actually change how we perceive “treats.”

1. The Homeostatic Circuit: This is the body’s fuel gauge. It involves the hypothalamus and hindbrain, which manage basic hunger and energy levels. It’s the circuit that tells you, “I’ve had enough calories for today.”

These new weight-loss pills do more than just settle your stomach; they speak directly to the brain’s reward center to help quiet the “food noise” that leads to overeating.

This is a “proof of concept” study. It proves the mechanism exists, but it doesn’t yet guarantee that a pill will be a side-effect-free “cure” for overeating in humans.

Humanized glucagon-like peptide 1 receptor (GLP1R) mouse models are used to investigate the neural circuitry through which small-molecule GLP1R agonists modulate feeding, with implications for how these orally delivered weight-loss drugs engage brain reward circuits.

New DNA-Based Therapy Can Help Lower ‘Bad Cholesterol’ Without Statins, Finds Study

Scientists may have found a powerful new way to lower “bad” cholesterol, which did not involve the use of statin medicines. In a recent study, researchers used tiny DNA-based molecules to cut levels of LDL (bad) cholesterol by nearly 50% in animal models. This was done without the side effects that are often linked to statins. If these results stay consistent in large human trials, the therapy could become an important option for people who cannot tolerate statins or who still have high cholesterol despite taking them. The study was led by Carles J. Ciudad and Veronica Noe from the University of Barcelona’s Faculty of Pharmacy and Food Sciences and the Institute of Nanoscience and Nanotechnology (IN2UB), working with Nathalie Pamir at the University of Oregon in Portland (United States). It was published in the journal Biochemical Pharmacology.

High LDL cholesterol is one of the biggest risk factors for heart attacks and strokes because it leads to the build up fatty plaques in arteries. Drugs like statins work well for many, but some people suffer from muscle aches, digestive issues, or liver problems and have to stop them. However, the new approach is different. Instead of changing how the liver handles fats, it targets a specific protein in the blood that controls how much LDL stays circulating.

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