Research & 
Publications

Although vertebrates cannot synthesize the natural disaccharide trehalose, exogenous administration of trehalose to mammalian cells may be beneficial for protein misfolding disorders. In this issue, DeBosch et al. show that trehalose may also be useful in treating nonalcoholic fatty liver disease and identify inhibition of cellular glucose import through SLC2A (also known as GLUT) transporters as a mechanism by which trehalose stimulates autophagy through the adenosine monophosphate–activated protein kinase (AMPK).

The accumulation of lipids in hepatocytes that occurs in nonalcoholic fatty liver disease (NAFLD) can result in liver failure or liver cancer. Trehalose is a ubiquitous sugar that is present in the food consumed by animals. DeBosch et al. determined that trehalose blocked glucose uptake into cells by inhibiting glucose transporters in the plasma membrane, which induced a “starvation”-like response that activated autophagy even in the presence of adequate nutrients and glucose. Furthermore, providing trehalose to mice that are a model of NAFLD prevented lipid accumulation in the liver. As noted by Mardones et al. in the associated Focus, trehalose, which has been previously under investigation to treat neurodegenerative diseases characterized by toxic protein aggregates, may be a “silver bullet” for treating diseases resulting from inadequate cellular degradative metabolism.

Currently, it has been shown that there are differences in the regulation of the functioning of normal and tumour cells. Based on this, the term “cell reprogramming” was introduced, meaning the formation of a malignant phenotype. One of the factors that differs in the functioning of normal and tumour cells is the reduced pH level observed in tumour tissue (acidosis), in connection with which the present review discusses the emergence of a malignant phenotype.

This study discovered a new process called lactylation, where lactate modifies a protein called MRE11 in response to DNA damage. This modification helps MRE11 bind to DNA, aiding in DNA repair. Blocking lactylation weakened DNA repair and made cancer cells more sensitive to chemotherapy in lab experiments. This suggests that targeting lactylation could be a new way to improve cancer treatment by weakening DNA repair mechanisms in cancer cells.

This study investigated how different carbohydrates affect glycogen replenishment after exercise. Participants completed cycling exercises followed by a 4-hour recovery period

where they consumed glucose, galactose, or a mix of galactose and glucose. Results showed that glucose was more effective than galactose or the mix for replenishing muscle glycogen. However, muscle glycogen synthesis was similar between the mix of galactose and glucose and exclusive galactose ingestion.

This study looked at the relationship between artificial sweeteners and the risk of developing type 2 diabetes. Researchers analyzed data from over 105,000 participants and found that those who consumed higher amounts of artificial sweeteners had a higher risk of developing type 2 diabetes compared to non-consumers. This risk was also seen for specific types of artificial sweeteners, including aspartame, acesulfame potassium, and sucralose. These findings suggest that artificial sweeteners may not be safe alternatives to sugar and warrant further investigation by health authorities.

This study investigated the relationship between metabolic factors, particularly insulin resistance, and the presence of a unique type of cells called gemistocytes (GCs) in patients with glioblastoma multiforme (GBM). They analyzed medical records of GBM patients and found that those with GCs were more likely to have poorly controlled type 2 diabetes and obesity compared to those without GCs. Interestingly, in patients with poorly controlled diabetes, none of those with GCs were using insulin prior to diagnosis, unlike those without GCs. This suggests a potential link between metabolic factors and the presence of GCs in GBM patients, which warrants further investigation.

This study investigated the role of the insulin receptor (INSR) in breast cancer development using mouse models. They found that deleting INSR in mammary epithelial cells delayed tumor onset and reduced tumor burden in two different breast cancer mouse models. The deletion of INSR affected tumor initiation but not progression or metastasis. The study suggests that INSR plays a crucial role in promoting tumor formation in breast cancer and highlights its potential as a therapeutic target.

This study investigates the potential of mannose, a type of sugar, as an anticancer treatment. While cells typically use sugars for growth and division, mannose uniquely inhibits cancer cell division and increases sensitivity to chemotherapy. The study focuses on how mannose affects cancer cells lacking a protein called MPI. When MPI is absent, mannose builds up within cells as mannose-6-phosphate, disrupting energy production pathways and slowing cell growth. By removing the MPI gene in human cancer cells, researchers found that mannose treatment slowed cell division by preventing DNA doubling, a crucial step in cell division, and made the cells more vulnerable to chemotherapy. The study suggests that targeting the mannose pathway could lead to new cancer treatments, although further research is needed to understand the varied responses of cancer cells to mannose treatment.

This study explores a potential strategy to overcome resistance to standard and new treatments in acute myeloid leukemia (AML). Researchers found that inhibiting an enzyme called mannose-6-phosphate isomerase (MPI), which is involved in mannose metabolism, makes AML cells more sensitive to both cytarabine and FLT3 inhibitors. They discovered that disrupting mannose metabolism also affects fatty acid metabolism through a process involving the unfolded protein response (UPR). This leads to the accumulation of polyunsaturated fatty acids, causing lipid peroxidation and a type of cell death called ferroptosis in AML cells. These findings highlight the importance of metabolic changes in AML therapy resistance and suggest a new approach to target therapy-resistant AML cells by making them more susceptible to ferroptosis.

This study explored the potential of using mannose, a sugar, as a treatment for colorectal cancer (CRC). CRC is a major cause of death, and current therapy with 5-fluorouracil (5-FU) can be toxic and ineffective due to drug resistance. The researchers found that mannose could inhibit the growth of CRC cells and worked even better when combined with 5-FU. Mannose affected the activity of enzymes involved in a pathway called the pentose phosphate pathway (PPP), which is crucial for cancer cell growth. It also increased oxidative stress and caused DNA damage in CRC cells. Importantly, mannose treatment alone or with 5-FU was well tolerated and reduced tumor size in mice with CRC. This suggests that mannose, either alone or combined with 5-FU, could be a promising new treatment approach for CRC.

This study looked at whether combining glucose and galactose during exercise increases the body’s use of ingested galactose. Fourteen endurance-trained participants exercised on four occasions while drinking beverages containing either galactose, glucose, or a mix of both. The mix reduced the amount of galactose in the blood but didn’t increase the use of ingested galactose during exercise. However, the mix was still a good source of energy during exercise, similar to glucose alone. This suggests that combining galactose and glucose could be an alternative energy source during exercise.

This study investigated how a ketogenic diet, which is low in carbohydrates and high in fat, affects pancreatic cancer and its response to chemotherapy. Using mouse models of pancreatic cancer, researchers found that a ketogenic diet changes the metabolism of tumors, making them more sensitive to chemotherapy. Specifically, the combination of a ketogenic diet and chemotherapy significantly slowed tumor growth and improved survival compared to chemotherapy alone. These findings led to the initiation of a clinical trial to test this approach in patients with metastatic pancreatic cancer.

This study aimed to investigate the safety and effects of a ketogenic diet (KD) on body composition, blood parameters, and survival in breast cancer patients undergoing chemotherapy. Sixty patients were divided into two groups: one receiving KDs and the other following a standard diet. Results showed that the KD group had reduced fasting blood sugar levels and increased ketone body levels compared to baseline. Additionally, BMI, body weight, and fat percentage were significantly lower in the KD group at the end of the study. No severe adverse effects were reported, and overall survival was higher in the KD group, particularly in neoadjuvant patients. These findings suggest that combining chemotherapy with a KD may improve biochemical parameters, body composition, and overall survival in breast cancer patients with no significant side effects.

This study explores the concept of food addiction and its role in obesity. It suggests that certain high-glycemic-index carbohydrates may trigger addictive behaviors similar to those seen with substance abuse. Evidence shows that these carbohydrates can affect brain chemistry in a way that leads to cravings and addictive-like responses. Understanding this link between food and addiction could help in developing better treatments for obesity, focusing not only on reducing food intake and increasing physical activity but also on addressing addictive behaviors related to certain types of food.

D-tagatose is a naturally existing rare monosaccharide having prebiotic properties. Minimal absorption, low metabolizing energy, and unique clinical properties are the characteristics of D-tagatose. D-tagatose gained international attention by matching the purpose of alternate sweeteners that is much needed for the control of diabetes among world population.

This study looked at how different sugars affect energy use and fat burning in twelve adults. They drank water with glucose, fructose, or galactose, and their energy levels were measured before and after. The results showed that all sugars initially increased energy use, but galactose and glucose caused a quicker return to normal levels compared to fructose. Surprisingly, there wasn’t a big difference in fat burning or energy use between the sugars when consumed as a drink.

This study aimed to change how muscle cells use energy by replacing glucose with galactose during their growth. They found that using galactose increased the cells’ ability to burn fatty acids and glucose. Additionally, cells grown with galactose had more mitochondria and stored more fat. Interestingly, these cells were better at switching between using fats and glucose for energy. This suggests that using galactose could be beneficial for studying conditions like insulin resistance and mitochondrial disorders in muscle cells.

This study aimed to find out how ingesting two different sugars, galactose and glucose, before exercise affects the use of fuel during the workout. Nine trained male cyclists were involved. They each did three rounds of cycling at 60% of their maximum capacity for 2 hours after not eating overnight. Before the exercise, they drank a fluid containing either a placebo, galactose, or glucose without knowing which. Scientists used special equipment to measure how much fat and carbohydrates the cyclists’ bodies were burning during exercise.

The results showed that peak carbohydrate burning from the drink was higher when they drank glucose compared to galactose, but the average rates were similar. Glucose was better at providing extra energy in the first hour of exercise, while galactose was better in the last hour. Glucose also caused higher rates of burning the sugar in the blood and liver during the exercise. However, overall, there were no significant differences in total carbohydrate or fat burning between the different conditions.

In conclusion, drinking glucose before exercising gives a quick burst of extra energy at the beginning, but galactose becomes the main source of fuel later on and reduces the body’s need to use stored sugars in the liver.

Oxygen free radicals are produced during stress, are unstable, and potentially interact with other cellular components or molecules. This reactivity can influence cellular function, including a prolongation in tissue recovery following exercise.

Dental plaque develops when early bacterial colonizers adhere to the acquired pellicle (saliva-derived proteinous coating on the tooth surface) followed by adhesion of late interspecies colonizers to form this type of biofilm (coaggregation).

Animal experiments in BALB/c-mice and in DBA/2-mice confirmed that lectin blockade with D-galactose containing receptor analogues can inhibit metastatic spread into the liver.

80 stomach adenocarcinoma patients (T1-3, NO, MO) were enrolled into a prospectively randomized clinical study. 40 patients were perioperatively treated with D-galactose (treatment group: 1.9 g/kg BW and per day) or D-glucose-containing electrolyte infusions (control group: n = 40).

The influence of different galactose concentrations on the cariogenic effect of Streptococcus mutans (strains: DSM 20381 and DSM 20523) in a sucrose diet (33%) was examined in an animal experiment. The treated Wistar rats were free of pathogenic germs at the beginning of the experiment.