Recent Progresses on Diabetes

Nearly 500 million people in the world suffer from diabetes, mainly type 2 diabetes, and this number is expected to soar in the next few years. Diabetes is also associated with many chronic diseases including heart disease, atherosclerosis, nerve damage, vision loss and wound healing disorders. It brings a huge health burden and economic burden. The urgency of this situation has made scientists desperately looking for better ways to prevent and control diabetes. The following are some of the latest progresses in diabetes research.

1 Abnormal T cells found in pancreatic tissue may reveal a new mechanism for the pathogenesis of type 1 diabetes

Scientists from La Jolla Institute of Immunology and other institutions have successfully targeted T cells with abnormal functions in the body’s pancreas (even in healthy people) through research.

The pancreas is full of clusters of cells called pancreatic islets. For most people, there is a type of beta cell in the pancreatic islets that can help the body make insulin to regulate the body’s blood sugar level. However, in patients with type 1 diabetes, the body’s T cells will move to pancreatic islets by mistake and kill beta cells. Previously, it was believed that the presence of autoreactive T cells in the pancreas is the exact sign of the onset of type 1 diabetes. However, in this study, the researchers found that even in the pancreatic tissue of healthy people, there may be a large number of such autoreactive T cells. The results of the study indicate that type 1 diabetes may not be caused by abnormal T cells attacking β cells, but some abnormalities in the pancreas induce the attack process of T cells. Recently, the research report was published in Science Advances.

2 Electromagnetic field exposure is expected to be used to develop new strategies for the treatment of diabetes

Treatment of diabetes usually requires daily medication or insulin injections. But in a new study, researchers from the University of Iowa and other institutions proposed another potential treatment option: electromagnetic field effects therapy. They found that exposing mice with type 2 diabetes to electrostatic and static magnetic fields can increase their insulin sensitivity and reduce blood sugar. The relevant research results were published in Cell Metabolism on October 6, 2020, entitled “Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes“. Previous studies have shown that cells can use electromagnetic fields to migrate, and this migration is mediated by a molecule called superoxide. Superoxide is a kind of active oxygen molecule that seems to function like a molecular antenna and can receive electromagnetic signals. Patients with type 2 diabetes have elevated levels of superoxide, which are related to vascular problems and diabetic retinopathy. In order to study how these electromagnetic fields might work, the researchers eliminated superoxide molecules in the livers of these mice and found that electromagnetic field exposure had no effect on blood sugar or insulin resistance. The researchers pointed out that they believe that superoxide molecules are sending signals to cells to adapt them to electromagnetic field exposure and subsequently improve blood sugar. They admitted in the paper that the role of many proteins is still unclear, and further exploration of their mechanism of action will be the subject of future research.

3 Exercise may effectively reduce the risk of heart disease in diabetic patients

Scientists from the University of Otago and other institutions have revealed how exercise can help reduce the risk of heart disease caused by diabetes. Researchers pointed out that exercise can induce the heart to release microRNAs, which can help increase protein production and improve the structure and function of the heart. Researcher Professor Daryl Schwenke said that this special microRNA can be adversely changed in the early stages of diabetes, so microRNA may be used as a reliable early marker to help detect whether diabetic patients will develop heart disease. Researchers have found that exercise can increase the production of good microRNAs and reduce the impact of bad microRNAs on the health of the body. Exercise can also effectively improve the regulation of microRNAs, thereby helping to inhibit the occurrence and progression of heart disease. At the same time, the researchers also pointed out that pharmacological drugs can also be used to increase the production of good microRNA. This research was published in Circulation Research.

4 Taking NRTI drugs for HIV and hepatitis B may prevent diabetes

Researchers from the University of Virginia School of Medicine and other research institutions have discovered that a group of drugs used to treat HIV and hepatitis B may be reused to prevent type 2 diabetes. Studies have found that patients taking these drugs have a 33% lower risk of diabetes. Researchers found that a drug called lamivudine significantly improved insulin sensitivity in human cell samples and diabetic mouse models, and HIV-1 or hepatitis B patients taking NRTI (nucleoside reverse-transcriptase inhibitor) were less likely to develop diabetes by more than 30%. These researchers studied the effects of lamivudine and two other similar drugs in human cell samples, and all three drugs have been shown to be helpful in preventing diabetes. Related research results were recently published in Nature Communications.

5 A balanced intake of carbohydrates and fats may be effective in preventing diabetes

Scientists from the Agricultural Research Service of the United States Department of Agriculture have discovered through research that high levels of carbohydrate intake may help regulate the expression of special genes in the body, thereby helping to reduce the risk of many metabolic diseases such as obesity, hypertension, type 2 diabetes. The bad news, however, is that the intake of large amounts of fat can cause a variety of health problems. Researchers have found that a person’s dietary habits may affect the activity level of the CPT1A gene, resulting in positive or negative health problems. High carbohydrate intake may be related to lower levels of CPT1A gene expression, while high fat intake is directly related to the high-level expression of CPT1A gene. Researcher Chao-Qiang Lai pointed out that this study can help us understand the molecular mechanism that affects the health of the body through balanced nutrition from the perspective of a single gene, CPT1A. The researchers also pointed out that a balanced intake of carbohydrates and fats may be the best way to effectively prevent metabolic diseases such as diabetes.

6 Interpretation and application of diabetes disease model is challenged by new research

Experimental models are essential for understanding the mechanism of diabetes and developing better drugs. To date, the most common diabetic disease model uses the toxic compound STZ to destroy insulin-producing cells in the pancreas. STZ is a drug that is toxic to the beta cells that produce insulin in the mouse pancreas. When these beta cells are destroyed, it will cause insufficient insulin production, which will limit the energy of human cells to absorb glucose. STZ has been used in many studies to build rodent diabetes models, and has been widely used by pharmaceutical companies to test the efficacy of anti-diabetic drugs. Now, researchers from Umeå University and the Karolinska Institute have presented new evidence that challenges this model. The results of the study show that although β cells are indeed destroyed, this is not the main reason for the development of diabetes. Instead, they used advanced imaging and molecular biology techniques to show that the vast majority of beta cells still exist, but pancreatic islets of different sizes are affected to varying degrees. Importantly, the researchers showed that the remaining affected insulin-producing cells lost their identity and transformed into a more immature state, which in turn led to increased blood sugar levels and insulin cell damage. Ulf Ahlgren, a professor at the Center for Molecular Medicine (UCMM), said: “This means that the loss of insulin-producing cells in this model can easily be overestimated.”

7 Special amyloid fibers associated with the development of early-onset type 2 diabetes

Scientists from Leeds University and other institutions have identified for the first time the structure of protein fibers associated with the onset of early-onset type 2 diabetes. Amylin is a protein that can regulate the body’s blood sugar level. This small peptide hormone can aggregate and accumulate to form amyloid fibrils, and these aggregates are the signs of type 2 diabetes. The formation of amyloid fibers is also directly related to the occurrence of many other diseases, including Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. The researchers compared the dextrin fiber (wild type) in dextrin from most people with the genetic mutant fiber called S20G in the body of patients with early-onset type 2 diabetes and found that all wild-type fibers have two dextrin fibers, some S20G fibers also have two dextrin fibers, but the researchers found a S20G fiber with three dextrin fibers in each layer. This indicates that fibers can form a template and lock more dextrin fibers on it, which may explain why the S20G mutant protein can aggregate faster, and it is also directly related to the rapid occurrence of diseases.

8 Loss of special kinases in the liver may induce type 2 diabetes

Scientists from Centennial College and other institutions have found that the lack of a special enzyme called SphK2 (sphingosine kinase 2) in the liver may cause the body to appear obvious insulin resistance and glucose intolerance, and they are symptoms of early type 2 diabetes. After conducting research using a mouse model, the researchers found that the lack of SphK2 enzymes in the liver promotes the accumulation of the fat product sphingosine, thereby impairing the function of insulin in the liver. SphK2 is an important participant in the body’s insulin regulation process. Related research results may help to develop new therapies for the treatment of diabetic patients. The research was published in Proceedings of the National Academy of Sciences.

9 Intestinal flora may not be involved in the onset of gestational diabetes in women

Maternal overweight and obesity increase the risk of gestational diabetes. Recently, researchers have discovered that the composition of the intestinal flora is directly related to the occurrence of overweight and a series of metabolic diseases. However, researchers do not know whether the intestinal flora is also involved in the occurrence of gestational diabetes. Scientists from Turku University and other institutions have carried out a clinical trial to investigate the effects of two food supplements-fish oil and probiotics (containing Rhamnosus HN001 and Bifidobacterium Lactococcus 420) on the risk of gestational diabetes. Researchers have found that the composition and function of intestinal microbes may not be involved in the occurrence of gestational diabetes in obese and overweight women. In addition, there does not seem to be any difference in the gut microbiome between women without gestational diabetes and women with gestational diabetes. The results of this study show that the combination of fish oil and probiotics can regulate the composition of the gut microbes of participants, especially women who do not suffer from gestational diabetes. In the later stage, researchers still need further research to analyze whether the intestinal flora of women with gestational diabetes is more difficult to be modified or improved with food supplements. This research was published in Gut.

10 How the brain regulates the relief of diabetes symptoms

Type 2 diabetes affects 10% of the American population. It is closely related to obesity and can cause serious health problems, including heart disease, vision loss, kidney failure, dementia, incurable infections and nerve damage. Previous studies have shown that a single surgical injection of a protein called fibroblast growth factor 1 can restore the blood sugar levels of rodents with type 2 diabetes to normal levels and maintain them for weeks to months. However, little is known about how this growth factor works in the brain to produce this lasting benefit. The researchers discovered an extracellular matrix assembly called a “peripheral neural network”, which fuses together groups of neurons involved in blood sugar control. Fibroblast growth factor 1 can repair the peripheral nerve network damaged by diabetes, so it can alleviate the symptoms of diabetes. Related research was published in Nature Communications and Nature Metabolism.