Tag Archives: Type 2 diabetes

Age 40+ With Diabetes Should Be a Priority for the COVID-19 Vaccine | Instant News

People with type 2 diabetes as young as 40 face a disproportionately increased risk of dying from COVID-19 infection, suggesting a British analysis of three large-scale data sets highlighting the need to prioritize vaccination in younger groups of vulnerable patients.

Research it published February 8 in the journal Diabetology.

Most European countries have prioritized COVID-19 vaccination for people with type 2 diabetes, but usually only age 50 and over. However, data from the current study suggest that this age limit should be lowered.

“It is important to remember that the risk of dying from COVID-19 in middle-aged people with diabetes is very low in absolute terms compared to the elderly,” said lead researcher Andrew P. McGovern, MD, of Royal Devon & Exeter Hospital, Exeter. , United Kingdom, in a press release from its agency.

However, he said that “strategies for determining priority groups for vaccination must take into account the disproportionate relative risk of COVID-19 death in middle-aged people with type 2 diabetes whose risk of COVID-19 has already increased with their age.”

McGovern informed Medscape Medical News that the magnitude of the effect of type 2 diabetes on deaths from COVID-19 is “absolutely shocking” about the new findings, and “not what you expected.”

Therefore, he said it was imperative that diabetics be put “in line” to get the vaccine “in the right place, and clearly in countries where vaccine rollout will be slower, it is more important.”

Bridget Turner, director of policy and improvement campaigns at Diabetes UK, which funded the study, said the results provide “important new insights into how much type 2 diabetes adds to the overall risk of dying from coronavirus at different ages, particularly the additional risk of that condition. increases in middle age. “

“The UK has made good progress in prioritizing those most vulnerable for vaccination, which includes all adults with diabetes,” he added in a press release, “but we need to continue to work with pace to identify and protect those people at a greater level. high risk. “

The Relationship Between COVID-19 Death and Diabetes Is Complex

The authors note that the association between COVID-19-related death and type 2 diabetes is not only a “co-effect of diabetes and age-related risk” but appears to be a “more complex” relationship, with “a disproportionately higher relative risk of excess relative risk.” death in young people with diabetes. “

To investigate this, they examined data from two UK population-based studies that previously reported age-specific hazard ratios for diabetes-related COVID-19 deaths:

  • Open safely, which includes 17.2 million people, 8.8% of whom have diabetes, and has an overall 90-day mortality rate of 0.06%.

  • QCOVID, comprising 6 million people, of whom 7% had diabetes, and had an overall 97-day mortality rate of 0.07%.

The team also looked at data from type 2 diabetes patients with severe COVID-19 from the COVID-19 Hospitalization in England Surveillance System (CHESS), which contained 19,256 patients were admitted to critical care in the UK, 18.3% of whom had diabetes.

The 30-day hospital mortality rate in this study was 26.4%.

They translated the death hazard ratio associated with COVID-19 infection in diabetics to “COVID-19 age,” which equates to additional years of “risk of death” added to the individual’s chronological age if diabetes is present.

Taking the QCOVID dataset as an example, the results showed that the diabetes-related “COVID age” for someone aged 40 was 20.4 years; which would indicate that “the risk of death [for COVID-19] similar to a 60 year old without diabetes. “

The impact of diabetes on the risk of death from COVID-19 decreases with age, so that diabetic patients aged 50 have COVID-19 aged 16.4 years. This drops to 12.1 years in someone who is 60, and 8.1 years in someone who is 70, meaning the latter has the same risk of dying from COVID-19 as someone without diabetes who is 78 years old.

Similar results were obtained when the team looked at data from the OpenSAFELY study.

But when they looked at the effect of diabetes on the risk of dying from COVID-19 in the CHESS data set, it was less visible..

Just Looking At Diabetes Is Too Simple, But It’s An Easy Marker For Vaccination

The investigators acknowledge that “only considering age and diabetes status when assessing COVID-19-related risk … is an oversimplification,” because factors such as body mass index (BMI), diabetes duration, and glycemic control are also known to play an important role. authority.

However, they said consideration of these factors was “impractical for vaccine rollout at the population level.”

“The time-critical nature of the COVID-19 vaccination population requires pragmatic group level priority, which is the approach initiated by the government so far,” the team concluded.

This study was supported by Diabetes UK. Study author John M. Dennis was supported by an Independent Fellowship funded by the Research England’s Expanding Excellence in England (E3) fund and by the NIHR Exeter Clinical Research Facility. McGovern is supported by the NIHR Exeter Clinical Research Facility.

Diabetology. Published online February 8, 2021. Full text

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“Reconnecting” metabolism in insulin-producing cells may help the treatment of type 2 diabetes-health | Instant News

Researchers have discovered a previously unknown method by which pancreatic cells determine how much insulin they secrete.It could provide a promising new target to develop drugs to increase insulin production in diabetic patients Type 2 diabetes.

In two recently published papers Cell metabolismScientists at the University of Wisconsin-Madison and their colleagues pointed out that an overlooked enzyme called pyruvate kinase is the main way for pancreatic beta cells to sense sugar levels and release the right amount of insulin.

Through several proof-of-concept experiments conducted on rodent and human pancreatic cells, the research team found that drugs that stimulate pyruvate kinase not only increase insulin secretion, but also have other metabolic protective effects on the liver, muscles, and red blood cells. Research results indicate that activation of pyruvate kinase may be a new way to increase insulin secretion to fight type 2 diabetes, but more research is needed before any new treatments are available.

Matthew Merrins, professor of medicine at the University of Western Australia School of Medicine and School of Public Health, who is in charge of this work, said: “Too much insulin will lower blood sugar to dangerous levels, and too much insulin can lead to diabetes.” The question to ask is: How do nutrients such as glucose and amino acids open up the beta cells in the pancreas to release the right amount of insulin?”

This work is based on a careful analysis of the contradictory timing of key biochemical events, when it was generally understood how pancreatic beta cells respond to nutrients in the blood. The researchers pointed out a new and richer model to understand how to control this important process to resolve these contradictions.

For decades, scientists have believed that mitochondria, the energy generators in cells, trigger insulin secretion. This is a natural explanation, because mitochondria produce the high-energy molecule ATP, and in the process deplete the low-energy form of ATP, ADP. The decline in ADP stimulates calcium, the ultimate trigger for the release of stored insulin.

But time makes no sense. Mitochondria are most active when insulin secretion has already begun, not before. In addition, the mitochondria will stall before they exhaust enough ADP to trigger insulin secretion.

The clues to resolve these obvious paradoxes came from the study of cardiomyocytes in the 1980s. At the time, scientists discovered that pyruvate kinase (which converts sugar into energy and does not rely on mitochondria) may also severely deplete ADP. This process occurs near the ADP sensor protein involved in insulin release in the pancreas. Mellins’ team believes that perhaps the pancreas uses this proximity to fine-tune insulin release.

In the initial experiment, the researchers provided sugar and ADP to pancreatic cell slices containing pyruvate kinase. Enzymes engulf these two components and deplete ADP. Since pyruvate kinase is located near the ADP sensor protein that triggers insulin secretion, it has a great effect.

“This is one of the important concepts in our paper: The location of the metabolism is critical to its function,” Merrins said.

The researchers used mouse and human islets, clusters of cells that release insulin, to try to stimulate the activity of pyruvate kinase. The drug that activates this enzyme increases the release of insulin four-fold, but only if there is enough sugar around-pyruvate kinase cannot be forced to release too much insulin.

Merrins said: “Pyruvate kinase does not change the amount of fuel that enters the cell, but only changes the way the fuel is used.” “Drugs with active pyruvate kinase can strongly promote insulin secretion without causing excessive insulin release. Hypoglycemia.”

Overall, they found a more complicated way, which is evidence of how pancreatic beta cells decide when and how much insulin they release, similar to a two-stroke engine. In the first cycle, pyruvate kinase processes blood sugar and consumes ADP. Mitochondria maintain this process by supplying more material to pyruvate kinase, which can cause ADP levels to collapse and ultimately stimulate enough calcium to enter the cell to release insulin.

In the second cycle, mitochondria transition from adding material to pyruvate kinase to producing the high-energy molecule ATP, which is necessary for the complete release of insulin. Then, the process will reset.

In an accompanying study by colleagues at Yale University Mellins, researchers studied how pyruvate kinase activator affects the metabolism of healthy and obese rats. In a series of experiments, they found that activating pyruvate kinase can increase insulin secretion and insulin sensitivity, while improving glucose metabolism in the liver and red blood cells. This type of treatment may be useful for patients with type 2 diabetes, who cannot produce enough insulin and therefore have abnormal glucose metabolism.

Mellins said: “The therapeutic idea here is that we can rearrange our metabolism to trigger insulin secretion more effectively while improving the function of other organs.

(This story was posted from a telecommunications company feed and has not been modified.)

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Research finds that specific brain cells trigger sugar consumption and cravings | Instant News

New research has identified specific brain cells that control how much sugar you eat and how hungry you are for sweet foods.

Most people enjoy sweets from time to time. However, unchecked “sweets” can lead to excessive consumption of sugary foods and chronic health problems such as obesity and type 2 diabetes. Understanding the biological mechanisms that control sugar intake and preference for sweetness may have important implications for controlling and preventing these health problems.

The new research is led by Dr. Matthew Potthoff, associate professor of neuroscience and pharmacology at Carver University in Iowa, and Dr. Matthew Gillum at Copenhagen University in Denmark. The research focuses on the action of a hormone called fibroblast growth. Factor 21 (FGF21). This hormone is known to play a role in energy balance, weight control and insulin sensitivity.

This is the first study to truly identify where this hormone works in the brain, and provides very cool insights into how to regulate sugar intake. “

Matthew Potthoff, a member of the Eagle Diabetes Brotherhood Research Center at UI and the Iowa Neuroscience Institute

Potthoff and his colleagues previously discovered that FGF21 is made in the liver in response to elevated sugar levels and plays a role in the brain to suppress sugar intake and preference for sweetness.

Based on this discovery, the team now shows for the first time which brain cells respond to FGF21 signaling and how this interaction helps regulate sugar intake and sweetness preferences. The study was published in the journal Cell metabolism, Also revealed how hormones mediate their effects.

Although FGF21 is known to function in the brain, because hormone receptors are expressed at very low levels, it is difficult to “see”, so determining the exact cellular target becomes complicated. Using various techniques, the researchers were able to accurately identify which cells express the FGF21 receptor. By studying these cells, studies have shown that FGF21 targets glutamatergic neurons in the brain to reduce sugar intake and sweet taste preference. The researchers also showed that the effect of FGF21 on specific neurons in the hypothalamus of the peritoneum reduces sugar intake by enhancing the sensitivity of neurons to glucose.

Several drugs based on modified forms of FGF21 have been tested as treatments for obesity and diabetes. The new discovery may cause the new drug to more precisely target the different behaviors controlled by FGF21, which may help control how much sugar a person eats.


Journal reference:

Jensen-Cody, so, Wait. (2020) FGF21 signaling to the hypothalamus glutamatergic neurons in the hypothalamus inhibits carbohydrate intake. Cell metabolism. doi.org/10.1016/j.cmet.2020.06.008.


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Heart enlargement related to autoimmunity is associated with the risk of heart failure in type 1 diabetes | Instant News

People with type 1 diabetes, especially those with poor glycemic control, are at a very increased risk for cardiovascular disease than the general population. Even more confusing, in individuals with type 1 diabetes, many cardiovascular risk factors are not in line with known risk factors associated with type 2 diabetes.

Dr. Myra Lipes, Investigator in the Immunobiology Section at the Joslin Diabetes Center at Harvard Medical School, has worked for more than a decade to understand what causes an increased risk of cardiovascular disease in patients with type 1 diabetes and what can be done about that.

Heart failure in particular has recently been recognized as an important type 1 complication with a national register-based study that shows a tenfold increase in the risk of heart failure in individuals with poor glycemic control. In addition, there is a higher case fatality rate in type 1 diabetes than in type 2 diabetes, which suggests different mechanisms for heart failure might be involved in type 1 diabetes.

Myra Lipes, Investigator in the Immunobiology Section at the Joslin Diabetes Center at Harvard Medical School

Given the burden of heart failure in type 1 diabetes, early identification of patients with certain risks is very important.

New research from Dr.’s lab Lipes in Joslin showed that in people with type 1 diabetes without known cardiovascular disease, the presence of autoantibodies to cardiac muscle protein is associated with evidence of cardiac magnetic resonance imaging (CMR) that shows an increase in left ventricular volume (the main heart pumping chamber), increased muscle mass and reduced pumping function (ejection fraction), a feature associated with a higher risk of failure in the general population. This new study was published in Circulation.

Antibodies are usually produced by the immune system and circulate in the blood, playing an important role in the body’s defense against infection. In people who tend to be autoimmune, the body misidentifies its own protein as a threat and attack. This is what happens with type 1 diabetes – the immune system thinks the pancreatic beta cells are the invaders and destroy them. In this situation, antibodies are called autoantibodies. So, it might not be too surprising that this type 1 diabetes complication also involves an incorrect immune response to heart muscle cells.

Previous studies conducted by Dr. Lipes has shown that a mouse model of type 1 diabetes develops dilated cardiomyopathy (weakened heart muscle) and premature heart failure associated with the presence of autoantibodies directed against cardiac muscle protein. His group also showed that poor glycemic control in patients with type 1 diabetes – but not in those with type 2 diabetes – was associated with cardiac autoimmunity. Unexpected findings are similar rates of cardiac autoantibodies in patients with type 1 diabetes, who are young and without diabetes complications, and a cohort of heart failure with Chagas cardiomyopathy, which is thought to be caused by chronic inflammation of the heart muscle (“myocarditis”), increasing the likelihood of dysfunction myocardial associated subclinical autoimmune in type 1 diabetes “said Dr. Lipes.

In this study, Lipes wanted to determine whether the widening cardiac phenotype seen in mouse models and Chagas patients was also present in people with type 1 diabetes who have this circulating autoantibody. He and his team used data collected from participants involved in the Diabetes Control and Complications (DCCT) study post-Diabetes Epidemiology Intervention and Complications (EDIC) follow-up studies, and consisted of people who had type 1 diabetes for an average of 28 year. As part of this study, participants were imaged with CMR, a gold standard noninvasive imaging technique to assess the structure and function of the heart.

“In this study, we measured autoantibodies against cardiac muscle protein in blood samples taken from CMR imaging in 892 EDIC participants without known cardiovascular disease,” Lipes said. “And then we examined where the presence of heart antibodies was associated with CMR evidence of myocardial dysfunction.”

They found that although recent A1c levels were similar in participants with and without cardiac autoantibodies, the presence of cardiac autoantibodies identified patients with worse glycemic control in the past, indicating that cardiac autoantibodies were a marker of long-term glycemic exposure. In addition, they found that CMR scanning of people with two or more autoantibodies showed an enlarged heart. They sorted patients into categories based on the number of circulating autoantibodies, which indicates that people with more of these specific autoantibodies have clearer changes in the heart. This finding did not weaken after adjusting for traditional cardiovascular risk factors, suggesting this change was mainly due to cardiac autoimmunity.

They know from previous research that the heart can have structural and functional changes related to the metabolic problems of diabetes itself; However, this relationship is relatively simple. For example, higher A1C levels are associated with slightly smaller left ventricular volume that is not clinically significant. But this research shows that higher A1C levels can trigger additional autoimmune responses that damage the heart in different and clearer ways that lead to enlargement and worse function, features that are known to be associated with a higher risk of heart failure.

“This points to a new process that involves the heart and is associated with poor glycemic control in type 1 diabetes,” Lipes said.

Because cardiac autoantibodies can be detected in a simple blood test, this study opens new avenues for detecting potential heart failure in patients with type 1 diabetes.

“Given the high burden of heart failure in type 1 diabetes, heart antibodies can allow early identification of people at higher risk of heart failure,” Lipes said. “And, of course, understanding the main causes of heart failure is important because it can lead to therapeutic approaches that are targeted at improving outcomes in these patients.”


Journal reference:

Sousa, G.R., et al. (2020) Cardiac Immunity Associated with Subclinical Myocardial Dysfunction in Type 1 Diabetes Mellitus Patients. Circulation. doi.org/10.1161/CIRCULATIONAHA.119.044539.


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