Type 2 diabetes who eat low-carb may discontinue medication 

Adults with type 2 diabetes on a low-carbohydrate diet may see benefits to their beta-cell function allowing them to manage their disease better and possibly discontinue medication, according to new research. Beta-cells are endocrine cells in the pancreas that produce and release insulin, the hormone that controls blood sugar levels. More than 38 million and over 90% of them have type 2 diabetes. Type 2 diabetes most often develops in people 45 or older, but more and more children, teens and young adults are also developing the disease. People with type 2 diabetes have a compromised beta-cell response to blood sugar, possibly due in part to eating too many carbohydrates. Beta-cell failure or insufficiency on top of insulin resistance is responsible for the development and progression of type 2 diabetes. This study shows people with type 2 diabetes on a low-carbohydrate diet can recover their beta-cells, an outcome that cannot be achieved with medication. People with mild type 2 diabetes who reduce their carbohydrate intake may be able to discontinue medication and enjoy eating meals and snacks that are higher in protein and meet their energy needs. The researchers gathered data from 57 adults with type 2 diabetes, half on a low-carbohydrate diet and the other half on a high-carbohydrate diet and examined their beta-cell function and insulin secretion at baseline and after 12 weeks. All of the participants' meals were provided. People on the carbohydrate-restricted diet ate 9% carbohydrates and 65% fat, and participants on the high-carbohydrate diet ate 55% carbohydrates and 20% fat. The researchers found those on a low-carbohydrate versus a high-carbohydrate diet saw improvements in the acute and maximal beta-cell responses that were 2-fold and 22% greater, respectively. Black adults on a low-carbohydrate diet saw 110% greater improvements in the acute beta-cell response and White adults had improvements in the maximal beta-cell response that were 48% greater than their respective counterparts on the high-carbohydrate diet. This research received financial support from the National Institute of Diabetes and Digestive and Kidney Diseases, the Nutrition Obesity Research Center of the University of Alabama at Birmingham, the Diabetes Research Center, and the National Heart, Lung, and Blood Institute.

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Six proteins implicated in early-onset preeclampsia

Pre-eclampsia is a life-threatening pregnancy complication marked by persistent high blood pressure that is even more serious when it occurs early in the first trimester. The exact cause of early-onset preeclampsia is unknown, and it is difficult to predict, prevent and diagnose. Now researchers report on six proteins that could be used as targets to diagnose and treat the condition. Preeclampsia's key symptom is high maternal blood pressure, and serious cases can lead to maternal organ failure, low infant birth weight, or maternal or fetal death. Preeclampsia before 34 weeks of pregnancy has a higher risk of severe outcomes, especially for the fetus. But it's difficult for health care providers to detect this condition before harmful symptoms appear, because little is known about what causes it. The researchers collected placenta tissue from 30 pregnant people, half with early-onset preeclampsia and half with healthy pregnancies. & used mass spectrometry to screen molecular fragments in each sample, followed by a software program to match the fragments to their associated proteins. This process pinpointed 59 proteins that were present in different amounts (either higher or lower) for preeclamptic placenta tissue samples versus healthy placenta tissue samples. The researchers chose 16 of these proteins to target with a different, more sensitive mass spectrometry method, which more precisely measured the amounts of each protein. Of these 16 proteins, six were present in statistically different amounts across tissue sample groups: Pre-eclamptic placenta tissue had higher levels of monocarboxylate transporter 4, ERO1-like protein alpha and pappalysin-2. These proteins are involved in synthesizing proteins and regulating growth hormones. Preeclamptic placenta tissue had lower levels of desmin, caldesmon and keratine 18. These proteins play key roles in cardiovascular complications, like an enlarged heart; blood flow in placental muscle cells; estrogen signaling and cell health in the uterus lining. Altogether, the results suggest that cardiovascular complications or the estrogen cycle could be linked to the development of early-onset preeclampsia.

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Immune cells prevent lung healing after viral infection 

Researchers have discovered a pathway by which immune cells prevent the lungs' protective barrier from healing after viral infections like COVID-19. The COVID-19 pandemic revealed how viral infections can cause long-lasting effects -- a condition called long COVID. Also known as post-acute sequelae of SARS-CoV-2, long COVID has left a devastating trail of people who continue to live with long-term debilitation after infection. One such manifestation is scarring of the lungs -- a condition known as post-acute sequelae of SARS-CoV-2 pulmonary fibrosis. Those with long COVID can present with a broad constellation of symptoms, including post-acute sequelae of SARS-CoV-2 pulmonary fibrosis, which can cause severe difficulty breathing that requires oxygen supplementation. Patients with the most severe breathing difficulty may also need a lung transplant. Without additional treatment options, many patients are often left with long-term disability and life-threatening complications. This study sought to understand the pathways that led to abnormal repair in the lungs that produced a scar-forming environment. The findings may lead to therapeutic strategies to prevent fibrotic lung disease after viral illnesses. Investigators established models of post-viral lung disease and used molecular profiling and imaging to identify immune cells called CD8+ T cells as a driving factor in preventing lung healing and repair post-infection. Moreover, the investigators used post-acute sequelae of SARS-CoV-2 pulmonary fibrosis patient cohorts to validate the abnormal immunologic pathways, corroborating the animal model work. Although we based the work on post-acute sequelae of SARS-CoV-2 pulmonary fibrosis, other viral pandemics in the past have also revealed that ability to cause lung scarring after infection -- like swine flu. These findings and similar studies could provide novel information into the pathobiology of other forms of lung fibrosis.

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Drug may stop migraines before the headache starts 

When taken at the first signs of a migraine, before headache pain begins, a drug called ubrogepant may be effective in helping people with migraine go about their daily lives with little or no symptoms, according to a new study. The study focused on people with migraine who could tell when an attack was about to happen due to early symptoms such as sensitivity to light and sound, fatigue, neck pain or stiffness, or dizziness. Improving care at the first signs of migraine, even before headache pain begins, can be a key to improved outcomes. The findings are encouraging, suggesting that ubrogepant may help people with migraine function normally and go about their day. The study involved 518 participants who had migraine for at least one year and two to eight migraine attacks per month in the three months before the study. All of the participants regularly experienced signs that a migraine would be starting within the next few hours. Participants were asked to treat two attacks during two months. Researchers divided participants into two groups. The first group received a placebo for their first set of pre-headache symptoms of migraine, followed by taking 100 milligrams (mg) of ubrogepant for their second instance of symptoms. The second group took ubrogepant for the first instance and placebo for the second instance. Participants evaluated limitations on their activity in their diary using a scale ranging from zero to five, with 0 meaning "not at all limited. 1, "a little limited"; 2, "somewhat limited"; 3, "very limited"; or 4, "extremely limited. Twenty-four hours after taking the drug or a placebo, 65% of people who took ubrogepant reported themselves as "not at all limited - I could do everything," or "a little limited," compared to 48% of those who took the placebo. Researchers found that as early as two hours post-medication, people who took the drug were 73% more likely to report that they had "no disability, able to function normally," than those who took the placebo. Based on the findings, treatment with ubrogepant may allow people with migraine who experience early warning signs before a migraine occurs to quickly treat migraine attacks in their earliest stages and go about their daily lives with little discomfort and disruption. This could lead to an improved quality of life for those living with migraine. The participants showed that based on their headache warning symptoms, they could reliably predict impending migraine headaches. These findings apply only to those with reliable warning symptoms.

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Researchers used mouse models and human post-mortem brain tissue to study the molecular underpinnings that may increase the risk of Alzheimer's after traumatic brain injury (TBI). Researchers found that TBI increases hyper phosphorylated, astro- and micro gliosis, synaptic dysfunction and cognitive impairments linked to developing Alzheimer's disease. Furthermore, they found that downregulation of BAG3 (Bcl-2-associated athanogene 3), a protein involved in protein clearance through the autophagy-lysosome pathway, contributes to the accumulation of hyper phosphorylated tau in neurons and oligodendrocytes after TBI in the mouse models and human post-mortem brain tissue with the history of TBI. Using an AAV-based approach of overexpressing BAG3 in neurons & found that BAG3 overexpression ameliorates tau hyper phosphorylation, synaptic dysfunction, and cognitive deficits, likely through the enhancement of the autophagy-lysosome pathway. Based on the findings & believe that targeting neuronal BAG3 may be a therapeutic strategy for preventing or reducing Alzheimer's disease-like pathology. This work builds on their earlier research that had identified BAG3 as a hub gene controlling tau homeostasis from non-diseased human post-mortem tissue. Since previous research using human tissue and mouse models shows that tau pathology increases after TBI, Scientists wondered if BAG3 may be a contributing factor to tau accumulation after TBI. Indeed that found that BAG3 dysfunction contributes to disruption of protein clearance mechanisms that results in tau accumulation in mouse models and in human post-mortem tissue with TBI and Alzheimer's.

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Crucial role of the cerebellum in social and cognitive functioning

Scientists shed light on the often-overlooked role of the cerebellum in both motor and social-cognitive processes. His research contributes to a growing shift in the field of neuroscience, which has traditionally focused on the cerebrum. For decades, the cerebellum was primarily associated with motor coordination. People with cerebellar abnormalities often experience motor issues. People struggle to smoothly touch their noses with a finger. These difficulties highlight the cerebellum's essential role in refining motor movements. The research extends beyond motor functions, exploring the cerebellum's involvement in social and cognitive abilities. The findings reveal that abnormalities in the cerebellum not only lead to motor deficits but are also linked to emotional and behavioral disorders. The research on individuals with autism, demonstrating how non-invasive brain stimulation techniques like magnetic stimulation can improve social task performance. Scientists have seen improvements in the sequence of cognitive tasks in people with autism through magnetic stimulation. Scientists now testing more complex tasks to see if these effects can be further enhanced, with the ultimate goal of developing practical treatments for people with autism. A notable breakthrough is the use of transcranial electrical stimulation, a more affordable and accessible technique compared to magnetic stimulation. While the effects of transcranial electrical stimulation are still limited, the research group is committed to further development, seeing its potential for wide-scale application in the future. This research offers a fresh perspective on the cerebellum's role and paves the way for new treatments for psychiatric and neurological conditions, such as autism spectrum disorders. The Scientists hope is to refine these techniques further to improve social and cognitive functions in people with autism.

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