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Eating almonds twice a day can help improve glucose metabolism as well as keep cholesterol levels in check, suggests a study. The study showed that almond consumption can improve blood sugar levels at the pre-diabetes stage, which may help prevent or delay the development of diabetes. In addition, almond consumption also reduced total cholesterol and ace bad" LDL-cholesterol significantly compared to the control group while maintaining "good" HDL-cholesterol levels.
"Lifestyle changes including improved nutrition and exercise targeted at teens and young adults have the potential to halt the progression from prediabetes to Type-2 diabetes. Results from this study show that the change does not have to be a major one -- simply including a twice-daily snack of almonds can make a difference," said principal investigator Jagmeet Madan, Professor, and Principal at Sir Vithaldis Thackersey College of Home Science in Mumbai. "The study results are very promising in showing how almonds improved total and LDL-cholesterol levels and reduced HbA1c levels in just 12 weeks of consumption," Madan added.
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For the study, the team included 275 participants (59 male, 216 female) with impaired glucose metabolism (prediabetes). The almond group ate 56 grams (about 2 one-ounce servings, or nearly 340 calories) of unroasted almonds every day for three months and the control group consumed a savory snack made using whole wheat flour, chickpea flour, salt, and Indian spices, with the same number of calories.
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Both the almond and savory snacks accounted for nearly 20 percent of participants' total calorie intake. In the almond group, HbA1c -- a measure of long-term blood sugar control that also serves as a diagnostic criterion for prediabetes and diabetes -- decreased significantly compared to the control group. There was a decrease in the fasting blood glucose in the almond group in comparison to the control group but was not statistically significant. (IANS/JC)
People with metabolic diseases like Type-2 diabetes and cancer as well as those exposed to organophosphate pesticides can be at an increased risk of Covid-19 infection, finds a new study performed in human lung airway cells. The study, led by Saurabh Chatterjee and the team from the University of South Carolina in the US, identified a basic mechanism linked with inflammation that could increase susceptibility to Covid-19 infection among people exposed to organophosphates.
The findings showed that people with Type-2 diabetes and cancer may also be at increased risk to Covid because they tend to exhibit the same type of inflammation. Exposure to organophosphate pesticides causes Gulf War Illness — a cluster of medically unexplained chronic symptoms that can include fatigue, headaches, joint pain, indigestion, insomnia, dizziness, respiratory disorders, and memory problems.
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The team examined whether exposure to the organophosphate pesticide chlorpyriphos and increased levels of interleukin 6 (IL-6) could increase the risk of SARS-CoV-2 infection. For six hours, they exposed human lung airway epithelial cells to either IL-6 or chlorpyriphos or to both in combination. Another group of cells received no exposure to serve as a control.
The researchers then treated the cells with the spike proteins that cover the outside of SARS-CoV-2. During infection, spike proteins bind with angiotensin-converting enzyme 2 (ACE2) receptors to our cells, starting a process that allows the virus to release its genetic material into the healthy cell. They found that cells exposed to IL-6 and the pesticide exhibited increased apoptosis — or controlled cell death — when the SARS-CoV-2 spike protein was present.
The cells exposed to both the pesticide and IL-6 also had significantly more ACE2 expression on the apical cell surface compared to cells that were unexposed or exposed to the pesticide alone. The apical membrane of airway cells faces the interior of the airway while the basolateral membrane touches the surrounding tissues. Increased ACE2 receptor expression on the apical surface means more viruses will attach to the cells, the researchers explained.
“Since people with obesity, Type-2 diabetes or cancer also have high circulatory IL-6 levels, we think people with these conditions will also have increased susceptibility to SARS-CoV-2 infection because of increased translocation of ACE2 receptor to the apical cell surface,” Chatterjee said. The findings will be presented at the virtual Experimental Biology (EB) 2021 meeting to be held on April 27-30. (IANS/JC)
Examining the role of cholesterol in both Alzheimer’s disease and Type-2 diabetes, researchers have identified a small molecule that may help regulate cholesterol levels in the brain, making it a potential new therapeutic target for Alzheimer’s disease. There is no known cure for Alzheimer’s disease and in the last decade, scientists have found increasing evidence linking the underlying causes of Type 2 diabetes and Alzheimer’s disease.
Type-2 diabetes occurs when insulin becomes less efficient at removing glucose from the bloodstream, resulting in high blood sugar that can cause abnormal cholesterol levels. A similar situation occurs in Alzheimer’s disease, but rather than affecting the body as a whole, the effects are localized in the brain.
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“Alzheimer’s and diabetes share many common causes,” said study co-author Gregory Thatcher, Professor at the University of Arizona College of Pharmacy.
“Our goal was to develop a way of identifying compounds that would counteract many detrimental changes that contribute to both Alzheimer’s and Type-2 diabetes,” Thatcher added.
When cholesterol rises, due to insulin resistance or other factors, the body starts a process is known as reverse cholesterol transport, during which specific molecules carry excess cholesterol to the liver to be excreted. Apolipoprotein E (APOE) is one of the proteins involved in reverse cholesterol transport. APOE is also the strongest risk factor gene for Alzheimer’s disease and related dementia, and an independent risk factor for Type 2 diabetes and cardiovascular disease.
Similarly, reduced activity of another cholesterol transporter, ATP-binding cassette transporter A1 (ABCA1), correlates with increased risk of cardiovascular disease, Type-2 diabetes, and Alzheimer’s disease. Increasing the activity of ABCA1 is expected to positively influence insulin signaling and reduce inflammation in the brain, making it a potential therapy for both Type-2 diabetes and Alzheimer’s disease.
In this study published in the journal ACS Pharmacology and Translational Science, Thatcher and the research team designed a way to identify small molecules that improve the function of ABCA1 in the body while avoiding unwanted effects to the liver. (IANS/SP)