Exercise improves memory in Diabetic rats

University of Tsukuba led researchers shows that moderate exercise may improve hippocampal memory dysfunction caused by type 2 diabetes and that enhanced transport of lactate to neurons may be the underlying mechanism.

Type 2 diabetes is characterized by impaired glucose metabolism and can cause central nervous system-related complications, such as memory dysfunction. The hippocampus is an essential brain component for normal memory formation. However, the effect of impaired glycometabolism on hippocampal-mediated memory in type 2 diabetes patients is not known.

In a new study, researchers centered at the University of Tsukuba investigated whether hippocampal glucose metabolism and memory function are altered in a rat model of type 2 diabetes. Based on the idea that exercise normalizes glycometabolism and improves memory function, the research team also investigated the effects of exercise on hippocampal glycometabolism and memory formation.

The hippocampal function was evaluated by placing the rat in a circular pool and testing its ability to remember the location of a platform that would allow it to escape from the water. “This is a well-established method for measuring spatial learning and memory,” study first author Takeru Shima says.

Type 2 diabetic rats needed more time to escape the water and find the platform. However, after 4 weeks of moderate exercise, they were able to find the platform much faster. “This indicated that exercise significantly improved spatial memory impairments in type 2 diabetic rats,” Shima explains.

Glycogen levels are altered in tissues of diabetes patients, leading to a variety of complications. However, glycogen levels have not yet been investigated in the hippocampus. “We showed for the first time that glycogen levels are significantly higher in the hippocampus of diabetic rats,” corresponding author Hideaki Soya says.

Interestingly, a single bout of exercise reduced hippocampal glycogen levels and this correlated with an increase in lactate levels. Lactate is an energy substrate and neuromodulator in the hippocampus and is known to enhance memory formation. Lactate is transferred to neurons through monocarboxylate transporters (MCTs). “MCT2 expression was significantly lower in the hippocampus of type 2 diabetic rats,” Soya says, “dysregulated MCT2-mediated neuronal uptake of lactate is a possible etiology of memory dysfunction in type 2 diabetes, and that elevated hippocampal glycogen may be an adaptive change to compensate for the decreased lactate utilization”.

4 weeks of moderate exercise further enhanced glycogen levels and normalized MCT2 expression in the hippocampus of type 2 diabetic rats.” These findings suggest that disrupted MCT2-mediated uptake of lactate by neurons contributes to memory dysfunction in type 2 diabetic rats.

The findings indicate that moderate exercise could be used to treat memory impairment in patients with type 2 diabetes by promoting the transfer of glycogen-derived lactate to hippocampal neurons. Further research is needed to see if this correlates in human beings.

Citation: Shima, Takeru, Takashi Matsui, Subrina Jesmin, Masahiro Okamoto, Mariko Soya, Koshiro Inoue, Yu-Fan Liu, Ignacio Torres-Aleman, Bruce S. McEwen & Hideaki Soya. “Moderate exercise ameliorates dysregulated hippocampal glycometabolism and memory function in a rat model of type 2 diabetes.” Diabetologia 2016 pp: 1-10.
DOI: 10.1007/s00125-016-4164-4
Research funding: Ministry of Education, Culture, Sports, Science and Technology – Japan, Japan Society for the Promotion of Science.
Adapted from press release by University of Tsukuba.

Role of nerve growth factor in glucose metabolism

Research led by a Johns Hopkins University biologist demonstrates the workings of a biochemical pathway that helps control glucose in the bloodstream, a development that could potentially lead to treatments for diabetes.

In a paper published in the current issue of Developmental Cell, Jessica Houtz, a graduate student working with Rejji Kuruvilla in the Department of Biology at Johns Hopkins, shows that a protein that regulates the development of nerve cells also plays a role in prompting cells in the pancreas to release insulin, a hormone that helps to maintain a normal level of blood sugar. The research on insulin represents a detour for Kuruvilla, whose work has focused on development of the peripheral nervous system. She has studied a group of proteins called neurotrophins, and in particular nerve growth factor [NGF]. These proteins nurture the growth of neurons, the cells of the nervous system.

It has been known for some time that neurons and the pancreatic beta cells, or β-cells, that reside in clusters called islets of Langerhans and produce insulin, have many similarities in molecular makeup and signaling receptors. Receptors are proteins on cell surfaces that respond to particular chemicals and have critical roles in biochemical pathways. Both neurons and pancreatic β-cells have the receptors for neurotrophins.

It turns out that particular nerve growth factor [NGF] performs a function in the mature pancreas that has nothing to do with supporting neurons. Specifically, the research team traced a chain of biochemical signals showing that elevated blood glucose causes particular nerve growth factor  to be released from blood vessels in the pancreas, and that the particular nerve growth factor signal then prompts pancreatic β-cells to relax their rigid cytoskeletal structure, releasing insulin granules into the blood stream. Although β-cells also makeparticular nerve growth factor, Kuruvilla and her team found that it was the particular nerve growth factor released from the blood vessels that is needed for insulin secretion.

Using genetic manipulation in mice and drugs to block particular nerve growth factor [NGF] signaling in β-cells, they were able to disrupt distinct elements of this signaling sequence, to show that this classical neuronal pathway is necessary to enhance insulin secretion and glucose tolerance in mice. Importantly, Kuruvilla and colleagues found that particular nerve growth factor’s ability to enhance insulin secretion in response to high glucose also occurs in human β-cells.

It is not yet clear how this system is affected in people with diabetes. “We are very interested in knowing whether aspects of this pathway are disrupted in pre-diabetic individuals,” Kuruvilla said. It would be of interest to determine if particular nerve growth factor [NGF] or small molecules that bind and activate particular nerve growth factor receptors in the pancreas could be of potential use in the treatment of type-2 diabetes. These are questions to be pursued in further research.

Citation: Houtz, Jessica, Philip Borden, Alexis Ceasrine, Liliana Minichiello, and Rejji Kuruvilla. “Neurotrophin Signaling Is Required for Glucose-Induced Insulin Secretion.” Developmental Cell 39, no. 3 (2016): 329-345.
DOI:http://dx.doi.org/10.1016/j.devcel.2016.10.003 
Research funding: NIH
Adapted from press release by John Hopkins University

Research finds bi-directional association between fatty liver disease and heart disease

Researchers have shown that a bi-directional relationship exists between fatty liver disease and cardiovascular disease. Fatty liver disease can lead to increased cardiovascular disease risk and vice versa. The findings, which appear in the Journal of Hepatology, are important in understanding the link between fatty liver disease and cardiovascular disease, which continues to be one of the major causes of morbidity and mortality worldwide.

Due to the increased prevalence of obesity, non-alcoholic fatty liver disease has become the most common liver disease in the U.S., affecting 20-30 percent of the adult population. Obesity is also an independent risk factor for cardiovascular disease — so both diseases exist in many patients. Previous studies have shown that there is a link between fatty liver and cardiovascular disease however it is not fully understood if fatty liver disease precedes or develops after cardiovascular disease.

Using data from participants in the Framingham Heart Study, researchers saw that individuals with fatty liver disease developed cardiovascular diseases such as high blood pressure and type 2 diabetes within six years. In a parallel analysis, individuals with high blood pressure, type 2 diabetes, or high triglycerides had a higher likelihood of developing fatty liver disease.

In our study, we observed a bi-directional association between fatty liver and cardiovascular disease,” explained corresponding author Michelle Long, MD, assistant professor of medicine at Boston University School of Medicine (BUSM), who also is a gastroenterologist at Boston Medical Center (BMC). “We observed that fatty liver was an important factor in the development of high blood pressure and diabetes and the opposite also stands true – various cardiovascular diseases were associated with the development of fatty liver disease over six years,” she added.

Long believes this study highlights the need to develop both preventative and treatment strategies for fatty liver disease in order to improve the cardiovascular health of all people.

Citation: Ma, Jiantao, Shih-Jen Hwang, Alison Pedley, Joseph M. Massaro, Udo Hoffmann, Raymond T. Chung, Emelia J. Benjamin, Daniel Levy, Caroline S. Fox, and Michelle T. Long. “Bidirectional relationship between fatty liver and cardiovascular disease risk factors.” Journal of Hepatology (2016).
DOI: http://dx.doi.org/10.1016/j.jhep.2016.09.022
Funding: NIH/National Heart, Lung and Blood Institute, Boston University School of Medicine.

Adapted from press release by Boston University School of Medicine.

Research shows advances in development of hand held breathalyzers to diagnose Diabetes

For several years, scientists have been working toward “breathalyzers” that can diagnose various diseases without painful pinpricks, needles or other unpleasant methods. Now, one team has developed a new, portable breath analyzer that could someday help doctors diagnose diabetes noninvasively in the office. The report appears in the ACS journal Analytical Chemistry.

Many studies examining the hallmarks of diabetes in exhaled breath have shown that elevated levels of acetone are strongly linked to diabetes. Detecting the concentrations of any given substance in breath in a simple way, however, is a major challenge. Breath contains a complex mix of compounds, including water, carbon dioxide and methane, that can throw results off. Mass spectrometry can do the job, but it’s not very practical for point-of-care testing. Robert Peverall and colleagues wanted to fill that void.

The researchers created a hand-held device with an adsorbent polymer that can trap acetone from exhaled breath, then release it into a cavity where a laser probes its concentration. They tested the accuracy of the device on the breath of healthy subjects under different conditions, such as after overnight fasting or exercising, and compared results with mass spectrometry readings. The measurements were a close match and covered a wide range of concentrations, including those that would suggest a patient has undiagnosed type-1 diabetes, or has problems controlling their blood glucose. Adding to the practicality of the device, the researchers say it could be re-used many times.

Citation: Blaikie, Thomas PJ, John Howard Couper, Gus Hancock, Philip L. Hurst, Robert Peverall, Graham Richmond, Grant AD Ritchie, David Taylor, and Kevin Valentine. “A portable device for measuring breath acetone based on sample preconcentration and cavity enhanced spectroscopy.” Analytical Chemistry (2016).
DOI: http://dx.doi.org/10.1021/acs.analchem.6b02837
Adapted from press release by American Chemical Society

Protein biomarkers to screen early type 1 diabetes mellitus

Certain proteins in the blood of children can predict incipient type 1 diabetes, even before the first symptoms appear. A team of scientists at the Helmholtz Zentrum München, partners in the German Center for Diabetes Research (DZD), reported these findings in the ‘Diabetologia’ journal.

The work was based on two large studies that are intended to explain the mechanisms behind the development of type 1 diabetes (BABYDIAB and BABYDIET*). The study participants are children who have a first-degree relative with type 1 diabetes and who consequently have an increased risk of developing the disease due to the familial predisposition. Type 1 Diabetes is an autoimmune disease and often young children go through asymptomatic phase characterized by presence of auto antibodies in the blood.

A team of scientists, led by Dr. Stefanie Hauck, head of the Research Unit Protein Science and the Core Facility Proteomics, and Prof. Dr. Anette-G. Ziegler, Director of the Institute of Diabetes Research (IDF) at the Helmholtz Zentrum München, analyzed blood samples from 30 children with autoantibodies who had developed type 1 diabetes either very rapidly or with a very long delay. The researchers compared the data with data on children who displayed neither autoantibodies nor diabetes symptoms. In a second step with samples from another 140 children, the researchers confirmed the protein composition differences that they found in this approach.

“Altogether, we were able to identify 41 peptides from 26 proteins that distinguish children with autoantibodies from those without,” reports Dr. Christine von Toerne. Striking in their evaluations: A large number of these proteins are associated with lipid metabolism. “Two peptides – from the proteins apolipoprotein M and apolipoprotein C-IV – were particularly conspicuous and were especially differently expressed in the two groups,” von Toerne adds. In autoantibody-positive children, it was furthermore possible to reach a better estimate of the speed of the diabetes development using the peptide concentrations of three proteins (hepatocyte growth factor activator, complement factor H and ceruloplasmin) in combination with the age of the particular child.

The researchers are confident that the protein signatures they have discovered will be helpful as biomarkers for future diagnostics.

Citation: Christine von Toerne, Michael Laimighofer, Peter Achenbach, Andreas Beyerlein, Tonia de las Heras Gala, Jan Krumsiek, Fabian J. Theis, Anette G. Ziegler, Stefanie M. Hauck. “Peptide serum markers in islet autoantibody-positive children”. Diabetologia (2016).
DOI: http://dx.doi.org/10.1007/s00125-016-4150-x
Adapted from press release by Helmholtz Zentrum München

Non alcoholic blueberry-blackberry beverage shown to have anti diabetic properties in mice

Blueberries, and berries in general, are among foods labeled as “diabetes superfoods” by the American Association of Diabetes. Food science researchers at the University of Illinois have found that fermenting berries may improve their antidiabetic potential even more.

Previous research has shown that dietary blueberries may play a role in reducing hyperglycemia in obese mice, therefore de Mejia and colleagues wanted to determine if a fermented, dealcoholized blueberry-blackberry beverage would enhance the potential of the phenolic compounds in the berries that are responsible for reducing diabetic markers.

A new study shows that the fermented berry beverage did reduce the development of obesity and blood glucose levels in mice on a high-fat diet. The researchers had already determined that the berries, when fermented at low temperatures, resulted in an improved and higher concentration of anthocyanins. Anthocyanins, found in the pigments of fruits such as blueberries, grapes, and apples, have been shown to promote insulin sensitivity, decrease blood glucose levels in the blood, and enhance insulin secretion. A previous cell culture study with the alcohol-free blueberry-blackberry wine, showed good results toward inhibiting enzymes related to glucose absorption.

The beverage included a ratio of 70 percent fermented blackberries to 30 percent fermented blueberries. The berries were collected from varieties grown at U of I’s Dixon Springs Agricultural Research Station in southern Illinois. Alcohol was removed from the beverage by rotoevaporation and was replaced with water. Some of the sugars left over after fermentation were also removed in the process.

During the study, groups of mice with diet-induced obesity and hyperglycemia were given the fermented berry beverage or the beverage with higher or lower enriched concentrations of the anthocyanins (0.1x, 1x, or 2x). Another group was given sitagliptin, a commonly used medication for diabetes, and another group was given water only. All groups ate the same diet, calories, and amount of sugars otherwise.

While benefits were seen in all groups drinking the fermented beverage, de Mejia says the group on the highest concentration of anthocyanins (2x) showed the greatest results, comparable to what was observed in the group on sitagliptin. This included no increase in body weight, which de Mejia says was a surprise.

The researchers also observed that glucose was deposited into tissue more than absorbed by and present in the blood, as well. “You want to avoid high glucose in the blood stream, and you want uptake into muscle, liver, and organs, and to keep the level in plasma and blood normal. We saw a reduction of glucose in the blood with the beverage, even in the beverage before it was enhanced,” de Mejia says.

They also saw an effect on oxidative stress in the obese mice.  “We saw that in the animals on 2x the enriched anthocyanins, the oxidative species went down, meaning they were kind of protected against oxidation. From that stand point, it was very positive looking at the oxidative stress of the animals because that can damage protein and DNA.”

Producing this berry wine, complete with the benefits of fermentation but without the alcohol, provides an opportunity for wine makers, de Mejia says. While the berry wine may not be able to replace medications for diabetics, de Mejia says it could help reduce the amount of medication needed; always under the doctor’s supervision and approval.

“There needs to be more studies to see how the anthocyanins work in the presence of medication, to see if they work synergistically, for example. Then, maybe, you could decrease the amount of the drug. All of these drugs for diabetes have adverse effects after so many years of use, even the safest ones.

Citation: Johnson, Michelle H., Matthew Wallig, Diego A. Luna Vital, and Elvira G. de Mejia. “Alcohol-free fermented blueberry–blackberry beverage phenolic extract attenuates diet-induced obesity and blood glucose in C57BL/6J mice.” The Journal of nutritional biochemistry 31 (2016): 45-59. DOI: http://dx.doi.org/10.1016/j.jnutbio.2015.12.013
Adapted from press release by University of Illinois College of Agricultural, Consumer and Environmental Sciences (ACES)

Protein galectin-3 plays role in insulin resistance and glucose intolerance

By removing the protein galectin-3 (Gal3), a team of investigators led by University of California School of Medicine researchers were able to reverse diabetic insulin resistance and glucose intolerance in mouse models of obesity and diabetes.

By binding to insulin receptors on cells, Gal3 prevents insulin from attaching to the receptors resulting in cellular insulin resistance. The team led by Jerrold Olefsky, MD, professor of medicine in the Division of Endocrinology and Metabolism at UC San Diego School of Medicine, showed that by genetically removing Gal3 or using pharmaceutical inhibitors to target it, insulin sensitivity and glucose tolerance could be returned to normal, even among older mice. However, obesity remained unchanged.

“This study puts Gal3 on the map for insulin resistance and diabetes in mouse model,” said Olefsky, associate dean for scientific affairs and senior author of the study. “Our findings suggest that Gal3 inhibition in people could be an effective anti-diabetic approach.”

Olefsky and other researchers have been studying how chronic tissue inflammation leads to insulin resistance in type 2 diabetes. In the paper, published in the journal Cell on November 3, researchers explain that inflammation requires macrophages — specialized cells that destroy targeted cells. In obese adipose tissue (fat), for example, 40 percent of cells are macrophages. Macrophages in turn secrete Gal3, which then acts as a signaling protein attracting more macrophages, thus resulting in the production of even more Gal3.

Furthermore, investigators identified bone marrow-derived macrophages as the source of Gal3 that leads to insulin resistance. More importantly, researchers found that Gal3 is secreted by macrophages, and can then cause insulin resistance in liver, fat cells, and muscle cells independent of inflammation.

Gal3 has previously been connected to other diseases. Olefsky will continue to study Gal3 depletion as a possible therapeutic target for nonalcoholic steatohepatitis as well as heart and liver fibrosis.

Citation: Hematopoietic-Derived Galectin-3 Causes Cellular and Systemic Insulin Resistance
Pingping Li, Shuainan Liu, Min Lu, Gautum Bandyopadhyay, Dayoung Oh, Takeshi Imamura, Andrew M.F. Johnson, Dorothy Sears, Zhufang Shen, Bing Cui, Lijuan Kong, Shaocong Hou, Xiao Liang, Salvatore Iovino, Steven M. Watkins, Wei Ying, Olivia Osborn, Joshua Wollam, Martin Brenner, Jerrold M. Olefsky. Cell 2016 vol: 167 (4) pp: 973-984.e12
DOI: http://dx.doi.org/10.1016/j.cell.2016.10.025
Adapted from press release by University of California San Diego

Research finds potential cause of chronic inflammation in diabetic patients

Inflammation is one of the main reasons why people with diabetes experience heart attacks, strokes, kidney problems and other, related complications. Now, in a surprise finding, researchers at Washington University School of Medicine in St. Louis have identified a possible trigger of chronic inflammation. The study is available Nov. 2 as an advance online publication from the journal Nature.

Immune cells (shown in green) produce fatty acids that contribute
to diabetes-related inflammation. Credit: Semenkovich lab
Washington University School of Medicine

Semenkovich’s team made genetically altered mice that could not make the enzyme for fatty acid synthase (FAS) in immune cells called macrophages. Without the enzyme, it was impossible for the mice to synthesize fatty acids, a normal part of cell metabolism.

“We were surprised to find that the mice were protected from diet-induced diabetes,” said first author Xiaochao Wei, an instructor of medicine. “They did not develop the insulin resistance and diabetes that normally would have been induced by a high-fat diet.”

Through a series of experiments in the animals and in cell cultures, the researchers, including Douglas F. Covey, a professor of developmental biology and biochemistry, and Daniel S. Ory, MD, a professor of medicine and of cell biology and physiology, found that if macrophages could not synthesize fat from within, the external membranes of those cells could not respond to fat from outside the cells. That prevented the cells from contributing to inflammation.

But eliminating inflammation altogether is not the answer to preventing diabetic complications because inflammation is also vital for clearing infectious pathogens from the body and helps wounds heal. Still, Semenkovich said the new findings may have profound clinical implications.

“An inhibitor of fatty acid synthase actually is now in clinical trials as a potential cancer treatment,” he explained. “And other drugs have been developed to inhibit fatty acid synthase in diabetes, too. One possibility that our work suggests is that altering the lipid content in the cell membrane may help block cancer metastases and complications of diabetes.”

Drugs currently in use to block fatty acid synthase, as well as other developing strategies, potentially could allow for chronic inflammation to be blocked, without co
mpletely eliminating the ability of macrophages to fight infection. The researchers also plan to take a look at existing drug compounds that change the lipid composition in cells.

Citation:Wei X, Song H, Rizzo MG, Sidhu R, Covey DF, Ory DS, Semenkovich CF. Fatty acid synthesis configures the plasma membrane for inflammation in diabetes. Nature. Nov. 2, 2016.
DOI: http://dx.doi.org/10.1038/nature20117
Adapted from press release by Washington University School of Medicine

Researchers reveal wound healing function of heat shock protien 60 (Hsp60) in mice

National Institutes of Health researchers have identified a novel role for a gene known as heat shock protein 60 (Hsp60), finding that it is critical in tissue regeneration and wound healing. The study found that topical treatment of an Hsp60-containing gel dramatically accelerates wound closure in a diabetic mouse model.

The study also describes the mechanism by which this works, finding that Hsp60 protein is released at the site of injury, signaling wound healing to initiate. The findings, reported by researchers at the National Human Genome Research Institute (NHGRI), the National Eye Institute (NEI), and their colleagues, may help in the development of effective therapeutics for accelerating wound closure in diabetic patients, as well as for normal wound healing and scar reduction.

“This study proposes an unusual role for a well-known gene,” said Shawn Burgess, Ph.D., head of NHGRI’s Developmental Genomics Section and senior author on the study, which was published  in the journal npj Regenerative Medicine. “This gene is found in every organism from bacteria to man. We have shown that in vertebrates, it has a surprising role in immunity that is essential for wound healing.”

Protein products of the Hsp60 gene are known primarily for their role in ensuring that other proteins are folded correctly. The Hsp60 protein has also been reported to serve as a signaling molecule that induces an inflammatory response to bacterial infection from a cut. Based on previous findings that the Hsp60 protein was necessary for an inflammatory response, the researchers hypothesized that the molecule might also be involved in an organisms’ ability to regenerate.

Using zebrafish — an ideal model for this work because fish can regenerate many tissues, including fins — the researchers used targeted mutagenesis, making specific and intentional changes to the DNA sequence of a gene, to “knock out” Hsp60 from the genome. The mutant fish appeared to develop normally, but when the researchers wounded them by injuring the cells involved in hearing or amputating a caudal fin, the fish were unable to regenerate their cells and fins, respectively.

Using fluorescently tagged leukocytes (immune cells that flock to the site of injury as part of the inflammatory response under normal conditions), the researchers demonstrated that without the Hsp60 gene, there were significantly reduced numbers of leukocytes at the injury site. This suggested that the Hsp60 protein was somehow acting as an attractant that promoted inflammation, a necessary component of wound healing.

“When we injected Hsp60 directly to the site of injury, the tissue surrounding the wound started to regenerate faster,” said Dr. Burgess. “That’s when we got really excited.” However, the most striking finding from the study was that actually applying a topical treatment of the Hsp60 protein to a puncture wound in diabetic mice stimulated complete healing after only 21 days. Mice without the treatment did not show improvement over the same time frame.

Although promising, this finding has only been shown in mice and is yet to be tested in humans.
“We hope that topical treatment with Hsp60 will act the same way in humans,” said Dr. Burgess. “And we believe it will, but more work is needed. We also want to know if it will help any wound heal, not just wounds encountered by people with diabetes. Will it reduce scarring and increase the speed of healing?”

This study reveals a potential for therapeutic development, but also highlights the value of basic science research. The fundamentals of cell signaling in wound healing and tissue regeneration are still poorly understood, with basic science research helping to clarify many important aspects of this complicated process.

Citation: Extracellular HSP60 triggers tissue regeneration and wound healing by regulating inflammation and cell proliferation. Authors: Wuhong Pei, Katsuya Tanaka, Sunny C Huang, Lisha Xu, Baoying Liu, Jason Sinclair, Jennifer Idol, Gaurav K Varshney, Haigen Huang, Shuo Lin, Robert B Nussenblatt, Ryoichi Mori & Shawn M Burgess
DOI: http://dx.doi.org/10.1038/npjregenmed.2016.13
Journal: npj Regenerative Medicine
Research funding: National Human Genome Research Institute, The National Eye Institute
Adapted from press release by NIH

Research shows link between impaired glucose tolerance and adverse cardiac structure and function.

A study of U.S. Hispanics with diabetes mellitus showed a link between impaired glucose regulation and adverse measures of cardiac function and structure. Researchers at Columbia University’s Mailman School of Public Health in collaboration with colleagues from Wake Forest Medical School and six other institutions extended previous knowledge regarding the concept of ‘diabetic cardiomyopathy, by also observing that these relationships emerged early and before the full onset of diabetes mellitus. The findings are published online in the journal Circulation: Cardiovascular Imaging.

Results were from the ECHO-SOL (Echocardiographic Study of U.S. Latinos) which examined chronic disease risk factors and related morbidity and mortality of 1,818 Hispanic/Latino men (43 percent) and women (57 percent) 45 years of age and older. Participants were recruited from the Bronx, New York; Chicago; Miami; and San Diego.

Glucose intolerance was defined as having a prediabetes hemoglobin of ?5.7 and <6.5 percent; diabetes mellitus was defined as a fasting glucose reading of ?126 mg/dL, and a hemoglobin of ?6.5 percent. Prediabetes was prevalent for 42 percent of the participants, and diabetes mellitus was reported by 28 percent with 47 percent uncontrolled and a hemoglobin of ?7.0 percent.

“Whether aggressive glucose-lowering therapy can prevent these cardiac alterations that lead to heart failure remains unknown, but it supports the notion that HbA1c <7% may be important for cardiac health," said Dr. Carlos J. Rodriguez, senior author and PI of the ECHO-SOL.

These findings also raise the possibility that primary prevention efforts targeting insulin resistance and glucose homeostasis might also be beneficial for optimal cardiac health and heart failure prevention although future studies are necessary. “If confirmed, these results would have high public health importance given the fact that Hispanics have elevated rates of Type 2 diabetes compared to the U.S. population overall. This is coupled with the fact that Hispanics are expected to account for 25 percent of the U.S. population by 2050,” noted Demmer.

Research funder: NIH/National Heart, Lung, and Blood Institute, NIH/National Institute on Deafness and Other Communication Disorders, NIH/National Institute of Dental and Craniofacial Research, NIH/National Institute of Diabetes and Digestive and Kidney Diseases

Adapted from press release by University Columbia, Mailman school of public health.