Love hormone effective in treating postpartum depression

A type of love hormone called Oxytocin, which is important in the regulation of social and maternal behavior, is also found helpful in treatment for many mental health disorders including postpartum depression.

The oxytocin receptor cells are present in the brain area and are thought to be involved in the regulation of maternal behavior. Moreover, the expression of oxytocin receptors in these cells are only present when estrogen is also present.

This implies that these cells are involved in inducing maternal behaviour. In addition, it confirms what many recent human studies have shown: there is a connection between altered expression of oxytocin receptors and postpartum depression.

“Many researchers have attempted to investigate the difference between the oxytocin system in females versus males, but no one has successfully found conclusive evidence until now. Our discovery was a big surprise,” said an associate professor and lead researcher of the study.

Postpartum depression contributes to poor maternal health and has negative effects on a child’s development. A number of studies have found that children of depressed mothers are at risk for a wide range of cognitive, emotional, behavioral and medical problems. Therefore, postpartum depression is a major public health concern that has significant adverse effects on both mother and child. About 10 to 20 percent of women experience postpartum depression after childbirth.

This new discovery opens doors to potential new treatments and drugs for postpartum depression targeting oxytocin receptor cells. “I think our discovery could be universal to all mammals that exhibit maternal behavior, including humans,” the author said.

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Experts Explain How Vit D Deficiency Can Cause Heart Failure

A daily dose of sunshine, which stimulates production of Vitamin D in the body, is vital not just for the well-being of your bones but may also be good for your heart.

The problem of vitamin D deficiency affecting bone health is well known for decades. For some years, scientists have also seen vitamin D deficiency as a factor that determines health of your heart. Now Indian researchers have deciphered how exactly vitamin D deficiency can cause heart failure.

The new study has shown that vitamin D deficiency alone can lead to heart failure, possibly through insulin resistance. It has found that cardiac insulin leads to functional deterioration of heart in animals with low vitamin D levels.

The utilization of glucose and fatty acids – key fuels for energy generation in heart – is adversely affected due to insulin resistance in heart cells. Insulin plays a critical role in regulation of cellular metabolism in many tissues in the body.

To study if vitamin D deficiency could cause cardiac damage similar to other risk factors like consumption of high fats and high calorie food, researchers designed an experiment with rats. They manipulated diets of animals and divided them into three groups – one with adequate vitamin D, second set had vitamin D deficiency, while the third group was fed with high fat and high fructose diet.

At the end of 20 weeks, it was found that the hearts of vitamin D deficient animals were failing. They showed molecular and functional changes similar to the hearts of rats in high fat high fructose diet group. “The cardiac dysfunction caused by vitamin D deficiency alone was very similar to that by the other risk factor – high calorie diet – sometimes even to a greater extent in some parameters. For example, cardiac inflammation was higher in vitamin D deficiency diet than high calorie diet,” researchers have observed in the study.

Researchers found greater expression of genes involved in enlargement of cardiac muscles. These findings were confirmed when scientists measured heart wall thicknesses, chamber internal diameters and contracting capacity of heart. Left ventricular posterior wall thickness was found to be increased in rats with vitamin D deficiency. This happens when cardiac workload increases and turns pathological if no remedial measures are taken, finally progressing to heart failure. In such condition, the pumping action of the heart can no longer meet the metabolic demands of the body.

“We have shown the link between vitamin D deficiency and cardiac dysfunction and how it may lead to heart failure. Vitamin D and its signalling modulate myocardial insulin sensitivity, the insufficiency of which induces impaired glucose utilization, remodeling response, and heart failure,” explained a senior scientist.

The group, in its study in 2016 involving a South Indian population, had shown that low vitamin D levels were associated with diabetes as well as diabetes plus coronary artery disease. However, it had not provided any cause-effect relationship. “Our study now tackles exactly that issue with animal experiments and provides conclusive evidence,” Dr. added.

The new findings have both public health and therapeutic implications. The insights gained on how vitamin D signalling affects myocardial insulin sensitivity may help scientists design new drugs for management of heart failure by targeting activation of vitamin D receptor.

With vitamin D deficiency emerging as a risk factor for heart disease, public health policies will have to take note of it since metabolic disorders are already a major health challenge in India. “We have evidence to show that widespread vitamin D deficiency in Indians definitely contributes to insulin resistance and diabetes. Our previous research and ongoing work in Indian population have indicated that supplementation with vitamin D may help in ameliorating insulin resistance and decreasing blood glucose levels,” commented a Dr.

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Molecules wired for obesity discovered

Researchers from across the globe have pinpointed a set of molecules that wire the body weight centre of the brain.

Research teams  tried to uncover key genes that guide the process of brain development.

"We know that the brain, in particular an area called the hypothalamus, has a very important role in the regulation of food intake and blood sugar," explains one of the researchers.

Researchers have focused on the hypothalamus for years in an effort to study the epidemic of obesity, which affects nearly 14 million children and adolescents in the United States. "What we don't yet understand," he says, "is how these circuits in the hypothalamus are being organised. We want to know how the brain puts itself together and what exactly governs that process." Understanding this is key because circuits must be established properly in order for the brain to ultimately perform complex functions like maintaining proper weight.

Why do certain brain cells connect to one area while specifically avoiding other, nearby cells? 

Researchers investigate how this precise wiring is achieved. Understanding how brain cells in the hypothalamus form these specific, complex connections and how this process can be adversely affected could provide insight into the development of childhood obesity. 

The researcher studied a group of molecules called semaphorins, which are found in abundance in the developing hypothalamus. Brain cells release semaphorins to communicate with other brain cells. These messages act as a sort of road map, guiding cells towards or away from other cells. But what happens to the brain when that road map is no longer functioning properly?

The Dr. who led the study, blocked semaphorin signaling in cells of the hypothalamus. She discovered that brain cells no longer grew the way they were supposed to, showing that semaphorin provide an essential map for them to follow. In addition to connections failing to establish, loss of semaphorin action in a preclinical model also caused elevated body weight. "What we are seeing is that semaphorins are guiding and shaping development of hypothalamic circuits that ultimately regulate calorie intake," explains the Dr.

A Prof. was also analysing genetic information from individuals with obesity. His team tested 1,000 DNA samples and found that individuals with early-onset obesity had more rare mutations in genes involved in semaphorin signaling than healthy individuals. The finding that people with obesity have rare mutations in semaphorin signaling shows that semaphorins are important in maintaining healthy body weight.

"We have now discovered the genes that establish the precise neural connections that form these circuits," says the Dr. who led the study and is co-first author on the paper. "This work provides new insights into the development of hypothalamic circuits that regulate appetite and metabolism."

This study gives a much clearer picture of what occurs in the developing brain. Semaphorin signaling appears to shape the physical architecture of the brain and influence circuitry governing body weight.

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Diabetic and struggling with weight loss? Things to know about diabetes and alcohol use

Repeated binge drinking can take a serious toll on your health. Studies have shown that heavy alcohol consumption puts you at a higher risk of certain health problems such as liver disease, heart ailments, stroke, brain damage, cancer, etc. Drinking too much can lead to weight gain because alcohol contains a lot of calories. Yet, when you have diabetes, it can be a little more complicated. Hence, people with diabetes are advised to be particularly cautious when it comes to drinking.
 
First of all, alcohol prevents the liver from performing its job, including regulating blood sugar. Alcohol can also interact with some diabetes medications. It can also worsen some complications of diabetes. If you’re living with diabetes and want to know whether it’s safe to consume alcohol, or how much is okay, read on below.

What you need to know about diabetes and alcohol use

Alcohol and your weight: Studies have shown that losing weight can help prevent or delay the onset of diabetes. A research published suggested that weight loss may even help reverse type 2 diabetes. However, researchers  suggest that alcohol intake may weaken long-term weight loss in people with overweight or type 2 diabetes. Their study showed that participants in the Intensive Lifestyle Intervention (ILI) group who abstained from alcohol consumption over the four-year period were able to lose more weight than those who drank any amount during the intervention. Moreover, since alcohol is very high in calories it can make it difficult for people to shed those extra pounds. Hence, diabetes who are trying to lose weight should be encouraged to limit alcohol intake.

Alcohol and your blood sugar levels: Drinking alcoholic beverages can cause fluctuations in blood sugar levels. For instance, consuming moderate amounts of alcohol may cause blood sugar to rise, heavy drinking can actually make your blood glucose levels drop within a few minutes of taking. 

Alcohol and your appetite: Alcohol can have a significant impact on your appetite and eating habits. It stimulates your appetite, making you overeat. This may affect your blood sugar control.

Alcohol and your liver: The liver stores glycogen, a form of glucose that the body reserves for future use. But drinking alcohol impairs the liver from doing its job. When you drink, your liver has to compromise with its function while trying to remove alcohol from your blood instead of working to regulate blood glucose.

Alcohol and your blood pressure: People with diabetes are more like to have high blood pressure, and having these conditions together can worsen both the diseases. Alcohol can lead to high blood pressure, which is a major risk factor for heart disease and stroke. Perhaps, being diabetic raises your risk for heart disease, stroke, kidney disease and other health issues.

If you are living with diabetes, it is always safe to check with your doctor to determine whether drinking alcohol is safe for you.

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Secrets of longevity protein revealed

Named after the Greek goddess who spun the thread of life, Klotho proteins play an important role in the regulation of longevity and metabolism. In a recent study, researchers revealed the three-dimensional structure of one of these proteins, beta-Klotho, illuminating its intricate mechanism and therapeutic potential.

The study findings, could have implications for therapies developed to treat a wide range of medical conditions, including diabetes, obesity, and certain cancers, the researchers said.

The Klotho family of two receptor proteins are located on the surface of cells of specific tissues. The proteins bind to a family of hormones, designated endocrine FGFs, that regulate critical metabolic processes in the liver, kidneys, and brain, among other organs. To understand how beta-Klotho works, the research team used X-ray crystallography, a technique that provides high-resolution, three-dimensional views of these proteins.

The researchers’ analysis yielded several insights. First, beta-Klotho is the primary receptor that binds to FGF21, a key hormone produced upon starvation. When bound to beta-Klotho, FGF21 stimulates insulin sensitivity and glucose metabolism, causing weight loss. This new understanding of beta-Klotho and FGF21 can guide the development of therapies for conditions such as type 2 diabetes in obese patients, the researchers said.

“Like insulin, FGF21 stimulates metabolism including glucose uptake,” said a senior author. “In animals and in some clinical trials of FGF21, it shows that you can increase burning of calories without changing food intake, and we now understand how to improve the biological activity of FGF21.” The authors also describe a new variant of FGF21 that has 10 times higher potency and cellular activity.

Additionally, the research team presented evidence of how a structurally-related enzyme, glycosidase, which breaks down sugars, evolved into a receptor for a hormone that lowers blood sugar—which may not be a coincidence, the researcher added.

Having untangled the structure of beta-Klotho, the researchers have a platform for exploring potential therapies for multiple diseases. By developing drugs that enhance the pathway, he said, researchers can target diabetes and obesity. Conversely, using agents that block the pathway, they hope to explore therapies for conditions such as liver cancer and bone diseases, among others.

“The next step will be to make better hormones, make new potent blockers, do animal studies, and move forward,” the researcher said.

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Here's how leaky calcium puts epileptics at heart risk

Sudden unexpected death in epilepsy (SUDEP) has long bedeviled doctors and now, a team of researchers may have found the cause of it.

In a paper, researchers from Baylor College of Medicine reported how a mutation in a gene involved in the regulation of calcium inside brain cells can help trigger blackouts of the brain stem, the center that controls heartbeat and breathing, and increase the risk of sudden unexpected death.

"SUDEP turns out to be the most common cause of premature death in people with epilepsy. It's not accidents or suicide, it's just this unexplained mortality," said senior author Dr Jeffrey L. Noebels.

He added, "Most people with epilepsy live long lives and do not seem to have an increased risk of SUDEP. But there is a subset of people at additional risk. We have been looking for genes that cause epilepsy to see if any of them might give us a clue as to who might be at risk. Specifically, we have been looking at genes that might explain what appears to be a collapse of the cardiac and respiratory system after a seizure."

In their years-long quest to understand the cellular and genetic mechanisms that may trigger SUDEP, Noebels and his colleagues studied the genes that are involved in the heart beat. Some of these genes are already well known to be related to sudden unexpected cardiac death.

"We wondered whether some of those same genes could also cause seizures if they were expressed in the brain, and, if so, whether those genes would also place people with epilepsy at risk, not only for having epilepsy, but an abnormal heart beat and risk of death," said Noebels. "In our first experiments we found several genes that actually filled that description: they are expressed in the brain and the heart, and mutations of those genes cause an abnormal heart beat and epilepsy in mouse models."

The researchers then found that these same genes carry an additional risk for a phenomenon called spreading depolarization, a slowly-progressing, temporary electrical blackout of a region in the brain. During a blackout, the brain cells in that area cease their activity until it is restored.

Noebels and colleagues studied another gene - RyR2 - which is also expressed in the heart and known to cause heart problems. They showed that RyR2, which is also expressed in the brain, also causes epilepsy in mice and sets up an electrical surge that makes a fatal blackout likely.

For Noebels and colleagues, the discovery of how the 'leaky' RyR2 increases the chances of SUDEP is a step forward toward a future in which neurologists could sit with a patient and their family and have a conversation about the possibility of offering an accurate prediction of the risks of SUDEP and effective interventions.

The study is published on the Proceedings of the National Academy of Sciences. 

 

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Metabolism is linked with gene regulation

In a discovery that holds promise for the understanding of many diseases, including cancer, researchers have discovered a new way by which metabolism is linked to the regulation of DNA - the basis of our genetic code.

The DNA wraps around specialised proteins called histones in the cell's nucleus.

Histones keep the DNA tightly packaged, preventing the expression of genes and the replication of DNA which are required for cell growth and division.

In order for critical functions to take place, histones need to be modified with the attachment of an acetyl-group, donated by a critical molecule called acetyl-CoA.

The research team, led by post-doctoral fellow Gopinath Sutendra from University of Alberta, discovered that an enzyme thought to reside only within mitochondria - Pyruvate Dehydrogenase Complex (PDC) - can actually find its way into the nucleus and do what it is designed to do in the mitochondria: generate acetyl-CoA.

This attachment relaxes the DNA, allowing for DNA replication and gene expression.
"This mechanism is called 'epigenetic regulation of DNA' and is important for normal functions like the growth of an embryo or brain functions or in common diseases like heart failure or cancer," Sutendra explained.

Until now, how the nucleus generates acetyl-CoA for histone acetylation had remained elusive.
Because the findings relate to how our DNA is regulated in general, this work may have far broader implications for many physiologic or pathologic conditions where epigenetic regulation is critical," Sutendra added.

"We are very excited about this new pathway linking energy production (the process known as metabolism) with gene regulation," researchers said in a paper published in the journal Cell.

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