Obesity is not a simple phenomenon at all. This has always been suspected, given the enormous amount of biological, statistical, epidemiological, food and socio-cultural data that lie behind it. Now, at least one new genetic, hormonal or alimentary mechanism is published annually on the topic, making the picture a “sea that extends into ocean”.
New research published in the journal Nature Medicine suggests that a new hormone called asprosine triggers hunger in the brain. The dott. Atul Chopra, a medical geneticist, assistant professor of Molecular and Human Genetics and of Molecular and cellular biology, at the Baylor College of Medicine in Houston, is one of the authors of the study. One of his previous research has allowed us to discover the hormone for the first time in 2016. The researchers later discovered that it is produced by fat and that regulates blood sugar levels, acting on the liver and “telling” it to release glucose. in the blood. Now, the team has shown that the hormone also affects the hypothalamus of the brain, regulating appetite and weight. When the hormone was discovered last year, Dr. Chopra only analyzed two patients with a very rare genetic disease called neonatal progeroid syndrome (NPS). One of the symptoms of the disease is extreme thinness, because the body is not able to accumulate fat.
The researchers were able to identify a genetic mutation of the NPS responsible for an asprosine deficiency. Significantly, the researchers also found that the hormone stimulates two types of neurons. There are two types of neurons involved in appetite control: one type, AgRP neurons, stimulates appetite while the other type, POMC neurons, suppresses it. Asprosine acts on both types of neurons in the opposite way, activates AgRP stimulating appetite neurons and disables POMC neurons that suppress appetite. “Our results give us the opportunity to treat obesity by regulating levels of asprosinemia, but much work still remains to be done, however, these findings potentially open the door to a whole new way of treating obesity,” says Dr. Chopra. Not only that, but asprosine is also a potential therapeutic target in the treatment of diabetes. Previous research by the authors found that the administration of anti-asprosine antibodies to diabetic mice reduced blood sugar levels. If men with diabetes respond in the same way as the asprosine antibody that diabetic mice do, this finding could lead to a new treatment for diabetes, which affects hundreds of millions of people globally.
And we pass on one of the factors that has been investigated more recently as a contributor to the appearance of obesity: stress. The researchers found that women who experienced traumatic events during their lifetime, or negative life events in the last 5 years were more likely to become obese, than women who had not experienced such events. The author Michelle A. Albert, from the Center for the Study of Adversity and Cardiovascular Diseases at the University of California, San Francisco, and colleagues recently presented their results at the Scientific Sessions 2017 of the American Heart Association. Previous research has shown that psychological stress can affect our eating habits. Dr. Albert says: “We know that stress affects behavior, including the fact that people are under or overweight as well as neurohormonal activity, partly increasing the production of cortisol, which is related to the increase of weight”. However, researchers note that little is known about how negative life experiences or traumatic events can influence the likelihood of a tendency toward obesity. This is what the Dr. Albert and colleagues tried to find out.
The researchers analyzed data from 21,904 middle-aged and elderly women who were part of the Women’s Health Study (WHS) 2012-2013. The team examined the number of self-reported traumatic events (such as a child’s death, physical abuse or a life-threatening illness) among women, as well as the number of negative life events (such as unemployment or being robbed) at home) in the last 5 years. They then examined whether these events were associated with the body mass index (BMI) or not. The researchers defined obesity with a BMI of 30 kilograms per square meter or higher and 23% of the study participants met this definition. The study revealed that women who experienced at least one traumatic event during their lifetime had 11% more likely to become obese than women who had not had traumatic events. The risk of becoming obese was 36% higher for women who had at least four negative life events in the last 5 years, compared to women who had no negative life events. The longer the negative life events last, the greater the risk of obesity.
Finally, there are news on feeding and weight regulation. One of the latest news concerns mulberries, sweet-tasting fruits that are believed to have a wealth of health benefits, including reducing cholesterol, improving blood sugar levels and a lower risk of cancer. The extracts of black mulberry leaves or bark are known to herbalists for their hypoglycaemic abilities, which makes them a pre-condition in the natural management of diabetes. Now, a team of Chinese researchers suggests that rutin, a naturally occurring flavonoid in mulberry, could also help treat obesity. The co-author of the study Wan-Zhu Jin, Ph.D., of the Institute of Zoology of the Chinese Academy of Sciences, and the team investigated the metabolic effects of rutin, in order to determine if the compound could stimulate weight loss. For their study, published in FASEB Journal, the team added rutin (1 milligram per milliliter) to the drinking water of two groups of mice. One group of mice was genetically obese, while the other group had diet-induced obesity. Both groups were fed on a regular diet throughout the duration of the study.
In both groups of mice, rutin was able to activate brown adipose tissue (BAT), or brown fat, which resulted in an increase in energy expenditure, improved glycemic homeostasis – that is, the balance of insulin and glucagon to maintain glucose levels – and fat reduction. Brown fat is activated by cold, activating the combustion of substrates and the production of heat. According to the researchers, rutin acts as a “cold mimetic” by activating a specific cascade of signals, which increases the activity of a gene called UCP1 and the number of mitochondria in brown fat. The UCP1 protein decouples the production of energy in the mitochondria, causing them to release in the form of heat. In addition, the team found that rutin activated the formation of fatty cells similar to brown fat in both the experimental models of obesity. Based on their findings, researchers believe that rutin can offer a new therapeutic approach to obesity and other conditions associated with excess weight.
Therefore, more data for one of the “biggest” problems on the globe, but also more solutions.
- edited by Dr. Gianfrancesaco Cormaci, PhD, specialist in Clinical Biochemistry.