Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By NICHOLAS BAKALAR Diabetes may be bad for the brain, especially if you are overweight. Researchers studied 50 overweight and 50 normal weight people in the early stages of Type 2 diabetes. All had been given a diagnosis within the previous five years. They compared both groups with 50 healthy control subjects. The scientists performed M.R.I. examinations of their brains and psychological tests of memory, reaction time and planning. Those with diabetes scored worse than the healthy controls on tests of memory and reaction times. M.R.I. scans revealed significant differences in brain areas related to memory, planning and the visual processing of information. Compared with the controls, those with Type 2 diabetes had more severe thinning of the cortex and more white matter abnormalities. Overweight people with diabetes had more brain deterioration than diabetic people of normal weight. Are these changes reversible? Probably not, according to a co-author, Dr. Donald C. Simonson of Brigham and Women’s Hospital in Boston. “When structural changes are seen on an M.R.I. scan, the processes leading up to them have probably been going on for years,” he said. “On the positive side, patients who maintain good control of their diabetes do seem to have a slower rate of deterioration.” The findings were published in Diabetologia. © 2017 The New York Times Company
By NICHOLAS BAKALAR A new study links diet soft drinks to an increased risk for stroke and dementia. Researchers studied more than 4,000 people over 45 who had filled out food-frequency questionnaires and had periodic health examinations between 1991 and 2001. The scientists tracked their health over the next 10 years and found 97 cases of stroke and 81 cases of dementia. The study, in the journal Stroke, found that compared with those who did not drink diet soda, people who drank one to six artificially sweetened drinks a week had twice the risk of stroke. There were similar, although weaker, associations for dementia risk. The reasons for the link remain unknown. The study adjusted for age, sex, education, physical activity, diabetes, smoking and many other characteristics that might affect the risks. But the senior author, Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine, said that there were additional variables the study could not address. For example, she said, people might have switched to diet soda because they already had cardiovascular problems. Still, she added, there are health benefits associated with some drinks, like tea or coffee, “but not with soda of any kind, either diet or not.” © 2017 The New York Times Company
By Knvul Sheikh Scientists have known for decades that what we eat can change the balance of microbes in our digestive tracts. Choosing between a BLT sandwich or a yogurt parfait for lunch can increase the populations of some types of bacteria and diminish others—and as their relative numbers change they secrete different substances, activate different genes and absorb different nutrients. And those food choices are probably a two-way street. Gut microbes have also been shown to influence diet and behavior as well as anxiety, depression, hypertension and a variety of other conditions. But exactly how these trillions of tiny guests—collectively called the microbiome—influence our decisions on which foods to stuff into our mouths has been a mystery. Now neuroscientists have found specific types of gut flora help a host animal detect which nutrients are missing in food, and then finely titrate how much of those nutrients the host really needs to eat. “What the bacteria do for appetite is kind of like optimizing how long a car can run without needing to add more petrol to the tank,” says senior author Carlos Ribeiro, who studies the eating behaviors of Drosophila melanogaster, a type of fruit fly, at Champalimaud Center for the Unknown in Lisbon. In a paper published Tuesday in PLoS Biology Ribeiro and his team demonstrated how the microbiome influences drosophila’s nutritional decisions. First, they fed one group of flies a sucrose solution containing all the necessary amino acids. Another group got a mix that had some of the amino acids needed to make protein but lacked essential amino acids that the host cannot synthesize by itself. For a third group of flies, the scientists removed essential amino acids from the food one by one to determine which was being detected by the microbiome. © 2017 Scientific American,
Link ID: 23538 - Posted: 04.26.2017
By NICHOLAS BAKALAR Drinking sugary beverages is associated with markers of accelerated aging and early signs of Alzheimer’s disease, a new study reports. Researchers used data on more than 4,000 people over 30, examining their brains with M.R.I. and measuring memory with psychological tests. All completed well-validated food frequency questionnaires. Sugary beverage intake is an indirect measure of how much sugar we get in our diets, which is difficult to measure precisely. The authors defined “sugary beverage” to include sodas as well as fruit juices, which may contain added sugars. The study, in Alzheimer’s & Dementia, found that on average, the more sugary drinks consumed, the lower the total brain volume and the lower the scores on memory tests. Brain shrinkage is tied to an increased risk of Alzheimer’s disease. Compared with those who drank no sugary drinks, those who drank one or two a day had a reduced brain volume equivalent to 1.6 years of normal aging, and lower memory scores equivalent to 5.8 years of aging. Those who drank more than two had decreased brain volume equivalent to two years of normal aging and lower memory scores by the equivalent of 11 years. The researchers controlled for diabetes, blood pressure, cholesterol, smoking and many other health and behavioral characteristics. “Although we can’t prove cause and effect, these data suggest that we should be cautious about drinking sugary beverages,” said the lead author, Matthew P. Pase, a senior research fellow at Boston University. “They’re empty calories that contribute to weight gain and metabolic disease.” © 2017 The New York Times Company
By Clare Wilson Could fasting boost your brainpower? A stomach hormone that stimulates appetite seems to promote the growth of new brain cells and protect them from the effects of ageing – and may explain why some people say that fasting makes them feel mentally sharper. When ghrelin was first discovered, it became known as the hunger hormone. It is made by the stomach when it gets empty, and whenever we go a few hours without food its levels rise in our blood. But there is also evidence that ghrelin can enhance cognition. Animals that have reduced-calorie diets have better mental abilities, and ghrelin might be part of the reason why. Injecting the hormone into mice improves their performance in learning and memory tests, and seems to boost the number of neuron connections in their brains. Now Jeffrey Davies at Swansea University, UK, and his team have found further evidence that ghrelin can stimulate brain cells to divide and multiply, a process called neurogenesis. When they added the hormone to mouse brain cells grown in a dish, it switched on a gene known to trigger neurogenesis, called fibroblast growth factor. If the same effect happens in animals, this could be how ghrelin exerts its effects on memory, says Davies, whose work was presented at the British Neuroscience Association conference this month. © Copyright Reed Business Information Ltd.
By Meredith Knight A complex cascade of biochemical signals determines what we eat, when we eat and how much we eat. Our digestive tracts and fat cells are known to secrete hormones that drive our hunger levels and our sense of satisfaction after eating. Now a new player has come to the table, our bones. A paper published this March in Nature shows bone cells secrete a hormone called lipocalin 2—and it has a surprising effect in mouse experiments of reducing appetite and stabilizing blood sugar independently of other hormones Stavroula Kousteni, a physiologist at Columbia University College of Physicians and Surgeons, and her colleagues showed 90 percent of the hormone lipocalin 2 was produced by osteoblasts, bone cells that create the chemicals necessary to build new bone. Because of its chemical structure scientists previously thought fat cells made the hormone. Lipocalin 2 is released after eating and reaches peak levels about an hour after a meal. When researchers genetically designed mice with defective lipocalin 2 genes in bone, the mice had 20 percent more body fat than mice that had the defective gene inserted into fatty tissue. The animals also ate 16 percent more chow. When mice with the broken gene were injected with lipocalin 2, their feeding behavior returned to normal. Injections of the hormone even reduced eating and improved blood sugar and insulin regulation in healthy mice. “In general, we found we could improve their metabolic phenotype,” Kousteni says. © 2017 Scientific American
Link ID: 23523 - Posted: 04.22.2017
Hannah Devlin Science correspondent They feel no pain, don’t get cancer and look like baggy-skinned sausages with teeth: the naked mole rat is already famously weird. Now scientists have discovered what could be the subterranean rodents’ strangest trait yet: they can survive without oxygen by switching to a metabolic strategy normally used by plants. By switching from a glucose-based metabolic system, which depends on oxygen, to one that uses fructose instead, mole rats can cope with nearly twenty minutes in air with 0% oxygen. Under the same conditions, a human would die within minutes. “The naked mole rat has simply rearranged some basic building-blocks of metabolism to make it super-tolerant to low oxygen conditions,” said Thomas Park, professor of biological sciences at the University of Illinois at Chicago, who made the discovery after studying the species for 18 years. The apparently unique metabolic strategy probably evolved along with the mole rats’ niche life-style, he said. The animals live in stuffy, hyper-crowded burrows, with chambers in which a hundred-odd colony mates sleep together in a heap of hairless bodies. Scientists were aware that oxygen supplies in the mole rats’ tunnels drop to levels that would be unsurvivable for other land mammals, but until now had not tested the limits of their ability to cope with oxygen deprivation, or how this works biologically. In the latest study, published in the journal Science, the team found that mole rats showed no ill effects after five hours breathing air with 5% oxygen – slightly lower that oxygen levels at the summit of Everest. Laboratory mice, by contrast, died within ten minutes. © 2017 Guardian News and Media Limited
Link ID: 23519 - Posted: 04.21.2017
Sarah Boseley in Amsterdam The city of Amsterdam is leading the world in ending the obesity epidemic, thanks to a radical and wide-reaching programme which is getting results even among the poorest communities that are hardest to reach. Better known for tulips and bicycles, Amsterdam has the highest rate of obesity in the Netherlands, with a fifth of its children overweight and at risk of future health problems. The programme appears to be succeeding by hitting multiple targets at the same time – from promoting tap water to after-school activities to the city refusing sponsorship to events that take money from Coca Cola or McDonalds. It is led by a dynamic deputy mayor with the unanimous backing of the city’s politicians. From 2012 to 2015, the number of overweight and obese children has dropped by 12%. Even more impressive, Amsterdam has done what nobody else has managed, because the biggest fall has been amongst the lowest socio-economic groups. It is in neighbourhoods like the Bijlmer in the south-east that the programme is changing lives. The Bijlmer is notorious, says Wilbert Sawat, coordinator and PE teacher at De Achtsprong primary school, and that’s why he wanted to work there. Other teachers do too, he says. “Here we can make a difference.
Link ID: 23493 - Posted: 04.15.2017
By CATHERINE SAINT LOUIS Halfway through February, I could no longer sleep through the night. At 2 a.m., I’d find myself chugging milk from the carton to extinguish a fire at the top of my rib cage. The gnawing feeling high in my stomach alternated with nausea so arresting I kept a bucket next to my laptop and considered taking a pregnancy test, even though I was 99 percent sure I wasn’t expecting. One day on the subway platform, I doubled over and let out a groan so pathetic it prompted a complete stranger to ask, “Are you all right?” Then I knew it was time to seek medical attention. New Yorkers don’t address strangers on the subway, I told myself. It’s like breaking the fourth wall. The next day, my primary care doctor told me I probably had an ulcer, a raw spot or sore in the lining of the stomach or small intestine. Here are some of the things I learned about ulcers during the odyssey that followed. ■ Anyone Can Get an Ulcer. Back in the 1980s, when doctors and most everyone else thought psychological stress or spicy foods led to ulcers, two Australian scientists discovered that the main culprit was actually a bacterium called Helicobacter pylori. That discovery eventually won them a Nobel Prize in 2005, and ushered in an era of using antibiotics to cure ulcers. But that didn’t wipe out ulcers altogether. Far from it. Indeed, my tribe of fellow sufferers are legion. Nearly 16 million adults nationwide reported having an ulcer in 2014,according to the Centers for Disease Control and Prevention’s National Center for Health Statistics. The largest group, roughly 6.2 million, were 45 to 64 years old. Those 18 to 44 accounted for 4.6 million, 65- to 74-year-olds for 2.6 million, and those 75 and older for 2.4 million. I got a blood test to see if I was infected with H. pylori; the test came back negative, so I didn’t need antibiotics. Regular use of nonsteroidal anti-inflammatory drugs, like ibuprofen or aspirin, can also lead to an ulcer, but I wasn’t taking those medicines. My ulcer turned out to be “idiopathic,” which is a fancy way of saying that doctors have no idea why it happened. © 2017 The New York Times Company
Link ID: 23490 - Posted: 04.14.2017
Tina Hesman Saey Some Pakistani people are real knockouts, a new DNA study finds. Knockouts in this sense doesn’t refer to boxing or a stunning appearance, but to natural mutations that inactivate, or “knock out” certain genes. The study suggests that human knockouts could prove valuable evidence for understanding how genes work and for developing drugs. Among 10,503 adults participating in a heart disease study in Pakistan, 1,843 people have at least one gene of which both copies have been knocked out, researchers report online April 12 in Nature. Researchers also drew blood from many of the participants and used medical records to study more than 200 traits, such as heart rate, blood pressure and blood levels of sugar, cholesterol, hormones or other substances. Studying how the knockout mutations affect those traits and health could point to genes that are potentially safe and effective targets for new drugs. Combining genetic data with medical information will provide “a rich dataset for many applications,” says Robert Plenge, a human geneticist formerly with the pharmaceutical company Merck. Scientists have traditionally learned about genes’ roles by deleting the genes from mice and then cataloging abnormalities in how those mice developed and behaved. Such animal research will always be needed, but studies of people naturally lacking certain genes “will change the nature of the scientific investigation of the genetic basis of human disease,” Plenge wrote in a commentary in the same issue of Nature. Often, a person will inherit a broken copy of a gene from one parent and a healthy copy from the other. But 39 percent of the people in this study had parents who were closely related — often first cousins — increasing the odds of inheriting two mutant copies of a gene. Of this study’s 1,843 participants, 1,504 had both copies of a single gene knocked out. The rest had more than one gene knocked out, including one person in whom six genes were predicted to be completely nonfunctional. |© Society for Science & the Public 2000 - 2017.
By ANAHAD O’CONNOR About a year and a half ago, Robin Collier and her husband, Wayne, were like millions of other Americans: overweight and living with Type 2 diabetes. Despite multiple diets, the couple could not seem to lose much weight. Then Ms. Collier’s doctor told her she was going to need daily insulin shots to control her diabetes. That was the motivation she needed. “I made up my mind right then and there,” said Ms. Collier, 62, an administrator at an accounting firm in Lafayette, Ind. “I said to myself, ‘I’m not going on insulin. I’m too young to have this disease.’” Instead, Ms. Collier and her husband entered a study sponsored by a company called Virta Health, one of a new crop of high-tech companies that have designed programs aimed at helping people prevent or even reverse their diabetes. On the program, patients video-chat with a remote Virta doctor, who consults with their primary care doctor, reviews their blood tests and medical history, and makes diet and drug recommendations. While studies show that a variety of different diets can benefit people with Type 2 diabetes, Virta, based in San Francisco, takes a low-carbohydrate approach, training patients to swap foods like pastries, pasta and sugary snacks for veggie omelets, almonds and salads with grilled chicken and beef. Every day, patients use an app to upload their blood sugar levels, blood pressure, body weight and other measurements. A health coach, usually a registered dietitian, monitors their data and checks in by phone, text or email to discuss any problems or just to provide daily encouragement. Today, Ms. Collier has lost 75 pounds and has avoided taking insulin. Her husband has lost 45 pounds and was able to stop two diabetes medications. Both are still in the program, which she called “life changing,” as part of an ongoing clinical trial. © 2017 The New York Times Company
Link ID: 23481 - Posted: 04.12.2017
By Jef Akst | Previous research has shown that high doses of broad-spectrum antibiotics can affect the behavior of adult animals, and numerous epidemiological studies have begun to link early-life antibiotic use to diverse ailments in humans. A study published last week (April 4) in Nature Communications adds to this growing literature, demonstrating that even low, clinically relevant doses of the classic narrow-spectrum antibiotic penicillin can trigger changes in the gut microbiome, in the blood-brain barrier and brain chemistry, and in the behaviors of mice exposed at a young age. Treating the mice with Lactobacillus rhamnosus bacteria, however, helped protect the mice against the effects of early-life, low-dose penicillin exposure. “There are almost no babies in North America that haven’t received a course of antibiotics in their first year of life,” McMaster University coauthor John Bienenstock, who is also the director of the Brain-Body Institute at St. Joseph’s Healthcare Hamilton, said in a press release. “In this paper, we report that low-dose penicillin taken late in pregnancy and in early life of mice offspring, changes behavior and the balance of microbes in the gut. While these studies have been performed in mice, they point to popular increasing concerns about the long-term effects of antibiotics. Furthermore, our results suggest that a probiotic might be effective in preventing the detrimental effects of the penicillin.” Bienenstock and colleagues gave pregnant female mice low doses of penicillin during their last week of gestation, and continued to treat their pups until they weaned a few weeks after birth. At six weeks old, mice exposed to the antibiotic were less social, slightly less anxious, and more aggressive than unexposed mice, the team reported. In the animals’ brains, the researchers found evidence of a thinned blood-brain barrier, as well as increased production of cytokines and heightened activity of a gene that has been linked to aggressive behavior. © 1986-2017 The Scientist
Ewen Callaway It may not be the most appetizing way to extend life but researchers have shown for the first time that older fish live longer after they consumed microbes from the poo of younger fish. The findings were posted to the bioRxiv.org preprint server on 27 March1by Dario Valenzano, a geneticist at the Max Planck Institute for Biology of Ageing in Cologne, Germany, and colleagues. So-called ‘young blood’ experiments that join the circulatory systems of two rats — one young and the other old — have found that factors coursing through the veins of young rodents can improve the health and longevity of older animals. But the new first-of-its-kind study examined the effects of 'transplanting' gut microbiomes on longevity. “The paper is quite stunning. It’s very well done,” says Heinrich Jasper, a developmental biologist and geneticist at the Buck Institute for Research on Aging in Novato, California, who anticipates that scientists will test whether such microbiome transplants can extend lifespan in other animals. Life is fleeting for killifish, one of the shortest-lived vertebrates on Earth: the fish hits sexual maturity at three weeks old and dies within a few months.The turquoise killifish (Nothobranchius furzeri) that Valenzano and colleagues studied in the lab inhabits ephemeral ponds that form during rainy seasons in Mozambique and Zimbabwe. © 2017 Macmillan Publishers Limited
Link ID: 23448 - Posted: 04.05.2017
SAN FRANCISCO — The nose knows when you’re tired. Sleep deprivation seems to increase the brain’s sensitivity to food smells, researchers reported March 27 at the Cognitive Neuroscience Society’s annual meeting in San Francisco. That might make snacks more enticing — helping explain why people who burn the candle at both ends tend to eat more and gain weight. Adults operating on only four hours of sleep inhaled food odors such as those from potato chips and cinnamon rolls, and nonfood smells like fir trees while undergoing functional MRI scans. (The scientists carefully controlled participants’ food intake throughout the day.) A few weeks later, the same participants repeated the experiment — this time with a full eight hours of sleep. When tired, participants showed greater brain activity in two areas involved in olfaction — the piriform cortex and the orbitofrontal cortex — in response to food smells than they did when well rested. That spike wasn’t seen in response to nonfood odors, says study coauthor Surabhi Bhutani, of the Northwestern University Feinberg School of Medicine in Chicago. Though preliminary, the results fit with previous research showing a link between sleep deprivation and both excessive calorie consumption and weight gain (SN: 8/24/13, p. 18). |© Society for Science & the Public 2000 - 2017
By Lizzie Wade Ask any biologist what makes primates special, and they’ll tell you the same thing: big brains. Those impressive noggins make it possible for primates from spider monkeys to humans to use tools, find food, and navigate the complex relationships of group living. But scientists disagree on what drove primates to evolve big brains in the first place. Now, a new study comes to an unexpected conclusion: fruit. “The paper is enormously valuable,” says Richard Wrangham, a biological anthropologist at Harvard University who was not involved in the work. For the last 20 years, many scientists have argued that primates evolved bigger brains to live in bigger groups, an idea known as the “social brain hypothesis.” The new study’s large sample size and robust statistical methods suggest diet and ecology deserve more attention, Wrangham says. But not everyone is convinced. Others say that although a nutrient-rich diet allows for bigger brains, it wouldn’t be enough by itself to serve as a selective evolutionary pressure. When the authors compare diet and social life, “they’re comparing apples and oranges,” says Robin Dunbar, an evolutionary psychologist at the University of Oxford in the United Kingdom and one of the original authors of the social brain hypothesis. Alex DeCasien, the new study’s author, didn’t set out to shake up this decades-long debate. The doctoral student in biological anthropology at New York University in New York City wanted to tease out whether monogamous primates had bigger or smaller brains than more promiscuous species. She collected data about the diets and social lives of more than 140 species across all four primate groups—monkeys, apes, lorises, and lemurs—and calculated which features were more likely to be associated with bigger brains. To her surprise, neither monogamy nor promiscuity predicted anything about a primate’s brain size. Neither did any other measure of social complexity, such as group size. The only factor that seemed to predict which species had larger brains was whether their diets were primarily leaves or fruit, DeCasien and her colleagues report today in Nature Ecology & Evolution. © 2017 American Association for the Advancement of Science
By Melissa Banigan Twenty years ago, I started experiencing what turned into a long list of seemingly unrelated health issues. Headaches, depression, insomnia, peripheral neuropathy, fatigue, joint pain, chest pain, shortness of breath, a lesion on my spine and a variety of uncomfortable gastrointestinal ailments. Over the past five years, things went from bad to worse as I also became lactose-intolerant, developed mild vitiligo (a condition that leads to loss of skin pigmentation) and major vertigo, experienced a series of low-grade fevers and started to have some memory loss that I referred to as brain fogs. Doctors told me that as an overworked single mother of 40, I might just need to figure out ways to get more sleep and relax. Some of what was happening, they said, might be attributed to the normal processes of aging. What was happening, however, didn’t feel normal. Always a voracious reader and a writer by profession, I could no longer focus on work, read even a page of a book or grip a pen long enough to write a grocery list. I often felt too exhausted to keep plans with friends. When I did pull myself off my couch to see them, I couldn’t concentrate on conversations, so I sequestered myself in my apartment and let my friendships fade. I had been a runner, a swimmer and a hiker, but just walking up a flight of stairs made me lose my breath so completely that I succumbed to inactivity. I did everything the doctors asked me to do. I changed my diet and sleep schedule, went to a physical therapist and saw specialists in neurology and rheumatology and even a mental-health therapist. I then also turned to massage therapists, herbalists and an acupuncturist. © 1996-2017 The Washington Post
Obese people who get surgery to lose weight have half the risk of developing heart failure as do patients who make lifestyle changes to shed excess pounds, a recent study suggests. “We were surprised by the large difference in heart failure incidence between the two groups,” said lead study author Johan Sundstrom of Uppsala University in Sweden. It’s possible that gastric bypass patients had a lower risk of heart failure because they lost more weight than the group trying to do so without surgery. Researchers also found that losing 22 pounds by any means was tied to a 23 percent drop in heart failure risk. The study team examined data on 25,805 obese people who had gastric bypass surgery, which reduces the stomach to a small pouch, and 13,701 patients who were put on low-calorie diets. After following half of the patients for at least four years, people who had gastric bypass were found to be 46 percent less likely to have developed heart failure. After one year, surgery patients had an average weight loss 41.4 pounds greater than that of those who relied on diet and exercise, the study found. After two years, surgery was associated with an average weight loss that was 49.8 pounds more than those who undertook lifestyle changes. Some previous research has linked obesity to heart failure, and a growing body of evidence suggests that obesity might directly cause the heart condition, Sundstrom said. While the new study wasn’t designed to prove a causal relationship, it adds more evidence in support of this possibility. © 1996-2017 The Washington Post
Link ID: 23372 - Posted: 03.19.2017
By Mitch Leslie It sounds like a crazy way to improve your health—spend some time on a platform that vibrates at about the same frequency as the lowest string on a double bass. But recent research indicates that the procedure, known as whole-body vibration, may be helpful in illnesses from cerebral palsy to chronic obstructive pulmonary disease. Now, a new study of obese mice reveals that whole-body vibration provides similar metabolic benefits as walking on a treadmill, suggesting it may be useful for treating obesity and type II diabetes. “I think it’s very promising,” says exercise physiologist Lee Brown of the California State University in Fullerton, who wasn’t connected to the study. Although the effects are small, he says, researchers should follow-up to determine whether they can duplicate them in humans. Plenty of gyms feature whole-body vibration machines, and many athletes swear the activity improves their performance. The jiggling does seem to spur muscles to work harder, possibly triggering some of the same effects as exercise. But researchers still don’t know how the two compare, especially when it comes to people who are ill. So biomedical engineer Meghan McGee-Lawrence of the Medical College of Georgia in Augusta and colleagues decided to perform a head-to-head comparison of exercise and whole-body vibration. The researchers tested mutant mice resistant to the appetite-controlling hormone leptin, resulting in obesity and diabetes. © 2017 American Association for the Advancement of Science.
Link ID: 23362 - Posted: 03.16.2017
An international team of researchers has conducted the first study of its kind to look at the genomic underpinnings of obesity in continental Africans and African-Americans. They discovered that approximately 1 percent of West Africans, African-Americans and others of African ancestry carry a genomic variant that increases their risk of obesity, a finding that provides insight into why obesity clusters in families. Researchers at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, and their African collaborators published their findings March 13, 2017, in the journal Obesity. People with genomic differences in the semaphorin-4D (SEMA4D) gene were about six pounds heavier than those without the genomic variant, according to the study. Most of the genomic studies conducted on obesity to date have been in people of European ancestry, despite an increased risk of obesity in people of African ancestry. Obesity is a global health problem, contributing to premature death and morbidity by increasing a person’s risk of developing diabetes, hypertension, heart disease and some cancers. While obesity mostly results from lifestyle and cultural factors, including excess calorie intake and inadequate levels of physical activity, it has a strong genomic component. The burden of obesity is, however, not the same across U.S. ethnic groups, with African-Americans having the highest age-adjusted rates of obesity, said Charles N. Rotimi, Ph.D., chief of NHGRI’s Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch and director of the Center for Research on Genomics and Global Health (CRGGH) at NIH. CRGGH examines the socio-cultural and genomic factors at work in health disparities — the negative health outcomes that impact certain groups of people — so they can be translated into policies that reduce or eliminate healthcare inequalities in the United States and globally.
By Abby Olena Researchers have shown that a hormone secreted by bone, called lipocalin 2 (LCN2), suppresses appetite in mice. The results, published today (March 8) in Nature, suggest that LCN2 crosses the rodents’ blood-brain barrier and binds a receptor in the hypothalamus. The team also found a link between body weight and LCN2 levels in people with type 2 diabetes. The authors “have identified a protein that’s secreted from bone that has a pretty significant impact on feeding behavior,” Lora Heisler of the University of Aberdeen in Scotland, who did not participate in the work, told The Scientist. “And the fact that they found that some supporting evidence in humans is really exciting.” “We have found a new role for bone as an endocrine organ, and that is its ability to regulate appetite,” said study coauthor Stavroula Kousteni of Columbia University in New York City. Scientists had previously identified LCN2 as a protein expressed in fat cells, but Kousteni and colleagues showed that it is enriched 10-fold in osteoblasts. When they generated mice without LCN2 in their osteoblasts, levels of the circulating hormone dropped 67 percent. These mice ate more than control animals and showed increases in fat mass and body weight. When the authors injected LCN2 into wild-type or obese mice, the rodents ate less food. The treated animals showed decreases in body weight, fat mass, and weight gain. LCN2 injections also led to increases in insulin levels and glucose tolerance, the scientists showed. © 1986-2017 The Scientist