Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By Gina Kolata You’d think that scientists at an international conference on obesity would know by now which diet is best, and why. As it turns out, even the experts still have widely divergent opinions. At a recent meeting of the Obesity Society, organizers held a symposium during which two leading scientists presented the somewhat contradictory findings of two high-profile diet studies. A moderator tried to sort things out. In one study, by Christopher Gardner, a professor of medicine at Stanford, patients were given low-fat or low-carb diets with the same amount of calories. After a year, weight loss was the same in each group, Dr. Gardner reported. Another study, by Dr. David Ludwig of Boston Children’s Hospital, reported that a low-carbohydrate diet was better than a high-carbohydrate diet in helping subjects keep weight off after they had dieted and lost. The low-carbohydrate diet, he found, enabled participants to burn about 200 extra calories a day. So does a low-carbohydrate diet help people burn more calories? Or is the composition of the diet irrelevant if the calories are the same? Does it matter if the question is how to lose weight or how to keep it off? There was no consensus at the end of the session. But here are a few certainties about dieting amid the sea of unknowns. What we know People vary — a lot — in how they respond to dieting. Some people thrive on low-fat diets, others do best on low-carb diets. Still others succeed with gluten-free diets or Paleo diets or periodic fasts or ketogenic diets or other options on the seemingly endless menu of weight-loss plans. Most studies comparing diets have produced results like Dr. Gardner’s: no difference © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25775 - Posted: 12.11.2018

Laura Beil Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons. Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old. Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find. With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain. “I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world. |© Society for Science & the Public 2000 - 2018.

Keyword: Parkinsons; Neuroimmunology
Link ID: 25765 - Posted: 12.08.2018

By Jonathan D. Grinstein It is well known that a high salt diet leads to high blood pressure, a risk factor for an array of health problems, including heart disease and stroke. But over the last decade, studies across human populations have reported the association between salt intake and stroke irrespective of high blood pressure and risk of heart disease, suggesting a missing link between salt intake and brain health. Interestingly, there is a growing body of work showing that there is communication between the gut and brain, now commonly dubbed the gut–brain axis. The disruption of the gut–brain axis contributes to a diverse range of diseases, including Parkinson’s disease and irritable bowel syndrome. Consequently, the developing field of gut–brain axis research is rapidly growing and evolving. Five years ago, a couple of studies showed that high salt intake leads to profound immune changes in the gut, resulting in increased vulnerability of the brain to autoimmunity—when the immune system attacks its own healthy cells and tissues by mistake, suggesting that perhaps the gut can communicate with the brain via immune signaling. Now, new research shows another connection: immune signals sent from the gut can compromise the brain’s blood vessels, leading to deteriorated brain heath and cognitive impairment. Surprisingly, the research unveils a previously undescribed gut–brain connection mediated by the immune system and indicates that excessive salt might negatively impact brain health in humans through impairing the brain’s blood vessels regardless of its effect on blood pressure. © 2018 Scientific American

Keyword: Obesity; Neuroimmunology
Link ID: 25754 - Posted: 12.06.2018

By Abby Ellin The issue was peanut butter. No matter what form it took — creamy, crunchy, straight from the jar or smeared between two slices of bread — it caused Sunny Gold enormous anxiety. In fact, the gooey spread posed such a threat that during her first few years of recovery from binge eating disorder, between 2006 and 2007, Ms. Gold, 42, a communications specialist in Portland, Ore., couldn’t keep it around the house. It was one of her favorite foods, and she feared she would binge on it. Just knowing it was there, lurking in her cupboard, made her feel “unsafe,” as she put it. And that’s when things got really tricky. Because her boyfriend at the time, John Pavlus, didn’t think twice about peanut butter — or any food, for that matter. When Ms. Gold, the author of “Food: The Good Girl’s Drug,” told him that it would be a casualty of her getting healthy, he was taken aback. “It was a bit uncomfortable for me at first,” Mr. Pavlus, a 40-year-old writer and filmmaker, admitted. He knew that Ms. Gold had grappled with binge eating since she was a teenager, but food was something they’d bonded over. So when she decided that she needed to “cut herself off,” he felt that he was losing something, “less for the practical inconvenience than the unexpected feeling of being subtly disconnected from her,” he said. “It was strange to think of these parts of our shared reality as being so radically — to me — redefined. Is peanut butter literally dangerous now? Does that mean I have to treat it that way too? Will it be like this forever?” Mr. Pavlus’s reaction is echoed by many romantic partners of someone with an eating disorder, many of whom — though certainly not all — are women. Partners often want to help, but simply don’t know how. © 2018 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 25734 - Posted: 11.30.2018

By Roni Caryn Rabin A. A deficiency of vitamin B12 can cause neurological and psychiatric problems that “can progress if left untreated, and can lead to irreversible damage,” said Dr. Donald Hensrud, director of the Mayo Clinic’s Healthy Living Program. Fortunately, it can be reversed fairly easily with vitamin pills or injections. Vitamin B12 is required for proper red blood cell formation, nerve function and DNA synthesis. It is naturally present in fish, meat, eggs and dairy products, as well as some fortified breakfast cereals and nutritional yeast products. Strict vegans who avoid animal products can develop a deficiency of B12 over time if they don’t take a supplement. But two-thirds of cases occur in the elderly, who are susceptible because they may not absorb adequate amounts of B12 from foods but who are not routinely tested, Dr. Hensrud said. Consequences of B12 deficiency can cause a range of symptoms that include fatigue, weakness, constipation, loss of appetite and weight loss. Other symptoms include difficulty maintaining balance, depression, confusion, dementia, poor memory and soreness in the mouth or tongue. B12 deficiency may also result in a form of anemia called megaloblastic anemia, which can also result from a deficiency of folic acid, another B vitamin. If anemia is detected on blood tests, levels of both vitamins should be checked. Neurological symptoms can, however, occur in the absence of anemia. Early treatment is critical to avoid potentially irreversible damage. Older adults are susceptible to B12 deficiency because they may have decreased secretion of hydrochloric acid in the stomach, which makes it difficult to absorb B12. Also vulnerable to B12 deficiency are those with gastrointestinal disorders like celiac disease or Crohn’s disease; those who have had weight loss or other gastrointestinal surgery; and those who use certain acid reflux drugs or the diabetes drug metformin. Individuals with pernicious anemia, which affects up to 2 percent of older adults, are also susceptible. © 2018 The New York Times Company

Keyword: Depression
Link ID: 25732 - Posted: 11.30.2018

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25711 - Posted: 11.24.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist.

Keyword: Obesity; Neuroimmunology
Link ID: 25710 - Posted: 11.24.2018

Abby Olena Anticipating something tasty can lead to a watering mouth and grumbling stomach, but these familiar responses aren’t the only ways the body prepares for nourishment. According to a study published today (November 15) in Cell, sensing food primes mice to process incoming nutrients by directions from the central nervous system to the liver. “It’s a great tour de force combining [several strategies] in one paper to then identify pathways by which food anticipation could alter hepatic metabolism,” says Christoph Buettner, a physician and researcher at Icahn School of Medicine at Mount Sinai in New York who was not involved in the study. “It’s interesting that even before your food hits your tongue or ends up in your stomach, there are changes that prepare an organism for nutrient storage.” Two types of cells in the brain’s hypothalamus have been shown in previous studies to play opposing roles in regulating how much an organism eats. AgRP neurons are turned on when energy stores are low, making an animal seek out food, while POMC neurons, activated when an animal is sated, inhibit eating. Up until a few years ago, the prevailing wisdom was that ingested food resulted in hormonal changes and subsequent neuronal activation after some lag time, says Jens Brüning, an endocrinologist and geneticist at the Max Planck Institute for Metabolism Research in Germany. But in 2015, researchers from the University of California, San Francisco, showed in mice that these neurons change their state of activation nearly instantaneously in response to the sight or smell of food. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25709 - Posted: 11.24.2018

By Gina Kolata Whenever I see a photo from the 1960s or 1970s, I am startled. It’s not the clothes. It’s not the hair. It’s the bodies. So many people were skinny. In 1976, 15 percent of American adults were obese. Now the it’s nearly 40 percent. No one really knows why bodies have changed so much. Scientists do a lot of hand-waving about our “obesogenic environment” and point to favorite culprits: the abundance of cheap fast foods and snacks; food companies making products so tasty they are addictive; larger serving sizes; the tendency to graze all day. Whatever the combination of factors at work, something about the environment is making many people as fat as their genetic makeup permits. Obesity has always been with us, but never has it been so common. Everyone — from doctors to drug companies, from public health officials to overweight people themselves — would love to see a cure, a treatment that brings weight to normal and keeps it there. Why hasn’t anyone discovered one? It’s not for lack of trying. Yes, some individuals have managed to go from fat to thin with diets and exercise, and have kept off the weight. But they are the rare exceptions. Most spend years dieting and regaining, dieting and regaining, in a fruitless, frustrating cycle. There is just one almost uniformly effective treatment, and it is woefully underused: only about 1 percent of the 24 million American adults who are eligible get the procedure. That treatment is bariatric surgery, a drastic operation that turns the stomach into a tiny pouch and, in one version, also reroutes the intestines. Most who have it lose significant amounts of weight — but many of them remain overweight, or even obese. Their health usually improves anyway. Many with diabetes no longer need insulin. Cholesterol and blood pressure levels tend to fall. Sleep apnea disappears. Backs, hips and knees stop aching. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25707 - Posted: 11.21.2018

Nicola Davis Being overweight can cause depression, researchers say, with the effects thought to be largely psychological. While previous studies have found that people who are obese are more likely to have depression, it has been unclear whether that is down to depression driving weight changes or the reverse. Now, in the largest study of its kind, experts say having genetic variants linked to a high body mass index (BMI) can lead to depression, with a stronger effect in women than men. What’s more, they say the research suggests the effect could be down to factors such as body image. “People who are more overweight in a population are more depressed, and that is likely to be at least partly [a] causal effect of BMI [on] depression,” said Prof Tim Frayling, a co-author of the study, from the University of Exeter medical school. Get Society Weekly: our newsletter for public service professionals Read more Writing in the International Journal of Epidemiology, the researchers from the UK and Australia describe how they used data from the UK Biobank, a research endeavour involving 500,000 participants aged between 37 and 73 who were recruited in 2006-10. The researchers looked at 73 genetic variants linked to a high BMI that are also associated with a higher risk of diseases such diabetes and heart disease. They also looked at 14 genetic variants linked to a high percentage of body fat but which were associated with a lower risk of such health problems. While the former group could be linked to depression through biological or psychological mechanisms, the latter would only be expected to have a psychological effect. © 2018 Guardian News and Media Limited

Keyword: Obesity; Depression
Link ID: 25677 - Posted: 11.13.2018

By Isabella Rolz Anais Garcia, 21, anxiously stares at the menu of a Bob Evans restaurant in Baltimore. Her dark brown eyes gravitate toward the Fit and Healthy section, which lists calories per meal. She takes a long time figuring out what to order and decides to go with her “safe meal,” a small stack of pancakes, with no butter, reduced-calorie syrup, a small bowl of fruit on the side and a cup of black coffee. “Restaurants are like battle zones for me, literal war zones,” she says. A ballerina who contended with anorexia nervosa for years, Garcia, who is 5-foot-1½ tall, has reached 105 pounds, a safer weight than the 79 pounds of a year ago. In her gray turtleneck sweater and casual black leggings, her extreme thinness remains apparent. “For the past five years, I’ve done nothing but hate and try to disown my body,” she says. Ballet celebrates the body — and thinness. Despite demands for change from dancers who have experienced problems and from psychologists specializing in eating disorders, the stereotype that a dancer must be elegant and lean persists. Ballerinas become vulnerable to self-consciousness about their bodies, and they face increased risk of anorexia, bulimia nervosa and other eating disorders. Generally, someone who develops an eating disorder has a predisposition, with several factors at play. For ballerinas, “it is of course the ballet culture,” which is competitive and demanding, says Linda Hamilton, a New York psychologist who has worked with ballerinas with eating disorders. But “you might also have a personality predisposition,” she says. “A perfectionist personality can make the dancer intolerant of any physical changes.” Sometimes, “the disorders start early, as young as 12,” she says, because the curves that come with puberty don’t fit the ballet look. © 1996-2018 The Washington Post

Keyword: Anorexia & Bulimia
Link ID: 25669 - Posted: 11.12.2018

By Kelly Servick SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating. “This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.” The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain. © 2018 American Association for the Advancement of Science

Keyword: Obesity; Neuroimmunology
Link ID: 25664 - Posted: 11.10.2018

/ By Susan D’Agostino I’d had intestinal distress before, but never like this. I was excreting not just waste, but blood and bits of my colon’s lining — up to 30 times per day. My abdominal pain hit deeper and felt less productive than the pain of giving birth, epidural-free, to my second child. Even shingles, which stung like a dental drill against my face, paled in comparison. Such was the agony of Clostridium difficile. Commonly known as C. diff., Clostridium difficile is an antibiotic-resistant superbug carried by approximately 5 percent of the adult population. The harmful gut bacterium is normally kept in check by other, good bacteria in the gut’s microbiome. But when the microbial balance is upset — for example, by a dose of antibiotics — C. diff. can gain a foothold. Left to multiply unchecked, it may kill its human host. In 2013, the Centers for Disease Control and Prevention estimated that 14,000 Americans die each year from C. diff. Thanks to an ill-considered decision by the U.S. Food and Drug Administration, and the willful ignorance of a string of doctors charged with my care, I was nearly one of them. Things started innocently enough. In early 2013, my doctor diagnosed me with a bacterial infection and prescribed an antibiotic. I had lived antibiotic-free for nearly four decades — a streak I was not inclined to break. But my doctor insisted on antibiotics, and I reluctantly complied. Soon after, my stomach turned against me. I went to an emergency room and was sent home with a prescription for vancomycin, an antibiotic reserved for serious bacterial infections. But the drug proved little match for the microbes that had bum-rushed my colon. My weight and fluid loss accelerated. My colon risked perforation. Copyright 2018 Undark

Keyword: Obesity
Link ID: 25663 - Posted: 11.10.2018

Tina Hesman Saey Timing is everything. Even how many calories a person burns while at rest depends on the hour. People burn about 129 more calories when resting in the afternoon and evening than in the early morning. But morning is better for burning carbohydrates, while fats are more likely to be burned in the evening, researchers report November 8 in Current Biology. The findings add to evidence that when people eat and sleep may be as important as what they eat for maintaining proper health (SN: 10/31/15, p. 10). Calories burned at rest fuel breathing, circulation and brain activity, while also helping to maintain body temperature. Researchers previously had conflicting evidence about whether a resting body burns calories at a fairly constant rate, or one that rises and falls in a daily — or circadian — rhythm. The study shows that a body’s resting metabolism is governed by circadian clocks, neuroscientist Jeanne Duffy of Brigham and Women’s Hospital in Boston and colleagues report. The study followed seven people kept in windowless rooms for three weeks, without any clues to the time of day. Each night, the seven went to bed four hours later than the previous night. That’s the equivalent of traveling around the world and crossing all time zones within a week. The schedule change allowed the researchers to study the natural body rhythms of each subject without outside influences. |© Society for Science & the Public 2000 - 2018.

Keyword: Biological Rhythms; Obesity
Link ID: 25658 - Posted: 11.09.2018

By David Prologo “Exercise isn’t really important for weight loss” has become a popular sentiment in the weight-loss community. “It’s all about diet,” many say. “Don’t worry about exercise so much.” This idea crept out amid infinite theories about dieting and weight loss, and it quickly gained popularity, with one article alone citing 60 studies to support and spread this notion like wildfire. The truth is that you absolutely can — and should — exercise your way to weight loss. So why is anyone saying otherwise? For 10 years, I have been studying the epidemic of failed weight-loss attempts and researching the phenomenon of hundreds of millions of people embarking on weight-loss attempts — then quitting. Meanwhile, exercise remains the most common practice among nationally tracked persons who are able to maintain weight loss over time. Ninety percent of people who lose significant weight and keep it off exercise at least one hour a day, on average. There are a few reasons that exercise for weight loss gets a bad rap. First, the public is looking, in large part, for a quick fix — and the diet and weight-loss industry exploits this consumer desire for an immediate solution. Many studies have shown that exercise changes your body’s composition, improves your resting metabolism and alters your food preferences. These plain and simple facts have stood the test of time, but go largely unnoticed compared to most sensationalized diet products (change through exercise over time is a much tougher sell than a five-day “cleanse”). Moreover, many people consider one hour a day for exercise to be unreasonable or undoable, and find themselves looking elsewhere for an easier fix. © 1996-2018 The Washington Post

Keyword: Obesity
Link ID: 25645 - Posted: 11.05.2018

Aimee Cunningham The appendix, a once-dismissed organ now known to play a role in the immune system, may contribute to a person’s chances of developing Parkinson’s disease. An analysis of data from nearly 1.7 million Swedes found that those who’d had their appendix removed had a lower overall risk of Parkinson’s disease. Also, samples of appendix tissue from healthy individuals revealed protein clumps similar to those found in the brains of Parkinson’s patients, researchers report online October 31 in Science Translational Medicine. Together, the findings suggest that the appendix may play a role in the early events of Parkinson’s disease, Viviane Labrie, a neuroscientist at the Van Andel Research Institute in Grand Rapids, Mich., said at a news conference on October 30. Parkinson’s, which affects more than 10 million people worldwide, is a neurodegenerative disease that leads to difficulty with movement, coordination and balance. It’s unknown what causes Parkinson’s, but one hallmark of the disease is the death of nerve cells, or neurons, in a brain region called the substantia nigra that helps control movement. Lewy bodies, which are mostly made of clumped bits of the protein alpha-synuclein (SN: 1/12/2013, p. 13), also build up in those neurons but the connection between the cells’ death and the Lewy bodies isn’t clear yet. Symptoms related to Parkinson’s can show up in the gut earlier than they do in the brain (SN: 12/10/2016, p. 12). So Labrie and her colleagues turned their attention to the appendix, a thin tube around 10 centimeters long that protrudes from the large intestine on the lower right side of the abdomen. Often considered a “useless organ,” Labrie said, “the appendix is actually an immune tissue that’s responsible for sampling and monitoring pathogens.” |© Society for Science & the Public 2000 - 2018.

Keyword: Parkinsons
Link ID: 25632 - Posted: 11.01.2018

A new study puts a fresh spin on what it means to “go with your gut.” The findings, published in Nature, suggest that gut bacteria may control movement in fruit flies and identify the neurons involved in this response. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study provides additional evidence for a connection between the gut and the brain, and in particular outlines how gut bacteria may influence behavior, including movement,” said Margaret Sutherland, Ph.D., program director at NINDS. Researchers led by Sarkis K. Mazmanian, Ph.D., professor of microbiology at the California Institute of Technology in Pasadena, and graduate student Catherine E. Schretter, observed that germ-free flies, which did not carry bacteria, were hyperactive. For instance, they walked faster, over greater distances, and took shorter rests than flies that had normal levels of microbes. Dr. Mazmanian and his team investigated ways in which gut bacteria may affect behavior in fruit flies. “Locomotion is important for a number of activities such as mating and searching for food. It turns out that gut bacteria may be critical for fundamental behaviors in animals,” said Dr. Mazmanian. Fruit flies carry between five and 20 different species of bacteria and Dr. Mazmanian’s team treated the germ-free animals with individual strains of those microbes. When the flies received Lactobacillus brevis, their movements slowed down to normal speed. L. brevis was one of only two species of bacteria that restored normal behavior in the germ-free flies.

Keyword: Movement Disorders
Link ID: 25630 - Posted: 11.01.2018

Sukanya Charuchandra L. Wu et al., “Human ApoE isoforms differentially modulate brain glucose and ketone body metabolism: Implications for Alzheimer’s disease risk reduction and early intervention,” J Neurosci, 38:6665­–81, 2018. Humans carry three different isoforms of the ApoE gene, which affects Alzheimer’s risk. Liqin Zhao of the University of Kansas and her colleagues previously found that the gene plays a role in brain metabolism when expressed in mice; in a new study, they looked for the pathways involved. LEAVING AN IMPRESSION Zhao’s team engineered female mice to express the human versions of either ApoE2, ApoE3, or ApoE4, and analyzed expression of 43 genes involved in energy metabolism in their cortical tissue. BLOCKADE Mice with ApoE2 showed higher levels of proteins needed for glucose uptake and metabolism in their brains relative to animals harboring the most common isoform in humans, ApoE3. Mice with ApoE4 had lower levels of such proteins. The brain tissue’s glucose transport efficiency also varied across the genotypes, and levels of a key glucose-metabolizing enzyme, hexokinase, were reduced in ApoE4 brains. However, ApoE2 and ApoE4 brains contained similar levels of proteins involved in using ketone bodies, a secondary source of energy, while ApoE3 brains had lower levels of those proteins. “Brain glycolytic function may serve as a significant mechanism underlying the differential impact of ApoE genotypes,” Zhao says. © 1986 - 2018 The Scientist.

Keyword: Obesity; Alzheimers
Link ID: 25613 - Posted: 10.25.2018

Laura Sanders Researchers have found a new link between gut and brain. By signaling to nerve cells in the brain, certain microbes in the gut slow a fruit fly’s walking pace, scientists report. Fruit flies missing those microbes — and that signal — turn into hyperactive speed walkers. With the normal suite of gut microbes, Drosophila melanogaster fruit flies on foot cover an average of about 2.4 millimeters a second. But fruit flies without any gut microbes zip along at about 3.5 millimeters a second, Catherine Schretter, a biologist at Caltech, and her colleagues report October 24 in Nature. These flies with missing microbes also take shorter breaks and are more active during the day. “Our work suggests that microbes assist in maintaining a certain level of locomotion,” Schretter says. An enzyme made by Lactobacillus brevis bacteria normally serves as the brakes, the researchers found. When researchers supplied the enzyme, called xylose isomerase, to flies lacking bacteria, the flies began walking at a slower, more normal pace. Xylose isomerase acts on a sugar that’s thought to influence nerve cells in fruit flies’ brains that control walking. For still mysterious reasons, the bacterial influence on walking speed occurred only in female fruit flies, not males. Studying that difference will be “a very interesting potential direction for this work,” Schretter says. |© Society for Science & the Public 2000 - 2018

Keyword: Obesity
Link ID: 25612 - Posted: 10.25.2018

By Mitch Leslie Male mice that work out spawn healthier offspring than their lethargic counterparts, according to a new study. Whether the results hold true for humans remains uncertain, but they support the notion that some of the benefits of exercise are somehow passed on to the next generation. “The science is solid, and it’s pretty exciting,” says epigeneticist Sarah Kimmins of McGill University in Montreal, Canada, who wasn’t connected to the work. Scientists already know that a parent’s bad exercise or dietary habits can affect their offspring. Mothers who are obese during pregnancy, for example, give birth to children who are more likely to be obese as adults and develop metabolic illnesses such as cardiovascular disease. Another study found that male rats that snarfed high-fat chow fathered offspring that didn’t respond normally to glucose, a hallmark of type 2 diabetes. To determine whether the opposite is true, molecular exercise physiologist Kristin Stanford of The Ohio State University College of Medicine in Columbus and colleagues fed male mice a fat-rich diet for 3 weeks. One group of animals had access to running wheels, scampering nearly 6 kilometers per night on average, but the rest were couch potatoes. After dissecting some of the rodents to obtain samples of their sperm, the researchers allowed the remaining mice to mate. Stanford and her colleagues tracked the resulting offspring until they were a year old, about middle age for a mouse. Even though the offspring of exercising and nonexercising dads all ate a high-fat diet their entire lives and didn’t get any physical activity, the offspring of healthy fathers seemed to inherit their dads’ metabolism. The progeny of the runners showed a better response to increases in blood glucose and had lower insulin levels—both hallmarks of a sound metabolism—the researchers report today in Diabetes. “Exercise was completely negating the effect of a high-fat diet” on the offspring, Stanford says. © 2018 American Association for the Advancement of Scienc

Keyword: Epigenetics; Obesity
Link ID: 25607 - Posted: 10.23.2018