Boston University scientists say that moderate daily exercise and dietary control might reverse immune dysfunctions found in people with obesity.
Overeating and a sedentary lifestyle are well-known risk factors for obesity, which is linked to hypertension, heart disease, diabetes, gum disease, certain cancers, and asthma.
Research has suggested that a change in immune function is a predecessor to all these diseases and researchers at Boston University Henry M. Goldman School of Dental Medicine (GSDM) have previously shown that obesity causes immune defects that make it hard to fight infection.
Until now, little was known about how diet and exercise affects immunity in obese people.
Researchers worked with diet-induced obese mice in four groups:
• lean mice on a standard chow diet
• obese mice on a high fat diet
• obese mice on a high fat diet on a moderate exercise plan for four weeks, and
• obese, high fat diet mice given moderate exercise and a four-week standard chow diet
Moderate daily exercise and dietary control dramatically restored immune function. Obese mice saw damaged cytokines—signaling molecules that help immune cells talk to each other—repaired and an improved ability to fight gum disease as measured by bone loss.
“The study underscores the necessity to correct two important factors in obesity—diet and exercise—to improve markers of immune dysfunction and bone loss,” says senior author Dr. Salomon Amar. “The correction of one factor only may not lead to any tangible changes.”...
Sunday, February 27, 2011
Treadmill the fountain of youth: study
Exercising on a treadmill for 45 minutes, three times a week, warded off the effects of premature aging in lab mice, a McMaster University study shows.
The researchers hope that when people see the dramatic difference between sedentary mice and those with the treadmill routine, it’ll give them an extra push to get off the couch.
Anything that motivates people to exercise is beneficial because it’s good for human health, decreasing rates of obesity and Type 2 diabetes while increasing longevity, said Dr. Mark Tarnopolsky of McMaster’s Michael G. DeGroote School of Medicine...
The researchers hope that when people see the dramatic difference between sedentary mice and those with the treadmill routine, it’ll give them an extra push to get off the couch.
Anything that motivates people to exercise is beneficial because it’s good for human health, decreasing rates of obesity and Type 2 diabetes while increasing longevity, said Dr. Mark Tarnopolsky of McMaster’s Michael G. DeGroote School of Medicine...
New research suggests that obesity and diabetes are a downside of human evolution
...In this study, which is the first to examine the effect of a human-specific CMAH genetic mutation in obesity-related metabolism and diabetes, Kim and colleagues show that the loss of CMAH's function contributes to the failure of the insulin-producing pancreatic beta cells in overweight humans, which is known to be a key factor in the development of type 2 diabetes. This gene encodes for an enzyme present in all mammalian species except for humans and adds a single oxygen atom to sialic acids, which are sugars that coat the cell surface.
To make their discovery, the researchers used two groups of mice. The first group had the same mutant CMAH gene found in humans. These mice demonstrated that the CMAH enzyme was inactive and could not produce a sialic acid type called NeuSGc at the cell surface. The second group had a normal CMAH gene. When exposed to a high fat diet, both sets of mice developed insulin resistance as a result of their obesity. Pancreatic beta cell failure, however, occurred only in the CMAH mutant mice that lacked NeuSGc, resulting in a decreased insulin production, which then further impaired blood glucose level control. This discovery may enhance scientific understanding of why humans may be particularly prone to develop type 2 diabetes. Results may also suggest that conventional animal models may not accurately mirror the human situation.
"The diabetes discovery is an important advance in its own right. It tells us a lot about what goes wrong in diabetes, and where to aim with new treatments," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but its implications for human evolution are even greater. If this enzyme is unique to humans, it must also have given us a survival advantage over earlier species. Now the challenge is to find the function of CMAH in defending us against microbes or environmental stress or both. This evolutionary science explains how we can win some and lose some, to keep our species ahead of the extinction curve."
To make their discovery, the researchers used two groups of mice. The first group had the same mutant CMAH gene found in humans. These mice demonstrated that the CMAH enzyme was inactive and could not produce a sialic acid type called NeuSGc at the cell surface. The second group had a normal CMAH gene. When exposed to a high fat diet, both sets of mice developed insulin resistance as a result of their obesity. Pancreatic beta cell failure, however, occurred only in the CMAH mutant mice that lacked NeuSGc, resulting in a decreased insulin production, which then further impaired blood glucose level control. This discovery may enhance scientific understanding of why humans may be particularly prone to develop type 2 diabetes. Results may also suggest that conventional animal models may not accurately mirror the human situation.
"The diabetes discovery is an important advance in its own right. It tells us a lot about what goes wrong in diabetes, and where to aim with new treatments," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but its implications for human evolution are even greater. If this enzyme is unique to humans, it must also have given us a survival advantage over earlier species. Now the challenge is to find the function of CMAH in defending us against microbes or environmental stress or both. This evolutionary science explains how we can win some and lose some, to keep our species ahead of the extinction curve."
Monday, February 14, 2011
Mapping obesity circuitry in brain
In the battle of the bulge, one important battalion is a set of brain cells expressing the melanocortin-4 receptor (MC4R). Via signals from the fat-derived hormone leptin, these neurons regulate feeding behavior and fat metabolism in an attempt to regulate body weight. But how leptin influences and acts on this brain circuitry is not fully understood.
Using mice with fluorescently-tagged MC4R, Masoud Ghamari-Langroudi, Roger Cone and colleagues analyzed how the activity of MC4R neurons of the paraventricular nucleus of the hypothalamus (PVN) are regulated by leptin and by metabolic state (i.e., fasting).
They report in the Jan. 4 Proceedings of the National Academy of Sciences that fasting increases firing of these neurons and that leptin administration returns the firing to normal levels. They also show that contrary to the conventional view that leptin indirectly regulates PVN neuron activity, it can also inhibit the activity of PVN neurons directly. Such details of the brain circuitry underlying energy balance could provide important clues to understanding – and combating – obesity.
Using mice with fluorescently-tagged MC4R, Masoud Ghamari-Langroudi, Roger Cone and colleagues analyzed how the activity of MC4R neurons of the paraventricular nucleus of the hypothalamus (PVN) are regulated by leptin and by metabolic state (i.e., fasting).
They report in the Jan. 4 Proceedings of the National Academy of Sciences that fasting increases firing of these neurons and that leptin administration returns the firing to normal levels. They also show that contrary to the conventional view that leptin indirectly regulates PVN neuron activity, it can also inhibit the activity of PVN neurons directly. Such details of the brain circuitry underlying energy balance could provide important clues to understanding – and combating – obesity.
Diet drug makers seeking new strategies
...The search for new drug pathways that alter the body’s metabolism, and the way calories are burned and stored as fat, gained momentum in 2009 when researchers from the University of Michigan, Vanderbilt University and Fudan University in Shanghai published a paper in the journal Cell exploring the relationship between inflammation in the fat tissue of mice and obesity and diabetes.
They focused on a protein that activates immune-system white blood cells that cause fat cells to swell.
In regular mice that were fed a high-calorie diet, the protein activated white blood cells, causing fat cells to swell. The mice gained weight and became insulin-resistant, a condition known as Type 2 diabetes.
Another group of mice were genetically engineered to lack the protein. Those animals were also overfed, but they didn’t gain weight. Instead, their bodies consumed more oxygen and produced greater amounts of another type of protein that generates body heat by burning fat tissue.
As an added benefit, the engineered mice didn’t develop diabetes.
They focused on a protein that activates immune-system white blood cells that cause fat cells to swell.
In regular mice that were fed a high-calorie diet, the protein activated white blood cells, causing fat cells to swell. The mice gained weight and became insulin-resistant, a condition known as Type 2 diabetes.
Another group of mice were genetically engineered to lack the protein. Those animals were also overfed, but they didn’t gain weight. Instead, their bodies consumed more oxygen and produced greater amounts of another type of protein that generates body heat by burning fat tissue.
As an added benefit, the engineered mice didn’t develop diabetes.
Mayo Clinic researcher's memory study leads to surprising obesity finding
Their mission was to solve a small but nagging mystery of Alzheimer's disease: How would the brain's ability to store information be affected if they "turned off" the obscure protein LRP1?
But Guojun Bu and his fellow researchers were in for a surprise. As they expected, mice whose brains had been wiped of the LRP1 gene showed Alzheimer's-like memory problems. But they also started to put on weight - fast.
The mice were lethargic. They were on their way to becoming diabetic. And they didn't seem to know when to stop eating.
In other words, they were a lot like the more than 72 million Americans who are obese...
But Guojun Bu and his fellow researchers were in for a surprise. As they expected, mice whose brains had been wiped of the LRP1 gene showed Alzheimer's-like memory problems. But they also started to put on weight - fast.
The mice were lethargic. They were on their way to becoming diabetic. And they didn't seem to know when to stop eating.
In other words, they were a lot like the more than 72 million Americans who are obese...
Sunday, February 06, 2011
Obesity resistant mechanisms in the Lean polygenic mouse model as indicated by liver transcriptome and expression of selected genes in skeletal muscle
Divergently selected Lean and Fat mouse lines represent unique models for a polygenic form of resistance and susceptibility to obesity development. Previous research on these lines focused mainly on obesity-susceptible factors in the Fat line.
This study aimed to examine the molecular basis of obesity-resistant mechanisms in the Lean line by analyzing various fat depots and organs, the liver transcriptome of selected metabolic pathways, plasma and lipid homeostasis and expression of selected skeletal muscle genes.
Results: Expression profiling using our custom Steroltalk v2 microarray demonstrated that Lean mice exhibit a higher hepatic expression of cholesterol biosynthesis genes compared to the Fat line...
This study aimed to examine the molecular basis of obesity-resistant mechanisms in the Lean line by analyzing various fat depots and organs, the liver transcriptome of selected metabolic pathways, plasma and lipid homeostasis and expression of selected skeletal muscle genes.
Results: Expression profiling using our custom Steroltalk v2 microarray demonstrated that Lean mice exhibit a higher hepatic expression of cholesterol biosynthesis genes compared to the Fat line...
Biochemistry analyses mouse resistance to obesity
Mechanisms that allow mice to resist developing obesity have been analysed using gel filtration chromatography by a team of French and Slovenian biochemistry and veterinary scientists...
Subscribe to:
Posts (Atom)