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A study by researchers at the University of Southern California (USC) found that overweight Hispanic children are at significant risk for pre-diabetes, a condition marked by higher than normal blood glucose levels that are not yet high enough for a diagnosis of diabetes. The persistence of pre-diabetes during growth is associated with progression in risk towards future diabetes, according to the study, which will be published in an upcoming issue of the journal Diabetes, and is now available online.

With a population of more than 35 million, Hispanics are the largest and fastest growing minority group in the United States. Despite the fact that Hispanics are at high risk for developing type 2 diabetes, few previous studies have looked at physiological causes of the disease within this population.

Researchers led by Michael I. Goran, Ph.D., professor of preventive medicine, physiology and biophysics and pediatrics, and director of the USC Childhood Obesity Research Center at the Keck School of Medicine of USC, followed a cohort of 128 overweight Hispanic children in East Los Angeles. The children were tested over four consecutive years for glucose tolerance, body mass index, total body fat and lean mass and other risk factors for type 2 diabetes. The study found that an alarming 13% of the children had what the scientists termed "persistent pre-diabetes".

Most prior studies examining pre-diabetes in overweight and obese children looked at a one-time assessment of metabolic risk factors for type 2 diabetes, but fluctuations over time led to poor reliability for these tests. In the new study, Goran and colleagues examined longitudinal data to look at a progression of risk factors over four years. Children were identified as having persistent pre-diabetes if they had three to four positive tests over four annual visits. The children who had persistent pre-diabetes had signs of compromised beta-cell function, meaning that their bodies were unable to fully compensate to maintain blood glucose at an appropriate level, and they had increasing accumulation of visceral fat or deposition of fat around the organs. Both of these outcomes point towards progression in risk towards type 2 diabetes.

"What this study shows is that doctors should be doing regular monitoring of these children over time, because a one-time checkup might not be enough to tell if they are at risk for developing diabetes," Goran says.

Visceral fat, which pads the spaces between abdominal organs, has been linked to metabolic disturbances and increased risk for cardiovascular disease and type 2 diabetes.

Increased obesity has been identified as a major determinant of insulin resistance. Lower beta-cell function is a key component in the development of type 2 diabetes, as the cells are unable to produce enough insulin to adequately compensate for the insulin resistance.

"To better treat at-risk children we need better ways to monitor beta-cell function and visceral fat buildup," Goran says. "Those are tough to measure but are probably the main factors determining who will get type 2 diabetes."

Future studies will examine different interventions, including improving beta-cell function and reducing visceral fat.

"The study provides great insight into the risk factors that lead to the progression towards type 2 diabetes in this population," says Francine Kaufman, professor of pediatrics at the Keck School of Medicine at USC and head of the division of endocrinology and metabolism at Childrens Hospital Los Angeles, who was not directly involved in the study. "Only by understanding how this devastating disease develops will be able to begin taking steps to prevent it".


Posted by: Evelyn    Source

Dr. Xingming Shi, bone biologist at the Medical College of Georgia Institute of Molecular Medicine and Genetics.

Credit: Phil Jones

A small protein may have a big role in helping you make more bone and less fat, researchers say.

"The pathways are parallel, and the idea is if you can somehow disrupt the fat production pathway, you will get more bone," says Dr. Xingming Shi, bone biologist at the Medical College of Georgia Institute of Molecular Medicine and Genetics.

He's found the short-acting protein GILZ appears to make this desirable shift and wants to better understand how it does it with the long-term goal of targeted therapies for osteoporosis, obesity and maybe more.

"Osteoporosis and obesity are two major public health problems, but people have no idea whether they have a connection," says Dr. Shi. Bone and fat do have a common source: both are derived from mesynchymal stem cells. Bone loss and fat gain also tend to happen with age and with use of the powerful, anti-inflammatory steroid hormones glucocorticoids. "When you age, your bone marrow microenvironment changes; the balance between the bone and fat pathway is broken," says Dr. Shi, a faculty member in the MCG Schools of Medicine and Graduate Studies. "You have more fat cells accumulate".

"The bones of elderly people or those who take glucocorticoids are yellow inside instead of red," he says. And it gets worse: in a classic vicious cycle, the more fat, the more cytokines that stimulate production of bone-destroying osteoclasts and inhibit bone-forming osteoblasts. He recently showed that even the stem cells change with age: their numbers and their ability to differentiate decrease.

Weight gain and bone loss are established side effects of glucocorticoids, whose wide-ranging uses include treatment for arthritis, asthma, infections and organ transplants. Ironically, glucocorticoids also induce a short burst of GILZ. GILZ, in turn, inhibits the transcription factor PPAR2, called the master regulator of adipogenesis, or fat production, as well as CCAAT/enhancer-binding proteins that turn on this fat-producing gene. One way GILZ does this is by binding to the regulatory region of PPAR2, Dr. Shi has shown.

To restore a healthier balance of bone and fat production, sustained GILZ action is needed. "When you permanently express GILZ, cells cannot differentiate into fat cells. Instead, you increase bone formation. People like this idea," says Dr. Shi, who has watched the mesynchymal stem cell production shift.

One point of controversy is that, at least in the lab, glucocorticoids seem to enhance bone formation. But Dr. Shi believes it's the short burst of GILZ at work there. He wants to know exactly how it works to see if it could offer a targeted therapy for osteoporosis and obesity and maybe a safer option for many who need glucocorticoids.

A recent $1.5 million, five-year grant from the National Institute of Diabetes and Digestive and Kidney Diseases is enabling Dr. Shi to further test his hypothesis about how GILZ represses PPAR2 and to see if GILZ over-expression in mice reduces PPAR2 expression and consequently increases bone and decreases fat. A long-term goal is to understand exactly how PPAR2 controls fat and bone production.

GILZ also is a powerful immune and inflammation suppressor. It inhibits two key inflammatory molecules, NF-kB and AP-1, which turn on inflammatory genes in response to cytokines, such as TNF- and IL-1, involved in rheumatoid arthritis and other inflammatory diseases, Dr. Shi showed in research published on the cover of the April 15 issue of Journal of Cellular Biochemistry That study notes GILZ's potential as a novel anti-inflammatory therapy.

In fact, Dr. Shi believes GILZ is a key factor mediating the anti-inflammatory effects of glucocorticoids. A long-acting version of GILZ or a similar substance would be needed to produce, for example, a powerful new arthritis treatment minus the undesirable effects. About 50 percent of arthritis patients who take glucocorticoids develop osteoporosis, he notes, worsening an already difficulty condition worse.

People can't take GILZ now, but another long-term goal is to develop a GILZ-like pill that would dramatically reduce fat production. Dr. Shi already has developed a cell line that continuously expresses GILZ.


Posted by: Evelyn    Source

Chips on the left are from potatoes infected with the zebra chip disease, which alters the sugar levels and causes the sugar to carmelize and give a burned appearance, according to Dr. Don Henne, Texas AgriLife Research assistant research scientist.

Credit: (Texas AgriLife Research photo by Kay Ledbetter)
Dr. Don Henne isn't wasting his degree when he's standing by the deep fryer waiting for potato slices to turn brown. He's conducting research that will help the potato industry and consumers.

Henne, an assistant research scientist in the Texas AgriLife Research plant pathology program in Amarillo, is one of a number of who are trying to find answers about zebra chip. Zebra chip is the latest disease to plague the potato industry, particularly those in the chipping business.

Dr. Charlie Rush, AgriLife Research plant pathologist and leader of the program, began working on the project at the request of local producers in early 2007. His work later became a part of the Zebra Chip State Initiative through the Texas Department of Agriculture.

The initiative brought together scientists from throughout the state and country to try to find answers for zebra chip, Rush said.

"When we first began working on it, the pathogen and vector were unknown," he said. "Only recently have scientists began pinning those down".

Rush said Henne was brought into the program in May because of his experience and background. His primary responsibility is to help understand the factors that impact disease onset and spread. Zebra chip is a disease that alters the sugar levels in the potato, Henne said. The sugar caramelizes and turns the chip brown when it is fried, giving it an off taste and burnt appearance. While it is not harmful, it is a cosmetic and taste concern for consumers.

Potato growers have had to abandon entire infected fields, costing as much as $2 million a year in damage, he said.

Henne, who has a degree in entomology, is trying to chase the potato psyllid, the insect that likely carries the pathogens which cause the disease. He is trying to find out what makes it move through a field, as well as when it moves and how fast.

He has visited grower fields from Weslaco to Pearsall and Olton to Dalhart already this year, as well as made contact with other zebra chip scientists around the nation to familiarize himself with this new chipping potato disease.

Zebra chip first appeared in Mexico and Guatemala in the early 2000s. It has been found in potato fields through South Texas and the Rio Grande Valley and now up into the South Plains and Panhandle regions.

The disease presents itself as curled leaves and stunted growth in the plant itself, and then the tubers exhibit a brown striped or mottled pattern when sliced, Henne said.

AgriLife Research and other researchers around the country have studied the vector or insect that transmits the pathogen, he said. Others are trying to identify the pathogen or bacteria that actually causes disease in the plant when the psyllid feeds on it.

Henne and other Amarillo-based scientists are working with commercial growers to monitor the movement of the insect and disease appearance. At the same time, they have established potato plots at the Texas AgriLife Research Station at Bushland and are doing some greenhouse work.

"We're focusing on the epidemiological aspects of the disease," Henne said. "We are trying to understand how the disease progresses in a potato field over time. We are looking at canopy structure, edge effect and how the insects are landing in fields and distributing the disease".

Henne and Dr. Fekede Workneh, an AgriLife Research quantitative plant disease epidemiologist, have planted six acres of potatoes at the Bushland station where they are looking at planting dates, canopy structure and insect dispersal.

Potatoes are planted in late March to early June in the Panhandle, so they are experimenting with planting dates May 2, May 28 and June 16 at Bushland to see if there is a relation between insect movement and disease severity.

"We are also working in the lab to graft diseased portions onto healthy plants to understand the movement of the disease through the plant," Henne said.

"We want to understand how the disease progresses so we can focus management practices on specific areas," he said. "Do the insects move up the plant, down or out from the stem? Some varieties have more canopy than others and is that acting as a natural bridge for insect movement?".

There is no adequate control for the insect or the disease at this time, he said.

Because there are other diseases that have similar symptoms as zebra chip, Henne said, one of the challenges they face is being able to correctly identify diseased plants in the field.

"When we find plants that appear to be infected, we bring the tubers back to the lab where they are sliced and fried to make the final determination," he said.

Henne said they hoped to have some management suggestions on how to help alleviate the problem for growers by the end of this year.


Posted by: Evelyn    Source

Scientists at the University of Minnesota have discovered a gene that may provide a clue as to why obesity rates increase with age. The research was published recently in the Proceedings of the National Academy of Sciences
Scientists in the lab of Kevin Wickman, Ph.D., associate professor of pharmacology at the University of Minnesota Medical School, removed a single gene from mice as part of a research study that's ongoing to understand how the brain controls heart function. While some cardiac deficiencies were detected in these mice, the scientists unexpectedly observed that these mice exhibited a predisposition to adult-onset obesity.

"This was not an outcome we expected, but now we have an animal model that may provide new insight into human obesity," said Wickman, co-author of the article.

By examining closely where this gene, termed Girk4, is expressed in the body, the scientists found especially high levels in the hypothalamus, a brain region involved in regulating food intake and energy expenditure. Wickman speculated that disruption of normal function in the hypothalamus may underlie the obesity seen in the mutant mice, but he acknowledges that more studies are needed to understand where and how this gene works, and consequently, why mice missing this gene develop obesity.

The age-dependence of the obesity seen in this mouse model mimics human obesity patterns, scientists said. Indeed, the likelihood of people developing obesity more than doubles between the ages of 20 and 60.

"This is a novel finding that may provide important new insight to the underlying cellular mechanisms that influence obesity," said Catherine Kotz, Ph.D., co-author of the article, scientist at the Minneapolis VA Medical Center and adjunct professor in the Department of Food Science and Nutrition at the University of Minnesota.


Posted by: Evelyn    Source

Healthy individuals who gain weight, even to a weight still considered normal, are at risk for developing chronic kidney disease (CKD), as per a research studyappearing in the September 2008 issue of the Journal of the American Society Nephrology (JASN). The study suggests that CKD should be added to the list of conditions that are linked to weight gain, including diabetes and hypertension.

Research has shown that obesity is associated with an increased risk of CKD, but no studies have looked at the effects of weight gain within the "normal" range of an individual's body mass index. To investigate, Drs. Seungho Ryu and Yoosoo Chang of the Kangbuk Samsung Hospital in Seoul, Korea, and their colleagues conducted a prospective study of individuals who were of a healthy weight and had no known risk factors for chronic kidney disease.

In Korea, all workers participate in either annual or biennial health exams, as mandatory by Korea's Industrial Safety and Health Law. As a result, the researchers had access to clinical data from thousands of individuals. For this study, they included 8,792 healthy men who participated in the health exams in 2002.

The scientists discovered a U-shaped association between weight change and development of CKD. Men who lost or gained a lot of weight (more than 0.75 kg per year) had the highest risk of developing CKD. Those whose weight changed minimally (within a range of -0.25 to