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Intense exercise training can help normalize muscle metabolism in people with type 1 diabetes, which could result in “clinically important health benefits,” Australian researchers report.

After 7weeks of sprint training, diabetics seemed to burn, or “oxidize,” fat more readily, while accumulating less lactate in their muscle tissue, Dr. Alison R. Harmer of the University of Sydney in New South Wales and her colleagues found. The researchers also found no adverse effects of intense exercise in the study participants, some of whom had poor blood glucose control.

In people without diabetes, high-intensity training can help reduce breakdown of glycogen, a molecule used to store energy in the body, in future bouts of intense exercise. And while lactate accumulates in the muscles with strenuous exercise, leading to fatigue and pain, training can help reduce this accumulation.

Just one study has looked at muscle metabolism in people with type 1 diabetes, the researchers note in the November issue of Diabetes Care. This investigation found that these individuals had less ability to burn energy in their muscle tissue, more fluctuation in glucose metabolism, and greater blood acidity.

To see if their hypothesis that training may help restore normal muscle metabolism for people with type 1 diabetes, the researchers had eight patients with the condition and seven healthy individuals complete 7 weeks of sprint training. Study participants performed 4 to 10 “all out” sprints on an exercise bike three times a week.

Before and after the 7 weeks of training, each study participant cycled to exhaustion. After training, the researchers found, cycling to exhaustion led to less accumulation of lactate in the muscles and blood and slower breakdown of both glucose and glycogen than before training in the diabetic individuals.

“The oxidative adaptations to high-intensity exercise training may confer clinically important health benefits in young patients with diabetes; however, this remains to be established,” Harmer and her team conclude.
Source: http://www.reuters.com/article/healthNews/idUSTRE4A49Z220081105

Regular moderate exercise helps people with diabetes to reduce fat in their livers, in turn potentially preventing liver failure and heart disease, U.S. researchers said on Friday.

People with type 2 diabetes, the most common form of the disease and one closely tied to obesity, often have elevated liver fat levels and are at high risk for a condition called nonalcoholic fatty liver disease.

Diabetics who did a six-month program of cardiovascular exercise and weight lifting three times a week cut the fat in their livers by about 40 percent in the study by researchers at Johns Hopkins University in Baltimore.

They said the study, which used magnetic resonance imaging scans, is the first to show exercise can get fat out of the livers of people with type 2 diabetes.

“What we were able to demonstrate pretty definitively is that yet another benefit of exercise is to help reduce liver fat,” Johns Hopkins exercise physiologist Kerry Stewart said in a telephone interview.

Stewart presented the findings at an American Association of Cardiovascular and Pulmonary Rehabilitation meeting in Indianapolis.

The condition, also known as hepatic steatosis, can lead to cirrhosis of the liver, liver failure, liver cancer and a higher risk for diabetes-related heart problems.

Seventy-seven men and women with diabetes, most of whom were overweight or obese, took part in the study.

About half were assigned to moderate exercise including 45 minutes of running on a treadmill, using a stair-climbing machine or riding a bicycle for 45 minutes three times a week, along with 20 minutes of lifting weights.

The others were not placed in any formal fitness program, and most got little physical activity. At the end of six months, they had no improvement in liver fat.

Those in the exercise group also improved their overall fitness, shedding weight, gaining muscle strength and losing abdominal fat.

Type 2 diabetes is a growing problem in the United States and many other countries, fueled by increasing obesity. The American Diabetes Association said about 24 million people in the United States have diabetes, mostly type 2.
source: http://www.reuters.com/article/healthNews/idUSN1944083420080919?sp=true

Maternal obesity has been associated with diabetic complications in the resulting offspring, according to experiments in mice reported recently by researchers at the University of Louisville.

Obesity is presently a worldwide health issue, and it is commonly considered a risk factor for diabetes, cardiovascular disease, and stroke. When a pregnant woman is obese, her children can be affected by malformation, functional abnormalities, obesity, and type II diabetes. Since, presently, over 18% of American women are classified as obese, and between 18 and 38% of pregnant women meet this criteria, it is an important issue in maternal and child health in this country. However, very little is known about the mechanism of the link between maternal obesity and diabetic effects in offspring.

To investigate this association, Dr. Jianxiang Xu and Junying Han of the University of Louisville first established a viable animal model to function similarly to maternal diabetes might in humans. Female mice, genetically predisposed to obesity and further marked with a yellow coat color, were mated with normal mice, whose offspring could then be classified by coat color for this obesity gene. The obesity prone mice were obese between 6 and 8 weeks of age, but maintained normal blood glucose levels. Offspring from these and from normal crosses were then fed with normal food for up to 15 weeks, then fed with a high fat diet, and examined by sex, and the mother’s obesity status. In this first portion of the study, the birth weight of offspring from obese mothers was 14% higher than in the control group.

When the offspring, at 50 weeks of age, were administered 2 mg glucose per kg body weight. This resulted in similar glucose levels in each group, but major differences in the serum insulin levels. Namely, in female offspring from obese mothers, there was a significant increase in serum insulin levels, while females from obese mothers and males showed no significant differences. This indicates that β cell function was impaired in the female offspring of obese mothers.

To confirm this link, a second experiment was performed. Pancreatic cells were isolated from 50 week old offspring to be tested in vitro for insulin excretion. Cells from mice with a normal diet showed normal secretion, but in the high fat diet, insulin secretion was sharply reduced in offspring from an obese mother, especially when exposed to a high glucose concentration. The measure of other enzymes related to glucose metabolism such as transketolase, GAPDH, and PFK in the cells of the 50 week old mice indicated a decrease in production by the β cells ranging from 31% to 70% for those born to an obese mother.

According to the researchers, this shows that obesity in pregnancy is a factor by itself to impaired glucose tolerance in offspring, which could contribute to the development of gestational diabetes in the mother and type II diabetes in the offspring. Additionally, since there are many mothers who are obese without displaying gestational diabetes, this obesity might be a greater factor in the health of their children than previously expected.
Source: http://www.medicalnewstoday.com/articles/115691.php