MONDAY, April 7 (HealthDay News) -- Use of the antipsychotic medication olanzapine may put a person at an increased risk for heart disease and type 2 diabetes, new findings show.

A team of French researchers studying the drug's effect on male rats found that, after consuming olanzapine over several weeks, the rodents' blood sugar levels rose significantly compared to rats not on the drug. This was especially noticeable after the rats ate meals with glucose in them. The rats consuming olanzapine did not gain weight or increase their food intake; however, the proportion of fat stored in their abdominal cavity was notably higher.

These changes are increased risk factors of metabolic syndrome, which puts an individual at greater risk of heart disease and type 2 diabetes.

"Based on these findings, we concluded that male rats treated with olanzapine experienced an early disruption of energy metabolism. This was a result of the fat tissue we observed and the impairment in blood sugar regulation which are both associated with metabolic syndrome and subsequent risk of diabetes," senior study author Dominique Hermier, of the Department of Human Nutrition, INRA, in Paris, said in a prepared statement.

The study was to be presented Monday at the Experimental Biology annual meeting, in San Diego.

Olanzapine is a part of the second generation of antipsychotics known as atypical antipsychotics being used to treat schizophrenia. These newer medicines have proven as effective as their predecessors in treating the delusions and hallucinations that accompany psychotic mental illness and even more effective in combating other symptoms, such as apathy. Side effects, though, include weight gain and a greater chance for developing metabolic syndrome. Physicians fear these side effects may cause their patients to stop taking their medicine.

"Atypical medications like olanzapine are of tremendous value in treating individuals with certain kinds of mental illness. Our hope is that through discoveries such as this one, such life-enhancing medicines can be further optimized," Hermier said.

More information

The American Heart Association has more about metabolic syndrome  .

FRIDAY, April 4 (HealthDay News) -- Elevated levels of uric acid in the blood may be an early sign of diabetic kidney disease in people with type 1 diabetes, a new study suggests.

Researchers at the Joslin Diabetes Center in Boston noted that increased uric acid levels may appear before any significant change in urine albumin levels, the standard screening test for diabetic kidney disease.

In the study, the researchers checked serum uric acid concentration and urine albumin levels in 675 patients with type 1 diabetes. The results showed that 311 patients had microalbuminuria (small amounts of the protein albumin in the urine), an early sign of diabetic kidney disease. The other 364 patients had normal urine albumin levels.

While none of the patients had higher levels of albumin (albuminuria), one in five did have some impairment of kidney function.

"Our research showed that loss of kidney function takes place even in the absence of albuminuria in patients with type 1 diabetes," study author Dr. Elizabeth T. Rosolowsky said in a prepared statement.

But she and her colleagues found that serum uric acid level was consistently related to kidney function. The higher the levels of uric acid in the blood, the lower the kidney function.

"The serum concentration of uric acid in these patients varied in a manner consistent with its having played a role in this early loss of kidney function," Rosolowsky said.

The findings, published in the May issue of the Clinical Journal of the American Society of Nephrology, suggest that treatments to reduce uric acid may help slow the decline of kidney function in diabetes patients.

"Thus we have the hope of having a means to thwart the loss of kidney function while function is still a relatively preserved stage," Rosolowsky said.

She noted that serum acid levels can be modified using drugs or by decreasing the amount of protein in a person's diet.

"If follow-up studies, already under way, demonstrate that serum uric acid concentration predicts the course of early decline in kidney function, then clinical trials would be justified to test whether modifying serum uric acid concentration also modifies the course of renal function decline in type 1 diabetic patients with high normoalbuminuria or microalbuminuria," Rosolowsky said.

More information

The National Kidney Foundation has more about diabetes and kidney disease  .

THURSDAY, March 20 (HealthDay News) -- Scientists have gained new insight into the workings of insulin, potentially laying the groundwork for an anti-aging treatment.

The research has only taken place in worms, a common model for this type of research, and it's too early to know if it will translate to humans. But worms whose insulin levels were adjusted lived a week longer than their typical two-week lifespan, the scientists said.

"It doesn't sound like much for a worm, but those percentages would be a lot for us," noted study co-author Dr. T. Keith Blackwell, senior investigator at Harvard Medical School's Joslin Diabetes Center, in Boston.

According to Blackwell, the findings -- which explore a genetic pathway in the worms -- provide new information about how insulin and lifespan might be related.

"We're understanding more and more about how cellular processes can really influence how we defend ourselves against challenges from the environment," he said.

The new findings are published in the March 21 issue of the journal Cell.

Insulin is best known as the hormone that allows healthy people to regulate blood sugar and is linked to a variety of problems in diabetics.

Insulin has other jobs, such as helping to regulate the burning of fuel by cells to provide energy, noted Blackwell, an associate professor of pathology at Harvard Medical School and faculty member at the Harvard Stem Cell Institute. Insulin also serves as a taskmaster, telling cells to process glucose, suppress tumors and respond to the daily challenges that our bodies face, he said.

In the new study, researchers looked into the effects of changing insulin levels in a species of tiny worm known as Caenorhabditis elegans. The worm has long been used in cutting-edge genetics research -- in fact, hundreds of the critters survived the 2003 Space Shuttle disaster intact, although their tiny lifespans prevented them from appreciating their brush with death for very long.

The Joslin researchers found that more insulin results in less activity by a gene-regulating protein called SKN-1. So, by lowering insulin levels, the study authors were able to boost levels of the protein and make the worms live longer.

The mechanism at work here seems to relate to how well cells defend themselves against damage. "From just being alive, your body is creating its own free radicals that can cause damage," Blackwell explained. "Your body has its own antioxidant systems that clean up damage and protect you from damage. We were able to push the activity of that system upward and make the animals live longer."

Previous research has shown that insulin controls the activity of another protein, known as FOXO, that also regulates genes.

The potential impact on people with diabetes is unclear. Diabetics are unable to produce enough insulin: people with the rarer type 1 diabetes produce no insulin, while those with type 2 diabetes don't produce enough.

Blackwell believes that the research does hold hope for people with a variety of diseases. "We're understanding more about mechanisms that can be harnessed in a way that pushes back this tide of cellular damage," he said. "There's a lot of therapeutic potential to defend against chronic diseases and potentially expand lifespans."

More information

There's more on insulin at the U.S. Food and Drug Administration.