[PHNUTR-L] Metabolic syndrome -- don't blame the belly fat

[Kathrynne Holden]

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Public release date: 16-Jul-2007
http://www.eurekalert.org/pub_releases/2007-07/hhmi-msd071607.php

Contact: Jennifer Michalowski
michalow at hhmi.org
301-215-8576
Howard Hughes Medical Institute

Metabolic syndrome -- don't blame the belly fat

Abdominal fat, the spare tire that many of us carry, has long been 
implicated as a primary suspect in causing the metabolic syndrome, a 
cluster of conditions that includes the most dangerous heart attack risk 
factors: prediabetes, diabetes, high blood pressure, and changes in 
cholesterol.

But with the help of powerful new imaging technologies, a team of Howard 
Hughes Medical Institute (HHMI) researchers at Yale University School of 
Medicine has found that insulin resistance in skeletal muscle leads to 
alterations in energy storage that set the stage for the metabolic syndrome.

Insulin resistance is a condition in which the body's cells become 
resistant to insulin, a hormone secreted by the pancreas that plays an 
essential role in regulating the carbohydrates, lipids, and proteins 
obtained from food.

The new study, published July 16, 2007, in the Proceedings of the 
National Academy of Sciences (PNAS), demonstrates that insulin 
resistance in skeletal muscle -- caused by decreased ability of muscle 
to make glycogen, the stored form of carbohydrate from food energy -- 
can promote an elevated pattern of lipids or fats in the bloodstream 
that underpins the metabolic syndrome.

The study was led by HHMI investigator Gerald I. Shulman and Kitt Falk 
Petersen, both of the Yale University School of Medicine. Coauthors of 
the paper were from Yale and Harvard Medical School.

The metabolic syndrome is a very common metabolic abnormality and the 
prevalence is growing. However, the underlying factors that cause it are 
poorly understood.” The syndrome afflicts more than 50 million Americans 
and roughly half of all Americans are predisposed to it, making it one 
of the nation's most serious human health issues.

To begin to shed light on the earliest molecular events that lead to the 
metabolic syndrome, Shulman and his colleagues used powerful new 
magnetic resonance imaging techniques to observe how nutrients are 
channeled in the body in both insulin resistant and insulin sensitive 
human subjects.

The subjects for the study were all young, lean, non-smoking, healthy 
individuals who were sedentary and matched for physical activity. Aside 
from insulin resistance in one cohort, these volunteers had none of the 
other confounding factors typically associated with obesity and type 2 
diabetes, which have been thought to play a key role in the pathogenesis 
of the metabolic syndrome.

"Our hypothesis was that the metabolic syndrome is really a problem with 
how we store energy from food,” Shulman explained. "The idea is that 
insulin resistance in muscle changes the pattern of energy storage."

After providing the study's subjects with two meals high in 
carbohydrates, Shulman and his colleagues turned to magnetic resonance 
spectroscopy to measure the production of liver and muscle triglyceride, 
the storage form of fat, and of glycogen, the storage form of 
carbohydrate. "What we found is that (insulin) sensitive individuals 
took the energy from carbohydrate in the meals and stored it away as 
glycogen in both liver and muscle," said Shulman.

In the insulin resistant subjects, the energy obtained from their 
carbohydrate rich meals was rerouted to liver triglyceride production, 
elevating triglycerides in the blood by as much as 60 percent and 
lowering HDL cholesterol (the “good cholesterol”) by 20 percent. "In 
contrast to the young, lean, insulin-sensitive subjects, who stored most 
of their ingested energy as liver and muscle glycogen, the young, lean, 
insulin-resistant subjects had a marked defect in muscle glycogen 
synthesis and diverted much more of their ingested carbohydrate into 
liver fat production,” Shulman and his colleagues reported.

"What we see," he noted, "is alterations in patterns of energy storage. 
An additional key point is that the insulin resistance, in these young, 
lean, insulin resistant individuals, was independent of abdominal 
obesity and circulating plasma adipocytokines, suggesting that these 
abnormalities develop later in the development of the metabolic syndrome."

The new findings promise to help untangle the early molecular events of 
a syndrome at the root of one of the world's most significant health 
issues. “Knowing how insulin resistance alters energy storage before it 
leads to more serious problems can help those susceptible prevent the 
onset of the metabolic syndrome,” Shulman said.

Another key observation was that skeletal muscle insulin resistance 
precedes the development of insulin resistance in liver cells, and that 
fat production in the liver is increased. “These findings also have 
important implications for understanding the pathogenesis of 
nonalcoholic fatty liver disease, one of the most prevalent liver 
diseases in both adults and children” Shulman said.

The good news, according to Shulman, is that insulin resistance in 
skeletal muscle can be countered through a simple intervention: exercise.
-- 
Kathrynne Holden, MS, RD < fivestar at nutritionucanlivewith.com >
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