Health for life

... and aid the breakdown of fat!

Researchers reporting in last months issue of the American Journal of Clinical Nutrition found that supplementing 30 grams/day of resistant starch to their volunteers diets resulted in a 33% increase in insulin sensitivity. As a result, subjects could clear glucose from their bloodstreams faster than those who did not receive the resistant starch.

A study last year in Nutrition and Metabolism found that replacing 5.4% of the carbohydrate in a meal* increased fat-oxidation (the breakdown of fat) and could decrease fat accumulation over time. The implications for resistant starchs use in weight management are encouraging.

* For example, if your meal contained 100 grams of carbohydrate, 5.4 grams would be replaced with resistant starch.

What is resistant starch (RS)?
Simply, its starch we eat that is not digested in the small intestine. It passes to the large intestine where it undergoes fermentation by bacteria. The HealthyEatingClub.com lists these foods as containing resistant starch:

• Intact wholegrain cereals/seeds/nuts, e.g. oats, rye, wheat, barley, semolina, corn, linseed, sesame
  
• Processed starchy foods, e.g. some breakfast cereals (cornflakes), white bread, rice, pasta
  
• Processed starchy foods with added RS called Hi-Maize (derived from corn)
  
• Legumes, e.g. lentils, beans (Legumes have the highest content of RS.)
  
• Unripe fruit, especially banana
  
• Cooked cold rice, cold pasta salad, cold boiled potato salad (Cooking and cooling food can increase RS content.)

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For some background on resistant starch:
Resistant Starch

For the American Journal of Clinical Nutrition study:
Insulin-sensitizing effects of dietary resistant starch and effects on skeletal muscle and adipose tissue metabolism

For the Nutrition and Metabolism study:
Resistant starch consumption promotes lipid oxidation

In the following study:

Reversal Of Diet-Induced Insulin Resistance With A Single Bout Of Exercise In The Rat: The Role Of PTP1B And IRS-1 Serine Phosphorylation, The Journal of Physiology, 2006

Researchers fed mice either a control diet or a high-fat diet for three months. The high-fat diet produced obese mice with greater insulin resistance.

Researchers then submitted some of the high-fat-fed, insulin-resistant, obese mice to a bout of exercise. The exercise increased insulin sensitivity in the obese mice, such that:

"The decrease in the glucose disappearance rate induced by the high-fat diet, returned to the basal levels 16 hours after acute exercise."

It did not return to basal levels in mice that did not exercise.

The authors hypothesized that the mechanism for this improved glucose uptake may be linked to the action of certain proteins known to regulate glucose metabolism in muscle cells.
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Another group of researchers hypothesized that the mechanism for improved glucose uptake after exercise may be related instead to activity of mitochondria in muscle.

In their study:

Setting The Stage: Possible Mechanisms By Which Acute Contraction Restores Insulin Sensitivity In Muscle, American Journal of Physiology - Regulatory, Integrative, and Comparative Physiology, 2008

When obese rats were exposed to bouts of exercise:

"Our group found that acute muscle contraction synergistically improved insulin-stimulated glucose transport in skeletal muscle. ... The improved insulin sensitivity was associated with a robust increase in mitochondrial energy flux."

How exercise works to improve insulin sensitivity may be under consideration, but that it works has been shown consistently.
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