Effect of Resistant Starch Consumption on Adiposity

This program endeavors to study the influence of resistant starch on fat metabolism and storage, and insulin sensitivity. Resistant starch has, in the past, been shown to reduce insulin and glucose excursion following a meal, improve long-term insulin sensitivity in rats, and increase beneficial microflora and the production of short chain fatty acids in the bowel which may reduce cancer risk. Due to the strong physical association between resistant starch and dietary fat, it is possible that consumption of resistant starch may alter fat absorption and, therefore, fat oxidation and storage. This program aims to examine this possibility in conjunction with the effect of chronic resistant starch consumption on insulin sensitivity in humans.

Program Director: (Click on name for biographical information)
Janine Higgins, Ph.D.
Higgins.Janine@tchden.org
(303) 837-2955

Purpose or description:
Currently, there is strong evidence linking dietary fat intake to the development of obesity but very little is known about the effects of carbohydrate subtype on this disease. However, recent evidence from both rat and human studies suggest that carbohydrate subtype may have direct effects on lipid metabolism. Dietary carbohydrates consist of simple carbohydrates, or sugars, and complex carbohydrates, or starches. Resistant starch (RS) is any starch that is not digested in the upper digestive tract but passes to the large bowel where it is an available substrate for fermentation. Rat data indicates that long-term RS feeding maintains insulin sensitivity relative to digestible starch (DS) feeding. In addition, it has been shown that RS feeding affects adipocyte morphology in rats, reducing cell size compared with DS-feeding. In humans, chronic RS feeding results in a reduction in fasting cholesterol and triglyceride concentrations relative to DS feeding.

The studies undertaken as part of this program aim to determine the effects of long-term RS feeding on adiposity and metabolic profile. The specific aims are: 1) to define the dose-response relationship between the RS content of the diet and postprandial glycemic/insulinemic response; 2) to measure adipocyte cell size in response to a high RS diet; 3) to correlate any changes in adipocyte morphology with body composition; 4) to measure insulin sensitivity in response to the RS content of the diet; 5) to determine the effects of the RS content of the diet on dietary fat storage and utilization. The optimal RS content in the diet, as determined by meal tests which defined the dose-response relationship between the RS content of the diet and postprandial/post-absorptive fat oxidation, is currently being used in a chronic RS feeding study. Subjects are randomly assigned to an RS- or DS-based diet for 12 weeks in a double cross-over, blinded design. One group of subjects will consume an RS-based diet for 12 weeks followed by a 4-week wash-out period and conclude the study with 12 weeks on a DS-based diet. The second group shall receive the two diet phases in reverse order (i.e. DS followed by RS). At the beginning and end of each diet phase, adipocyte cell size, body composition, macronutrient oxidation rate, insulin sensitivity, and fasting and postprandial blood lipids, glucose, and insulin concentrations will measured. By using this study to define the role of carbohydrate subtype on adiposity and the metabolic changes associated with obesity, we are moving a step closer to the overall aim of this research which is to develop an 'anti-obesity' diet. Such a diet would optimally combine the fat and carbohydrate subtypes which most effectively prevent adiposity and weight gain.

Techniques/Methods Utilized:

• Body composition is assessed using dual X-ray absorptiometry (DEXA)
• Macronutrient oxidation is measured via indirect calorimetry during a 24 hour stay in a whole room calorimeter. Non-protein respiratory quotient (RQ) is used to calculate absolute carbohydrate and fat oxidation. These values are then adjusted to account for adiposity.
• Meal fat oxidation is calculated from the collection of expired breath samples following ingestion of a mixed meal, accounting for 30% of daily caloric needs, which contains a small amount of radiolabelled fat, [1-14C]triolein. All breath samples are assessed for 14CO2 content.
• Meal fat storage is assessed by obtaining a gluteal fat biopsy and measuring the amount of 14C accumulated following ingestion of a mixed meal, accounting for 30% of daily caloric needs, which contains a small amount of radiolabelled fat, [1-14C]triolein (as described above).
• Insulin sensitivity is measured via an hyperinsulinemic-euglycemic clamp, in which insulin is infused at afixed rate to achieve steady state, mid-physiological serum insulin concentrations. Glucose is simultaneously infused at a variable rate in order to maintain euglycemia. The glucose infusion rate at euglycemia is a measure of insulin sensitivity.

Program Support:

This work is funded by a National Institutes of Health (NIH) R01 grant. All resistant starch foods are supplied by Penford Australia Limited

Staff and Collaborators: (Click on name for biographical information)
Dan Bessesen, M.D.
W. Troy Donahoo, M.D.
Janine Higgins, Ph.D.
James Hill

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