Resistant starch consumption promotes lipid oxidation

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Nutrition & Metabolism

Open Access

Research

Resistant starch consumption promotes lipid oxidation

Janine A Higgins*

, Dana R Higbee

, William T Donahoo

, Ian L Brown

Melanie L Bell

and Daniel H Bessesen

Address:

University of Colorado Health Sciences Center, Center for Human Nutrition, Denver, Colorado 80262. USA,

University of Vermont,

Department of Medicine, Burlington, Vermont 05405. USA,

University of Wollongong, Wollongong, NSW, 2522. Australia and

Preventive &

Social Medicine, University of Otago, Dunedin, New Zealand

Email: Janine A Higgins* - Higgins.Janine@tchden.org; Dana R Higbee - Dana.Higbee@uchsc.edu;
William T Donahoo - William.Donahoo@uvm.edu; Ian L Brown - ian.brown@nstarch.com;
Melanie L Bell - melanie.bell@stonebow.otago.ac.nz; Daniel H Bessesen - Daniel.Bessesen@uchsc.edu

* Corresponding author

resistant starchfat oxidationglucoseinsulinamylose

Abstract

Background: Although the effects of resistant starch (RS) on postprandial glycemia and
insulinemia have been extensively studied, little is known about the impact of RS on fat metabolism.
This study examines the relationship between the RS content of a meal and postprandial/post-
absorbative fat oxidation.

Results: 12 subjects consumed meals containing 0%, 2.7%, 5.4%, and 10.7% RS (as a percentage of
total carbohydrate). Blood samples were taken and analyzed for glucose, insulin, triacylglycerol
(TAG) and free fatty acid (FFA) concentrations. Respiratory quotient was measured hourly. The
0%, 5.4%, and 10.7% meals contained 50 µCi [1-

C]-triolein with breath samples collected hourly

following the meal, and gluteal fat biopsies obtained at 0 and 24 h. RS, regardless of dose, had no
effect on fasting or postprandial insulin, glucose, FFA or TAG concentration, nor on meal fat
storage. However, data from indirect calorimetry and oxidation of [1-

C]-triolein to

showed that addition of 5.4% RS to the diet significantly increased fat oxidation. In fact, postprandial
oxidation of [1-

C]-triolein was 23% greater with the 5.4% RS meal than the 0% meal (p = 0.0062).

Conclusions: These data indicate that replacement of 5.4% of total dietary carbohydrate with RS
significantly increased post-prandial lipid oxidation and therefore could decrease fat accumulation
in the long-term.

Background

Resistant starch (RS) is any starch that is not digested in
the small intestine but passes to the large bowel for fer-
mentation [1]. Retrograded amylose (a linear polymer of
glucose residues linked by (14) bonds; RS1), such as
cooked and cooled starchy foods like pasta salad, and

native starch granules (RS2), such as those found in high-
amylose maize starch and bananas, are the major compo-
nents of dietary RS. Calories from RS that are undigested
in the small intestine can be salvaged by fermentation to
short-chain fatty acids (SCFA; acetate, butyrate, proprion-
ate) by the microflora of the large bowel. Fermentation of

Published: 06 October 2004

Nutrition & Metabolism 2004, 1:8

doi:10.1186/1743-7075-1-8

Received: 14 August 2004
Accepted: 06 October 2004

This article is available from: http://www.nutritionandmetabolism.com/content/1/1/8

© 2004 Higgins et al; licensee BioMed Central Ltd.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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