Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats.

Damien P Belobrajdic,Anthony R Bird,Claus T Christophersen,Roger A King

doi:10.1186/1743-7075-9-93

Abstract

BackgroundAnimal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents. We aimed to determine whether RS dose-dependently reduces adiposity in obesity-prone (OP) and obesity-resistant (OR) rats.MethodsMale Sprague–Dawley rats (n=120) were fed a moderate-fat, high-energy diet for 4 wk. Rats that gained the most weight (40%) were classified as obesity-prone (OP) and obesity-resistant (OR) rats were the 40% that gained the least weight. OP and OR rats were randomly allocated to one of six groups (n=8 for each phenotype). One group was killed for baseline measurements, the other five groups were allocated to AIN-93 based diets that contained 0, 4, 8, 12 and 16% RS (as high amylose maize starch) for 4 wk. These diets were matched for total carbohydrate content. At 0, 4 and 7 wk from the start of the study insulin sensitivity was calculated by homeostasis model assessment of insulin resistance (HOMA-IR) and adiposity was determined by dual-energy X-ray absorptiometry (DXA). At 8 wk, rats were euthanized and fat pad weights, intestinal digesta short chain fatty acid (SCFA) pools and plasma gut hormone levels were determined.ResultsObesity prone rats gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in OR animals was significant only at 16% RS. Irrespective of phenotype, diets containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. All diets containing RS increased total SCFA pools in the caecum and lowered plasma GIP concentrations compared to the 0% RS, whereas plasma GLP-1 and PYY were increased when the diet contained at least 8% RS. Insulin sensitivity was not affected by RS.ConclusionRS in amounts that could be potentially consumed by humans were effective in reducing adiposity and weight gain in OP and OR rats, due in part to a reduction in energy intake, and changes in gut hormones and large bowel carbohydrate fermentation.

Highlights

Animal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents
Aziz et al [6] showed that in diet-induced obese rats, diets high in RS reduced body weight gain, fat pad weight and glycaemic response, and increased insulin sensitivity compared to a diet low in RS
We have shown previously that moderate to high levels of RS reduced the body weight of healthy non-obese rats compared to those fed a low-amylose control diet [7]

Summary

Introduction

Animal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents. Aziz et al [6] showed that in diet-induced obese rats, diets high in RS (as high-amylose maize starch; HAMS) reduced body weight gain (by 40%), fat pad weight and glycaemic response, and increased insulin sensitivity compared to a diet low in RS. These changes were dramatic they were achieved at levels of RS that are not readily achievable in the human diet. Because dietary intakes of RS in industrialised countries are low, it is important to establish minimal levels of RS that elicit favourable metabolic effects in obese and non-obese animals to assist in identifying appropriate levels for human intervention trials

Objectives

Methods

Results

Discussion

Conclusion