Part 2 of my series on the N=2 will be up early next week. In the meantime, here's a study, with full text.
M Denise Robertson, Alex S Bickerton, A Louise Dennis, Hubert Vidal, and Keith N Frayn
From the Introduction:
"...Insoluble fibers, such as resistant starch (RS), are nonviscous and thus have no effect on glucose absorption, yet they have been shown in short-term human studies (8) to increase insulin sensitivity. Despite epidemiologic evidence linking insoluble fiber intake to a reduced incidence of type 2 diabetes (9-11), the metabolic link between chronic RS ingestion and insulin sensitivity has yet to be proven in humans.
"One possible mechanism by which dietary RS intake might modulate insulin sensitivity is through alterations in fatty acid flux. Fatty acid metabolism is a key feature in determining tissue insulin sensitivity. Abnormalities in fatty acid storage and lipolysis in insulin-sensitive tissues with increased flux from adipose to nonadipose tissues such as skeletal muscle may be a critical event in the development of insulin resistance (12). The direct effect of RS consumption on fatty acid flux is unknown beyond studies that have measured fasting triacylglycerol and cholesterol concentrations after RS intervention (7). In isolation, short-chain fatty acids (SCFAs), which are produced during colonic fermentation of RS, inhibit adipose tissue lipolysis (13), but an in vivo effect of dietary RS intake has yet to be shown.
"We showed previously that short-term (24 h) high doses of RS (60 g/d) significantly elevate postprandial insulin sensitivity, with lower circulating concentrations of both NEFAs and SCFAs (8). In the present study, we assessed the effect of a more sustainable dose of RS of 30 g/d for 4 wk to allow the assessment of longer-term metabolic adaptation to RS. By using an integrative approach to this nutritional question, we have assessed adaptation to RS intake at the gene-tissue and whole-body levels in humans."