The decreased NEFA output from adipose tissue reflected a significant postprandial reduction in the rate of action of hormone-sensitive lipase, the enzyme responsible for the mobilization of stored triacylglycerol. There was no significant effect of RS intake on plasma triacylglycerol despite a significant reduction in the calculated rate of action of lipoprotein lipase. Although the release of NEFAs from adipose tissue was lower, the arterialized NEFA concentration and the total uptake of fatty acids by muscle were unchanged by supplementation
...propionate uptake was significant only after the high-RS diet. Butyrate uptake was not significant. Acetate uptake increased after RS supplementation across both tissues: as a function of increased plasma concentration (adipose tissue) and as increased fractional extraction (skeletal muscle). Propionate was present at much lower concentrations and had a higher fractional extraction across adipose tissue after the RS supplement
Adipose tissue itself is also an important site for maintaining glucose homeostasis, with total glucose removal increasing by 200% after RS supplementation. The metabolic fate of this additional glucose is at present unclear.
After RS supplementation, the peripheral concentrations of both acetate and propionate were increased, as was the rate of uptake into the specific tissues. SCFAs were recently shown to bind to the G protein–coupled receptors GPR41 and GPR43, which have been isolated from both adipose tissue and skeletal muscle. The function of these receptors is at present ill defined, but they have been proposed to trigger leptin release from adipocytes. Despite significantly higher SCFA concentrations, no significant change in plasma leptin or leptin mRNA was found after RS supplementation. SCFAs have been shown to inhibit adipose tissue lipolysis in vivo and thus may contribute to the observed reduction in lipolysis. However, this has never been reported physiologically after fiber intake. We found no relation between NEFA release from adipose tissue and SCFA concentrations, so additional mechanisms may be involved.
An interesting observation was the increase in the circulating concentration of total ghrelin after RS supplementation. This result is counterintuitive from what we know about the satiating effects of RS and the appetite-stimulating effects of ghrelin. Perhaps the systemic concentration of ghrelin is more relevant in determining its peripheral actions, independent of those induced within the hypothalamus. Elevations in plasma ghrelin have been linked to increased insulin sensitivity in numerous studies, although debate still exists as to the mechanism. It is hypothesized that the hyperinsulinemia of insulin resistance down-regulates ghrelin release and thus that elevated ghrelin is merely a consequence of the low insulin concentrations. In the present study, fasting ghrelin concentrations were significantly elevated with no significant change in fasting insulin concentrations, and thus it is doubtful that this mechanism is in place.
We have now shown insulin sensitization at the whole-body leve...In addition, we showed a reduction in adipose tissue lipolysis and an increase in the insulin sensitivity of skeletal muscle glucose clearance. These effects of RS may be due to changes in the peripheral metabolism of SCFAs or in the secretion of ghrelin...we have been able to show the metabolic changes induced by fermentable fiber at both the whole-body and the tissue level.