Impact of resistant starch on body fat patterning and central appetite regulation

Abstract

Background: Adipose tissue patterning has a major influence on the risk of developing chronic disease. Environmental influences on both body fat patterning and appetite regulation are not fully understood. This study was performed to investigate the impact of resistant starch (RS) on adipose tissue deposition and central regulation of appetite in mice.

Methodology and principle findings: Forty mice were randomised to a diet supplemented with either the high resistant starch (HRS), or the readily digestible starch (LRS). Using (1)H magnetic resonance (MR) methods, whole body adiposity, intrahepatocellular lipids (IHCL) and intramyocellular lipids (IMCL) were measured. Manganese-enhanced MRI (MEMRI) was used to investigate neuronal activity in hypothalamic regions involved in appetite control when fed ad libitum. At the end of the interventional period, adipocytes were isolated from epididymal adipose tissue and fasting plasma collected for hormonal and adipokine measurement. Mice on the HRS and LRS diet had similar body weights although total body adiposity, subcutaneous and visceral fat, IHCL, plasma leptin, plasma adiponectin plasma insulin/glucose ratios was significantly greater in the latter group. Adipocytes isolated from the LRS group were significantly larger and had lower insulin-stimulated glucose uptake. MEMRI data obtained from the ventromedial and paraventricular hypothalamic nuclei suggests a satiating effect of the HRS diet despite a lower energy intake.

Conclusion and significance: Dietary RS significantly impacts on adipose tissue patterning, adipocyte morphology and metabolism, glucose and insulin metabolism, as well as affecting appetite regulation, supported by changes in neuronal activity in hypothalamic appetite regulation centres which are suggestive of satiation.

Figure 1. The effect of HRS and LRS diets on average body weights over the 8-week dietary interventional period.

No significant difference was observed in the body weight between the two groups of animals [two way ANOVA with post-testing by Bonferonni correction, n = 16 and 20 for HRS and LRS groups, respectively.)

Figure 2. The effect of HRS and LRS on average weekly food and energy intake per mouse over the 8 week dietary intervention period.

Figure 2a: The effect of HRS and LRS on average weekly food intake per mouse over the 8 week dietary interventional period. Figure 2b: The effect of HRS and LRS on average weekly energy intake (KJ/mouse/week) over the 8 week dietary intervention period. [***, significance at level P<0.001, two way ANOVA with post-testing by Bonferonni correction, n = 16 and 20 for HRS and LRS groups, respectively.]

Figure 3. The effect of HRS and LRS diets on percentage adiposity over the 8 week dietary interventional period.

[***, significance at level P<0.001, two way ANOVA with post-testing by Bonferonni correction, n = 16 and 20 for HRS and LRS groups, respectively.]

Figure 4. Typical transverse abdominal MRI and associated segmented images of mice on HRS and LRS diets.

Figure 5. Representative baseline (pre-contrast) MRI images of the mouse brain showing assignment of regions of interest (ROIs) in various brain areas from which signal intensities (SI) were obtained.

Time course of changes in SI (as a percentage of baseline) before and at various times after IV manganese chloride infusion in the (A) ARC, (B) VMH and the (C) PVN. Data are presented as means of three consecutive image acquisitions±SEM. Significant differences were observed in the VMH, and PVN brain areas (P<0.05) but not in the ARC. Key: ARC, arcuate hypothalamic nucleus; VMH, ventromedial hypothalamic nucleus; PVN, paraventricular hypothalamic nucleus; LRS, low resistant starch diet; HRS, high resistant starch diet.