Abstract
BackgroundAdipose 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 FindingsForty mice were randomised to a diet supplemented with either the high resistant starch (HRS), or the readily digestible starch (LRS). Using 1H 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 SignificanceDietary 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.
Highlights
The link between obesity, adipose distribution, premature mortality and morbidity is one of the most enduring observations in the field of nutrition [1]
The increase in total weight of food consumed by individual mice in the HRS group did not fully compensate for the more energy dilute feed, this includes estimation of the energy recovery from the high resistant starch feed through fermentation
Maintenance for 8 weeks on either the LRS or HRS diets lead to similar weight gain but differences in whole body adiposity
Summary
The link between obesity, adipose distribution, premature mortality and morbidity is one of the most enduring observations in the field of nutrition [1]. This is suggestive of a change in adipocyte metabolism that may lead to a change in insulin sensitivity Fermentable carbohydrate such as RS and inulin has been demonstrated to increase the release of gut hormones with roles in appetite regulation and possibly, leptin release [9,11]. 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. Mice on the HRS and LRS diet had similar body weights total body adiposity, subcutaneous and visceral fat, IHCL, plasma leptin, plasma adiponectin plasma insulin/glucose ratios was significantly greater in the latter group. 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
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