Abstract
(1) High-fat (HF) diet leads to gut microbiota dysbiosis which is associated with systemic inflammation. Bacterial-driven inflammation is sufficient to alter vagally mediated satiety and induce hyperphagia. Promoting bacterial fermentation improves gastrointestinal (GI) epithelial barrier function and reduces inflammation. Resistant starch escape digestion and can be fermented by bacteria in the distal gut. Therefore, we hypothesized that potato RS supplementation in HF-fed rats would lead to compositional changes in microbiota composition associated with improved inflammatory status and vagal signaling. (2) Male Wistar rats (n = 8/group) were fed a low-fat chow (LF, 13% fat), HF (45% fat), or an isocaloric HF supplemented with 12% potato RS (HFRS) diet. (3) The HFRS-fed rats consumed significantly less energy than HF animals throughout the experiment. Systemic inflammation and glucose homeostasis were improved in the HFRS compared to HF rats. Cholecystokinin-induced satiety was abolished in HF-fed rats and restored in HFRS rats. HF feeding led to a significant decrease in positive c fiber staining in the brainstem which was averted by RS supplementation. (4) The RS supplementation prevented dysbiosis and systemic inflammation. Additionally, microbiota manipulation via dietary potato RS prevented HF-diet-induced reorganization of vagal afferent fibers, loss in CCK-induced satiety, and hyperphagia.
Highlights
IntroductionObesity has been characterized as a low-grade inflammatory state, and inflammation plays a critical role in both the exacerbation of obesity and the development of co-morbidities such as diabetes [2]
Prevalence of obesity has soared to 93.3 million people in the United States [1]
Obesity has been characterized as a low-grade inflammatory state, and inflammation plays a critical role in both the exacerbation of obesity and the development of co-morbidities such as diabetes [2]
Summary
Obesity has been characterized as a low-grade inflammatory state, and inflammation plays a critical role in both the exacerbation of obesity and the development of co-morbidities such as diabetes [2]. There is accumulating evidence that the chronic low-grade inflammation characteristic of obesity is at least partially controlled by the gut microbiota [3]. Microbiota composition changes with diet and is especially responsive to/can be modulated by dietary fats [5,6], sugars [7], and fibers [5,8]. Dysbiosis, has been associated with increased adiposity in both humans [9,10] and animal models [7,11]
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