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1.
Food Funct ; 13(18): 9481-9495, 2022 Sep 22.
Article in English | MEDLINE | ID: mdl-35993118

ABSTRACT

Obesity is a chronic disease that may lead to the development of metabolic diseases, cardiovascular diseases, and cancers and has been predicted to affect one billion adults by 2030. Owing to the pivotal role of the gut microbiota in health, including metabolism and energy homeostasis, dietary fiber, the primary energy resource for the gut microbiota, not only helps reduce appetite and short-term food intake but also modulates the structure of the gut microbiota. In this study, we investigated whether high-amylose maize (HAM), with a particular amount of dietary fiber, improves dysmetabolism and gut microbiota dysbiosis in diet-induced obese mice. Promisingly, the HAM dietary intervention not only reduced body weight gain, adipocyte hypertrophy, and dyslipidemia but also mitigated non-alcoholic fatty liver disease, insulin resistance, impaired glucose tolerance, and inflammation in the liver and epididymal white adipose tissues in high-fat diet (HFD)-fed obese mice. In addition, the HAM dietary intervention ameliorated gut microbiota dysbiosis in HFD-fed mice. Changes in families, genera, and species of gut biota that have a relative abundance of 0.01% in at least one group were scrutinized. At the species level, HAM dietary intervention increased Bifidobacterium pseudolongum, Bifidobacterium animalis, Bifidobacterium bifidum, and Lactobacillus paraplantarum and decreased Streptococcus agalactiae, Mucispirillum schaedleri, and Alistipes indistinctus. This change in the gut microbiota driven by the HAM diet was strongly associated with obesity-related indices, highlighting the nutraceutical potential of HAM for improving overall metabolic health. Taken together, this study demonstrates the potential of the HAM diet for mediating metabolic syndrome and gut microbiota dysbiosis.


Subject(s)
Gastrointestinal Microbiome , Amylose , Animals , Diet, High-Fat/adverse effects , Dietary Fiber , Dysbiosis/microbiology , Mice , Mice, Inbred C57BL , Mice, Obese , Obesity/metabolism , Zea mays
2.
Nutrients ; 13(9)2021 Sep 10.
Article in English | MEDLINE | ID: mdl-34579036

ABSTRACT

Metabolic syndrome and its associated conditions, such as obesity and type 2 diabetes mellitus (T2DM), are a major public health issue in modern societies. Dietary interventions, including microbiota-directed foods which effectively modulate the gut microbiome, may influence the regulation of obesity and associated comorbidities. Although research on probiotics and prebiotics has been conducted extensively in recent years, diets with the use of synbiotics remain relatively unexplored. Here, we investigated the effects of a novel synbiotic intervention, consisting of an adlay seed extrusion cooked (ASEC)-based prebiotic and probiotic (Lactobacillus paracasei and Bacillus coagulans) on metabolic disorders and microbial dysbiosis in high-fat diet (HFD)-induced obese mice. The ASEC-based synbiotic intervention helped improve HFD-induced body weight gain, hyperlipidemia, impaired glucose tolerance, insulin resistance, and inflammation of the adipose and liver tissues. In addition, data from fecal metagenomics indicated that the ASEC-based synbiotic intervention fostered reconstitution of gut bacterial diversity and composition in HFD-induced obese mice. In particular, the ASEC-based synbiotic intervention increased the relative abundance of families Ruminococcaceae and Muribaculaceae and order Bacteroidales and reduced that of families Lactobacillaceae, Erysipelotrichaceae, and Streptococcaceae in HFD-induced obese mice. Collectively, our results suggest that delayed dietary intervention with the novel ASEC-based synbiotic ameliorates HFD-induced obesity, metabolic disorders, and dysbiosis.


Subject(s)
Diet, High-Fat/adverse effects , Dysbiosis/chemically induced , Gastrointestinal Microbiome/drug effects , Prebiotics , Probiotics , Synbiotics , Adipose Tissue , Animal Feed/analysis , Animals , Bacteria/classification , Bacteria/genetics , Body Weight , Dyslipidemias , Insulin Resistance , Male , Mice , Obesity/chemically induced
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