Increasing evidence suggests that polyphenols have a significant potential in the prevention and treatment of risk factors associated with metabolic syndrome. The objective of this study was to assess the metabolic outcomes of two polyphenol-containing extracts from cinnamon bark (CBE) and grape pomace (GPE) on C57BL/6J mice fed a high-fat diet (HFD) for 8 wk. Both CBE and GPE were able to decrease fat mass gain and adipose tissue inflammation in mice fed a HFD without reducing food intake. This was associated with reduced liver steatosis and lower plasma nonesterified fatty acid levels. We also observed a beneficial effect on glucose homeostasis, as evidenced by an improved glucose tolerance and a lower insulin resistance index. These ameliorations of the overall metabolic profile were associated with a significant impact on the microbial composition, which was more profound for the GPE than for the CBE. At the genus level, Peptococcus were decreased in the CBE group. In the GPE-treated group, several key genera that have been previously found to be linked with HFD, metabolic effects, and gut barrier integrity were affected: we observed a decrease of Desulfovibrio, Lactococcus, whereas Allobaculum and Roseburia were increased. In addition, the expression of several antimicrobial peptides and tight junction proteins was increased in response to both CBE and GPE supplementation, indicating an improvement of the gut barrier function. Collectively, these data suggest that CBE and GPE can ameliorate the overall metabolic profile of mice on a high-fat diet, partly by acting on the gut microbiota.
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http://dx.doi.org/10.1152/ajpendo.00107.2017 | DOI Listing |
Food Funct
January 2025
Department of Nutrition and Food Hygiene, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Gut dysbiosis serves as an underlying risk factor for the development of hypertension. The resolution of this dysbiosis has emerged as a promising strategy in improving hypertension. Food-derived bioactive protein peptides have become increasingly more attractive in ameliorating hypertension, primarily due to their anti-inflammatory and anti-oxidant activities.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Background: The brain is shielded from the peripheral circulation by central nervous system (CNS) barriers, comprising the well-known blood-brain barrier (BBB) and the less recognized blood-cerebrospinal fluid (CSF) barrier located within the brain ventricles. The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host, including the development of neurological disorders like Alzheimer's disease (AD). However, the intricate mechanisms governing the interplay between the gut and brain remain elusive, and the means by which gut-derived signals traverse the CNS barriers remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, San Diego, La Jolla, CA, USA.
Background: Studies using Alzheimer's disease (AD) models suggest that gut bacteria contribute to amyloid pathology and systemic inflammation. Further, gut-derived metabolites serve critical roles in regulating cholesterol, blood-brain barrier permeability, neuroinflammation, and circadian rhythms. Recent studies from the Alzheimer's Disease Neuroimaging Initiative have shown that serum-based gut-derived metabolites are associated with AD biomarkers and cognitive impairment.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Pediatrics, West China Second University Hospital of Sichuan University, Chengdu, China.
Background: Irritable bowel syndrome (IBS) is a common gastrointestinal disease. Recently, an increasing number of studies have shown that Toll-like receptor 4 (TLR4), widely distributed on the surface of a variety of epithelial cells (ECs) and immune sentinel cells in the gut, plays a vital role in developing IBS.
Objectives: We sought to synthesize the existing literature on TLR4 in IBS and inform further study.
Nat Microbiol
January 2025
Institute of Digestive Disease and The Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China.
Hepatocellular carcinoma (HCC) is accompanied by an altered gut microbiota but whether the latter contributes to carcinogenesis is unclear. Here we show that faecal microbiota transplantation (FMT) using stool samples from patients with HCC spontaneously initiate liver inflammation, fibrosis and dysplasia in wild-type mice, and accelerate disease progression in a mouse model of HCC. We find that HCC-FMT results in gut barrier injury and translocation of live bacteria to the liver.
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