Background: It is not clear whether dietary grape seed proanthocyanidin (GSP) affects mammalian lipid metabolism via the gut microbiota.
Objective: The aim of this study was to evaluate the contribution of the gut microbiota to the effect of dietary GSP.
Methods: This study was divided into 3 separate experiments using Duroc × Landrace × Yorkshire pigs (50% male) weaned at day 28 and then fed the same basal diet (NC). In Experiment 1, 90 pigs were fed NC or NC with 250 mg GSP/kg (GSP) or 400 mg betaine/kg [positive control (PC)] for 28 d. In Experiment 2, 30 pigs were fed NC, GSP, or GSP with antibiotics (GSP + Abx) diets for 14 d. In Experiment 3, pigs were fed NC, NC plus 1 g sodium propionate/kg (SP), or NC plus 1 g sodium butyrate/kg (SB) diet for 14 d. Serum biochemical indexes, SCFA concentrations, and microbial composition were determined.
Results: In Experiment 1, compared with the GSP group, visceral adipocyte area was higher in the NC (28.6%) and PC (18.2%) groups (P ≤ 0.05). Colonic propionate and butyrate concentrations were 30.2% and 3.6% higher in the GSP group than in the NC group, respectively (P ≤ 0.05). In Experiment 2, compared with the GSP group, the NC group had a 108% higher Firmicutes to Bacteroidetes ratio and had 50.4%, 61.2%, and 82.3% lower abundance of Akkermansia, Alistipes, and Bacteroides, respectively (P ≤ 0.05); antibiotics removed these effects of GSP. In Experiment 3, serum peptide YY was 19.5% higher in the SP group than in the NC group (P ≤ 0.05), and it did not differ between the SB and NC groups (P > 0.05).
Conclusions: GSP affected lipid metabolism in weaned pigs, which is associated with changed gut microbiota and enhanced microbial propionate production. These findings provide potential mechanisms for GSP intake to improve lipid metabolism.
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http://dx.doi.org/10.1093/jn/nxz102 | DOI Listing |
Hepatol Int
January 2025
Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
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Commun Biol
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Division of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Changes in brain mitochondrial metabolism are coincident with functional decline; however, direct links between the two have not been established. Here, we show that mitochondrial targeting via the adiponectin receptor activator AdipoRon (AR) clears neurofibrillary tangles (NFTs) and rescues neuronal tauopathy-associated defects. AR reduced levels of phospho-tau and lowered NFT burden by a mechanism involving the energy-sensing kinase AMPK and the growth-sensing kinase GSK3b.
View Article and Find Full Text PDFActa Neuropathol Commun
January 2025
Department of Biological Sciences, Purdue University, 915 Mitch Daniels Blvd, West Lafayette, IN, USA.
Dementia refers to an umbrella phenotype of many different underlying pathologies with Alzheimer's disease (AD) being the most common type. Neuropathological examination remains the gold standard for accurate AD diagnosis, however, most that we know about AD genetics is based on Genome-Wide Association Studies (GWAS) of clinically defined AD. Such studies have identified multiple AD susceptibility variants with a significant portion of the heritability unexplained and highlighting the phenotypic and genetic heterogeneity of the clinically defined entity.
View Article and Find Full Text PDFBackground: The association between serum uric acid (SUA) and dyslipidaemia is still unclear in patients with type 2 diabetes mellitus (T2DM). This study aimed to examine the association between SUA and dyslipidaemia and to explore whether there is an optimal SUA level corresponding to the lower risk of suffering from dyslipidaemia.
Research Design And Methods: This cross-sectional study included 1036 inpatients with T2DM and the clinical data were extracted from the hospital medical records.
Cancer Lett
January 2025
Clinical and Health Sciences, University of South Australia, Adelaide, Australia; Department of Histopathology, Trinity College Dublin, St. James's Hospital, Dublin, Ireland. Electronic address:
Metabolic reprogramming is a hallmark of cancer, crucial for malignant transformation and metastasis. Chronic lymphocytic leukaemia (CLL) and prostate cancer exhibit similar metabolic adaptations, particularly in glucose and lipid metabolism. Understanding this metabolic plasticity is crucial for identifying mechanisms contributing to metastasis.
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