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Background: Obesity occurs when energy intake is excessive compared to energy expenditure, resulting in the excessive storage of triglyceride in adipose tissue.
Objective: The present study aimed to investigate the antiobesity effects of extracts (PF) in high-fat diet (HFD)-induced obese mice and 3T3-L1 adipocytes to demonstrate the lipid mechanisms underlying these effects.
Design: Mice were fed with a normal diet (AIN93G normal diet), HFD (60% HFD), Met (HFD containing metformin 250 mg/kg b.w.), PF50 (HFD containing PF 50 mg/kg b.w.), and PF100 (HFD containing PF 100 mg/kg b.w.) for 12 weeks.
Results: Body weight gain, adipose tissue weight, adipose tissue mass, and size of adipocytes were significantly decreased by PF supplementation in HFD-fed mice. Moreover, PF supplementation suppressed the adipogenesis and lipogenesis pathways and activated the lipolysis and thermogenesis pathways in the adipose tissues of HFD-fed mice.
Conclusions: PF treatment during the differentiation of 3T3-L1 cells suppressed adipogenesis and lipogenesis and PF treatment after differentiation activated lipolysis and thermogenesis. Thus, we suggest that PF is effective for weight loss by directly affecting the lipid metabolism of adipocytes.
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http://dx.doi.org/10.29219/fnr.v67.9374 | DOI Listing |
J Endocrinol Invest
September 2025
Key Laboratory of Immune Microenvironment and Inflammatory Disease Research in Universities of Shandong Province, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, China.
Purposes: Controversy has emerged regarding the impact of non-nutritive sweeteners (NNS) on body weight. This systematic review and meta-analysis of randomized controlled trials aims to assess the effect of NNS intake on body weight change.
Results: Of the 3327 studies retrieved, 19 met the eligibility criteria for inclusion in the meta-analysis.
Am J Pathol
September 2025
Department of Hepatology, Center of Infectious Diseases and Pathogen Biology, the First Hospital of Jilin University, Changchun, China; Jilin Provincial Key Laboratory of Metabolic Liver Diseases, Jilin University, Changchun, China; China-Singapore Belt and Road Joint Laboratory on Liver Disease Res
Aldehyde dehydrogenase 2 (ALDH2) is a critical enzyme involved in the detoxification of acetaldehyde. Although numerous studies have demonstrated the significance of ALDH2 in alcohol-associated liver disease (ALD), its role in alcohol-induced activation of liver progenitor cells (LPCs) has not been thoroughly investigated. Proteomic analysis of serum samples from patients with either normal ALDH2 genotype or ALDH2 mutation following alcohol consumption revealed that ALDH2 deficiency may suppress LPC proliferation.
View Article and Find Full Text PDFPoult Sci
August 2025
Jiangxi Provincial Key Laboratory of Poultry Genetic Improvement, Institute of Biological Technology, Nanchang Normal University, Nanchang, 330032, China. Electronic address:
Excessive abdominal fat deposition (AFD) in poultry reduces meat yield and efficiency. The gut microbiota regulates AFD through shifts in microbial composition and the production of metabolites. Reduced microbial diversity and fat-promoting taxa (e.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Food Science, Ishikawa Prefectural University, Nonoichi, Ishikawa, Japan.
Epidemiological studies in humans have suggested that tomato consumption and the compositional ratios of Prevotella, Megamonas, and Streptococcus in the intestinal microbiota are related to intestinal permeability. In this study, we investigated the causal relationship using Caenorhabditis (C.) elegans.
View Article and Find Full Text PDFFront Neurol
August 2025
Department of Pediatric Neuroscience, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
Background: Pediatric Huntington's disease (PHD), a rare and severe form of juvenile-onset Huntington's disease (JOHD), is associated with highly expanded CAG repeats in the gene and a rapidly progressive neurodegenerative course. Recent studies have suggested that glucose metabolism may be impaired in PHD due to reduced expression of glucose transporters in the brain, resembling aspects of GLUT1 Deficiency Syndrome (GLUT1DS).
Methods: We investigated glucose metabolism in two pediatric patients with genetically confirmed PHD (CAG repeats: 76 and 79) referred to our tertiary care center.