The underlying mechanisms for the detrimental consequences of a high-fructose diet in animal models are not clear. However, the possibility exists that fructose feeding facilitates oxidative damage. Thus, the aim of the present study was to assess, in weaning rats, the effect of a high-sucrose diet v. starch diet for 2 weeks on oxidative stress variables. Plasma lipid levels were measured and lipid peroxidation was evaluated by urine and plasma thiobarbituric acid-reactive substances (TBARS). The susceptibilities of several tissues to peroxidation were determined in tissue homogenates after in vitro lipid peroxidation. Antioxidant defence variables were evaluated by measuring plasma and heart vitamin E levels, and heart superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. Higher plasma triacylglycerol (P<0.01) and TBARS (P<0.01) levels were found in rats fed the sucrose diet as compared with the starch-fed group, whereas plasma alpha-tocopherol levels were significantly decreased in the sucrose-fed group compared with the starch-fed group (P<0.01). Higher urine TBARS (P<0.01) were found in the sucrose-fed group compared with the starch-fed group, suggesting increased production of these substances from lipid peroxidation in vivo. Higher susceptibility to peroxidation in heart, thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group. No statistical differences were observed for liver TBARS level between the two groups. Heart SOD activity was significantly decreased (P<0.001) in the sucrose-fed group compared with the starch-fed group, whereas heart vitamin E level and GPX activity were not different between the groups. However, the in vitro generation of superoxide radical in heart homogenate, measured by electron spin resonance detection and spin trapping, was not increased in the sucrose-fed group compared with starch-fed rats. Altogether, the results indicate that a short-term consumption of a high-sucrose diet negatively affects the balance of free radical production and antioxidant defence in rats, leading to increased lipid susceptibility to peroxidation.
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http://dx.doi.org/10.1079/BJNBJN2002524 | DOI Listing |
Life Sci
January 2025
Immuno-Endocrinology, Diabetes & Metabolism Laboratory, Instituto de Investigaciones en Medicina Traslacional (IIMT), CONICET - Universidad Austral, Pilar, Argentina; Facultad de Ciencias Biomédicas, , Universidad Austral, Pilar, Argentina. Electronic address:
Aims: Type 2 diabetes (T2D) is a prevalent metabolic disease linked to obesity and metabolic syndrome (MS). The glucolipotoxic environment (GLT) impacts tissues causing low-grade inflammation, insulin resistance and the gradual loss of pancreatic β-cell function, leading to hyperglycemia. We have previously shown that Compound A (CpdA), a plant-derived dissociative glucocorticoid receptor-modulator with inflammation-suppressive activity, displays protective effects on β-cells in type 1 diabetes murine models.
View Article and Find Full Text PDFChem Biol Interact
December 2024
Department of Gastroenterology and Hepatology, Hangzhou Red Cross Hospital, Hangzhou, China, 310003. Electronic address:
Nonalcoholic Steatohepatitis (NASH) is a common liver disease with limited treatment options. Oxymatrine (OMT) has been reported to treat liver diseases effectively. This study aims to explore the mechanisms of OMT in NASH.
View Article and Find Full Text PDFCirc Res
January 2025
Experimental Research Center, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, China (H.J.).
Background: Metabolic syndrome heightens cardiovascular disease risk primarily through increased arterial stiffness. We previously demonstrated the involvement of YAP (Yes-associated protein) in high-fat/high-sucrose diet (HFHSD)-induced arterial stiffness via modulation of PPM1B (protein phosphatase Mg/Mn-dependent 1B)-lysine63 (K63) deubiquitination. In this study, we aimed to elucidate the role and mechanisms underlying PPM1B deubiquitination in HFHSD-induced arterial stiffness.
View Article and Find Full Text PDFLife Sci
December 2024
State Key Laboratory of Animal Biotech Breeding, Institute of Animal Science, Chinese Academy of Agricultural Sciences (CAAS), Beijing 100193, China. Electronic address:
Aims: This study aimed to explore the molecular pathological mechanisms of the liver in metabolic disease-susceptible transgenic pigs via multiomics analysis.
Materials And Methods: The triple-transgenic (PNPLA3-GIPR-hIAPP) pig model (TG pig) was successfully constructed in our laboratory via the CRISPR/Cas9 technique previously described. Wild-type (WT) pigs and TG pigs after 2 or 12Â months of high-fat and high-sucrose diet (HFHSD) induction (WT2, TG2, WT12, and TG12 groups, respectively) were used as materials.
Mol Med
December 2024
Disease Prevention and Health Management Center, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310006, Zhejiang, China.
Background: Nonalcoholic fatty liver disease (NAFLD) has developed as a leading public wellness challenge as a result of changes in dietary patterns. Unfortunately, there is still a lack of effective pharmacotherapy methods for NAFLD. Wang's empirical formula (WSF) has demonstrated considerable clinical efficacy in treating metabolic disorders for years.
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