Background And Aims: A single high-fat meal may induce endothelial activation and dysfunction in both normal subjects and in patients with type 2 diabetes. The aim of this study was to assess the effect of a high-fat meal on endothelial function in patients with the metabolic syndrome.
Methods And Results: Twenty-five patients with the metabolic syndrome (ATP III criteria) were matched for sex, age and body mass index with 25 subjects without the metabolic syndrome. All subjects ate under supervision a high fat meal (760 calories) with 59% energy from fat, 12% energy from protein and 29% energy from carbohydrates. Compared with the control group, subjects with the metabolic syndrome had reduced endothelial function, as assessed with the l-arginine test, and higher circulating levels of TNF-alpha. Following the high-fat meal, both triglyceride and TNF-alpha levels increased more in subjects with the metabolic syndrome than in subjects without, while endothelial function decreased more in subjects with the metabolic syndrome. There was a significant relation between increases in TNF-alpha levels and decreases in endothelial function score in subjects with the metabolic syndrome (r=-0.39, P=0.03).
Conclusion: TNF-alpha levels are increased in subjects with the metabolic syndrome; moreover, a high-fat meal produces further increase in its levels associated with endothelial dysfunction.
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http://dx.doi.org/10.1016/j.numecd.2005.11.014 | DOI Listing |
PLoS One
January 2025
Specialist in Family and Community Medicine, Milladoiro Health Centre, Health Area of Santiago de Compostela, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Purpose: To determine the relationship between self-reported physical activity and the components of premorbid metabolic syndrome in patients treated in primary care according to sex.
Methods: Cross-sectional descriptive study conducted on a sample of 2,359 patients without cardiovascular disease or diabetes, included in the cohort of the IBERICAN study. Using ANOVA models and adjusting for age, economic status, employment situation, level of education, adherence to a Mediterranean diet, tobacco use and alcohol consumption, we estimated the association of the variables blood pressure, triglycerides, HDL cholesterol, blood glucose and waist circumference with the self-reported level of physical activity (sedentary, moderate, high, very high).
Diabetes
January 2025
Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
PPARγ is the pharmacological target of thiazolidinediones (TZDs), potent insulin sensitizers that prevent metabolic disease morbidity but are accompanied by side effects such as weight gain, in part due to non-physiological transcriptional agonism. Using high throughput genome engineering, we targeted nonsense mutations to every exon of PPARG, finding an ATG in Exon 2 (chr3:12381414, CCDS2609 c.A403) that functions as an alternative translational start site.
View Article and Find Full Text PDFBJU Int
January 2025
Department of Urology, Mayo Clinic Arizona, Phoenix, AZ, USA.
Objectives: To compare postoperative complication rates of patients with metabolic syndrome (MetS) with patients without MetS after holmium laser enucleation of the prostate (HoLEP) for management of benign prostatic hyperplasia (BPH).
Patients And Methods: We retrospectively reviewed patients aged >40 years who underwent HoLEP at our institution from 2007 to 2022. Criteria for MetS were diagnoses of at least three of the following: diabetes mellitus, hypertension, hyperlipidaemia, or obesity (body mass index ≥30 kg/m).
Rev Med Chil
September 2024
Hospital de Niños Dr. Roberto del Río, Santiago, Chile.
Hereditary tyrosinemia type 1 (HT-1) is an inborn error of metabolism caused by a defect in tyrosine (tyr) degradation. This defect results in the accumulation of succinylacetone (SA), causing liver failure with a high risk of hepatocarcinoma and kidney injury, leading in turn to Fanconi syndrome with urine loss of phosphate and secondary hypophosphatemic rickets (HR). HT-1 diagnosis is usually made in infants with acute or chronic liver failure or by neonatal screening programs.
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