The expansion of adipose tissue is regulated by insulin and leptin through sterol regulatory element-binding protein-1c (SREBP-1c), up-regulating lipogenesis in tissues by Stearoylcoenzyme A desaturase 1 (SCD1) enzyme, while adipose triglyceride lipase (ATGL) enzyme is key in lipolysis. The research objective was to evaluate the expression of Sterol Regulatory Element Binding Transcription Factor 1 (SREBF1), SCD1, Patatin Like Phospholipase Domain Containing 2 (PNPLA2), and leptin (LEP) genes in hepatic-adipose tissue, and related them with the increment and distribution of fat depots of individuals without insulin resistance. Thirty-eight subjects undergoing elective cholecystectomy with liver and adipose tissue biopsies (subcutaneous-omental) are included. Tissue gene expression was assessed by qPCR and biochemical parameters determined. Individuals are classified according to the body mass index, classified as lean (control group, n=12), overweight (n=11) and obesity (n=15). Abdominal adiposity was determined by anthropometric and histopathological study of the liver. Increased expression in omental adipose tissue (p=0.005) and in liver (p=0.01) were found in the obesity group. decreased expression in subcutaneous adipose tissue was significant in individuals with abdominal adiposity (p=0.017). Anthropometric parameters positively correlated with liver and the expression of liver with serum leptin. increased levels may represent lipid storage activity in omental adipose tissue. Liver increased expression could function as a primary compensatory event of visceral fat deposits associated to the leptin hormone related to the increase of adipose tissue.
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http://dx.doi.org/10.1055/a-0829-6324 | DOI Listing |
Cancer Med
January 2025
The Huntsman Cancer Institute at the University of Utah, Salt Lake City, Utah, USA.
Introduction: The purpose of this study was to evaluate the association between body composition, overall survival, odds of receiving treatment, and patient-reported outcomes (PROs) in individuals living with metastatic non-small-cell lung cancer (mNSCLC).
Methods: This retrospective analysis was conducted in newly diagnosed patients with mNSCLC who had computed-tomography (CT) scans and completed PRO questionnaires close to metastatic diagnosis date. Cox proportional hazard models and logistic regression evaluated overall survival and odds of receiving treatment, respectively.
Eur Heart J Cardiovasc Imaging
January 2025
Sorbonne Université, unité d'imagerie cardiovasculaire et thoracique, Hôpital La Pitié Salpêtrière (AP-HP), Laboratoire d'Imagerie Biomédicale, INSERM, CNRS, Institute of Cardiometabolism and Nutrition, ACTION Group, Paris, France.
Purpose: Epicardial adipose tissue (EAT) could contribute to the specific atherosclerosis profile observed in premature coronary artery disease (pCAD) characterized by accelerated plaque burden (calcified and non-calcified), high risk plaque features (HRP) and ischemic recurrence. Our aims were to describe EAT volume and density in pCAD compared to asymptomatic individuals matched on CV risk factors and to study their relationship with coronary plaque severity extension and vulnerability.
Materials And Methods: 208 patients who underwent coronary computed tomography angiography (CCTA) were analyzed.
Sarcopenia is defined as a muscle-wasting syndrome that occurs with accelerated aging, while cachexia is a severe wasting syndrome associated with conditions such as cancer and immunodeficiency disorders, which cannot be fully addressed through conventional nutritional supplementation. Sarcopenia can be considered a component of cachexia, with the bidirectional interplay between adipose tissue and skeletal muscle potentially serving as a molecular mechanism for both conditions. However, the underlying mechanisms differ.
View Article and Find Full Text PDFBackground: The activation of brown adipose tissue (BAT) is associated with improved metabolic health in humans. We previously identified the mitochondrial protein 4-Nitrophenylphosphatase Domain and Non-Neuronal SNAP25-Like 1 (Nipsnap1) as a novel regulatory factor that integrates with lipid metabolism and is critical to sustain the long-term activation of BAT, but the precise mechanism and function of Nipsnap1 is unknown.
Objectives: Define how the regulatory factor Nipsnap1 integrates with lipid metabolism.
Background: Type 2 Diabetes Mellitus (T2DM) is a significant public health burden. Emerging evidence links volatile organic compounds (VOCs), such as benzene to endocrine disruption and metabolic dysfunction. However, the effects of chronic environmentally relevant VOC exposures on metabolic health are still emerging.
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