Purpose Of Review: The lipolytic catabolism of stored fat in adipose tissue supplies tissues with fatty acids as metabolites and energy substrates during times of food deprivation. This review focuses on the function of recently discovered enzymes in adipose tissue lipolysis and fatty acid mobilization.
Recent Findings: The characterization of hormone-sensitive lipase-deficient mice provided compelling evidence that hormone-sensitive lipase is not uniquely responsible for the hydrolysis of triacylglycerols and diacylglycerols of stored fat. Recently, three different laboratories independently discovered a novel enzyme that also acts in this capacity. We named the enzyme 'adipose triglyceride lipase' in accordance with its predominant expression in adipose tissue, its high substrate specificity for triacylglycerols, and its function in the lipolytic mobilization of fatty acids. Two other research groups showed that adipose triglyceride lipase (named desnutrin and Ca-independent phospholipase A2zeta, respectively) is regulated by the nutritional status and that it might exert acyl-transacylase activity in addition to its activity as triacylglycerol hydrolase. Adipose triglyceride lipase represents a novel type of 'patatin domain-containing' triacylglycerol hydrolase that is more closely related to plant lipases than to other known mammalian metabolic triacylglycerol hydrolases.
Summary: Although the regulation of adipose triglyceride lipase and its physiological function remain to be determined in mouse lines that lack or overexpress the enzyme, present data permit the conclusion that adipose triglyceride lipase is involved in the cellular mobilization of fatty acids, and they require a revision of the concept that hormone-sensitive lipase is the only enzyme involved in the lipolysis of adipose tissue triglycerides.
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http://dx.doi.org/10.1097/01.mol.0000169354.20395.1c | 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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