Defective Lipolysis and Altered Energy Metabolism in Mice Lacking Adipose Triglyceride Lipase

By G. Haemmerle, A. Lass, R. Zimmermann, G. Gorkiewicz, C. Meyer, J. Rozman, G. Heldmaier, R. Maier, Christian Theussl, S. Eder and 5 more. Science, 2006

1,353 citations recorded by the source corpus.

Subfields: Biochemistry, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/11bc83a5ef5c6b9557833c8ebbd09ec2440baad2

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Citations in the corpus

Cardiac Metabolism and Its Interactions with Contraction, Growth, and Survival of the Cardiomyocte (2013, background): “lation and severe cardiomyopathy associated with decreased FAO.(63,64) However, cardiac-specific overexpression of adipose”
Lipolysis – A highly regulated multi-enzyme complex mediates the catabolism of cellular fat stores (2011, background): “In contrast to ATGL deficiency, hormone-sensitive lipase (HSL)deficient mice do not show increased fat deposition, are not overweight or obese, and lose WAT mass with increasing age [11,12,19,20].”
Regulation of lipolysis in adipocytes. (2007, neutral): “Global loss of desnutrin/ATGL gene function in mice resulted in increased weight gain and a shift in favor of carbohydrate over fat as a primary fuel source during fasting, indicating that in vivo desnutrin/ATGL likely also functions in adipose tissue lipolysis (43).”
Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, neutral): “Mice lacking ATGL have marked alterations in lipid metabolism with ectopic lipid accumulation in most tissues, manifesting dramatically with massive cardiac lipid accumulation leading to premature death (Haemmerle et al., 2006).”
Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis (2011, background): “The phosphorylation of perilipin A releases CGI-58, allowing it to interact with Pnpla2 to enhance the lipolysis of stored triglyceride”
Cardiac remodeling in obesity. (2008, background): “The mechanism for heart failure in ATGL KO mice remains to be completely characterized, but might be due in part to disruption of contractile units by increased lipid and increased fibrosis (127).”
Non Alcoholic Fatty Liver Disease, Hepatic Insulin Resistance and Type 2 Diabetes (2014, background): “Mice lacking ATGL have marked alterations in lipid metabolism, with ectopic lipid accumulation in most tissues.(88) Liver-specific deletion of ATGL renders mice prone to hepatic steatosis and decreased lipid oxidation.”
A tissue-specific atlas of mouse protein phosphorylation and expression. (2010, neutral): “Intriguingly, though no direct link has been identified between PKA and ATGL, the rate-limiting enzyme for initiation of triglyceride lipolysis (Haemmerle et al., 2006), we identified a putative PKA phosphorylation site on ATGL (Ser406) that could participate in lipolytic regulation.”
ATGL-mediated fat catabolism regulates cardiac mitochondrial function via PPAR-α and PGC-1 (2011, background): “, massive lipid accumulation in multiple tissues, severe skeletal- and cardiomyopathies, and premature deat”
FAT SIGNALS - Lipases and Lipolysis in Lipid Metabolism and Signaling (2012, background): “Recently it was shown that neither source of FA can generate PPAR ligands directly; rather, a cycle of FA esterification and rehydrolysis is required (Haemmerle et al., 2011) (Figure 2).”