Adipose triglyceride lipase (ATGL), highly expressed in adipose tissue, is associated with lipid droplets inside cells. The function of ATGL is to specifically hydrolyze triacylglycerol (TG) into free fatty acids. ATGL is the second TG lipase next to the hormone sensitive lipase (HSL) in adipose tissue for hydrolysis of TG. In a recent issue of Science, the phenotype of ATGL knockout mice was published. The knockout leads to an increase in adipose mass and triacylglycerol deposition in multiple tissues including heart, causing cardiac dysfunction and premature death. The mice had increased glucose utilization, increased glucose tolerance, and increased insulin sensitivity. Like CD36 KO mice, this is another example that less utilization of FFA may lead to insulin sensitization. Attached is the PDF file of the paper.

PTP1B is a tyrosine phosphatase that was shown to inhibit signaling activities of leptin and insulin receptors. Mice with global inactivation of PTP1B exhibit higher sensitivity to leptin and do not develop diet-induced obesity. However, the organ/tissue responsible for the metabolic phenotype of TP1B inactivation is not known. In Nature Medicine online publications, a new study using tissue-specific KO mice of PTP1B demonstrates that the brain is the organ. See attached PDF file.

ATGL paper in Science

 PTP1B paper in Nature Medicine


By Jianping at PBRC
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ATGL is Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu