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Dagmar KRATKY - Colloquia in Physiology & Vascular Biology


31. März 2023
12:00 - 13:00

Medical University Vienna, Center for Physiology and Pharmacology,
Institute of Physiology, Schwarzspanierstrasse 17, 1090 Vienna

Großer Hörsaal Physiologie (big lecture hall Physiology)

Lehrstuhl für Molekularbiologie und Biochemie
Neue Stiftingtalstraße 6/IV
8010 Graz
Website Kratky group


”Cytosolic and lysosomal lipid hydrolysis: insights from lipase-deficient mouse models”

Fatty acids (FA) are the most efficient substrates for energy production in vertebrates and are
essential components of the lipids that form biological membranes. Synthesis and storage of
triacylglycerols (TG) from FA represent a highly efficient strategy to stockpile energy-dense
substrate intracellularly and prevent FA-induced lipotoxicity. Enzymatic hydrolysis of TG by a
process called lipolysis is required to release the stored FA. Neutral lipolysis is defined as the
catabolism of TG stored in cellular lipid droplets (LD) by the sequential action of adipose
triglyceride lipase (ATGL), hormone-sensitive lipase, and monoglyceride lipase to release
glycerol and FA. The important role of ATGL in lipolysis became evident from observations in
Atgl-deficient mice, which accumulate TG in essentially all cells and tissues. In contrast to
intracellular neutral lipases that act on cytosolic LD, lysosomal acid lipase (LAL) hydrolyzes
TG and cholesteryl esters (CE) within lysosomes. As such, LAL participates in lipophagy, a
process in which a LD or a part of a LD) is engulfed by a double-membrane autophagosome,
which then fuses with a lysosome to form an autolysosome that degrades neutral lipids.
Mutations in the LAL-encoding LIPA gene are responsible for the development of LAL
deficiency in humans and mice, which is characterized by the accumulation of CE and TG
predominantly in hepatocytes, adrenal glands, the small intestine, and macrophages. The talk
will primarily focus on recent discoveries in cells and tissues of mutant mouse models with
global or cell-specific lipase deficiencies.

Host: Johannes SCHMID

Contact for questions: Helmut KUBISTA