Renate Schreiber (0000-0002-3475-157X)

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Our research focuses on neutral lipid metabolism. In particular, we are interested in how intracellular neutral lipid degrading enzymes (lipases) affect adipocyte health and mitochondrial function, and thus metabolic health. To address our hypotheses, we use biochemical methods, high-resolution respirometry, mammalian cells, and mouse models combined with state-of-the-art in vivo physiological phenotyping.

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University of Graz: Graz, AT

2024 to present | Senior Scientist and group leader (Institute of Molecular Biosciences)

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Renate Schreiber

https://orcid.org/0000-0002-3475-157X

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Biography

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Employment (6)

University of Graz: Graz, AT

University of Graz: Graz, AT

University of Graz: Graz, AT

University of Graz: Graz, AT

University College London: London, London, GB

University of Umea: Umea, SE

Education and qualifications (4)

Czech Academy of Sciences, Institute of Physiology: Prague, CZ

University of Graz: Graz, AT

University of Cambridge: Cambridge, Cambridgeshire, GB

University of Graz: Graz, AT

Professional activities (7)

BioHealth - Field of Excellence, University of Graz: Graz, AT

BioTechMed-Graz: Graz, AT

European Lipoprotein Club: Tutzing, DE

Journal of Lipid Research: Rockville, US

Austrian Atherosclerosis Society: Vienna, AT

Journal of Lipid Research: Rockville, US

Austrian Atherosclerosis Society: Vienna, AT

Funding (4)

Metabolic control of aging and disease

BioHealth Accelerator

Integrating exercise and NAD+ to reduce cardiometabolic risk

Lipid Hydrolysis: Cellular lipid degradation pathways in health and disease

Works (41)

The Potential Roles of Transacylation in Intracellular Lipolysis and Related Qssa Approximations

The lysosomal LAMTOR / Ragulator complex is essential for nutrient homeostasis in brown adipose tissue

p53 Regulates a miRNA-Fructose Transporter Axis in Brown Adipose Tissue Under Fasting

Optimized expression and purification of adipose triglyceride lipase improved hydrolytic and transacylation activities in vitro.

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis.

Advanced lipodystrophy reverses fatty liver in mice lacking adipocyte hormone-sensitive lipase.

Nicotinamide for the treatment of heart failure with preserved ejection fraction.

Distinct roles of adipose triglyceride lipase and hormone-sensitive lipase in the catabolism of triacylglycerol estolides.

Metabolic regulation of the lysosomal cofactor bis(monoacylglycero)phosphate in mice

Regulation of thermogenic adipocytes during fasting and cold

The Lipolysome—A Highly Complex and Dynamic Protein Network Orchestrating Cytoplasmic Triacylglycerol Degradation

Lipokine 5-PAHSA Is Regulated by Adipose Triglyceride Lipase and Primes Adipocytes for De Novo Lipogenesis in Mice

Of mice and men: The physiological role of adipose triglyceride lipase (ATGL)

N-acetylaspartate availability is essential for juvenile survival on fat-free diet and determines metabolic health

Hepatocyte-specific deletion of lysosomal acid lipase leads to cholesteryl ester but not triglyceride or retinyl ester accumulation

Low cardiac lipolysis reduces mitochondrial fission and prevents lipotoxic heart dysfunction in Perilipin 5 mutant mice

Lipolysis Triggers a Systemic Insulin Response Essential for Efficient Energy Replenishment of Activated Brown Adipose Tissue in Mice

Loss of ABHD15 Impairs the Anti-lipolytic Action of Insulin by Altering PDE3B Stability and Contributes to Insulin Resistance

Cold-Induced Thermogenesis Depends on ATGL-Mediated Lipolysis in Cardiac Muscle, but Not Brown Adipose Tissue.

Global Analysis of Plasma Lipids Identifies Liver-Derived Acylcarnitines as a Fuel Source for Brown Fat Thermogenesis.

Pharmacological inhibition of adipose triglyceride lipase corrects high-fat diet-induced insulin resistance and hepatosteatosis in mice.

Effects of two therapeutic dietary regimens on primary chylomicronemia in paediatric age: a retrospective data analysis

Hypophagia and metabolic adaptations in mice with defective ATGL-mediated lipolysis cause resistance to HFD-induced obesity.

G0/G1 Switch Gene 2 Regulates Cardiac Lipolysis.

Fasting-induced G0/G1 switch gene 2 and FGF21 expression in the liver are under regulation of adipose tissue derived fatty acids.

Adipose triglyceride lipase is involved in the mobilization of triglyceride and retinoid stores of hepatic stellate cells.

Lipolysis meets inflammation: arachidonic acid mobilization from fat.

Fibroblast growth factor 21 is induced upon cardiac stress and alters cardiac lipid homeostasis.

A switch from white to brown fat increases energy expenditure in cancer-associated cachexia.

Skeletal muscle triacylglycerol hydrolysis does not influence metabolic complications of obesity.

Cardiac-specific overexpression of perilipin 5 provokes severe cardiac steatosis via the formation of a lipolytic barrier.

Cholesteryl ester accumulation and accelerated cholesterol absorption in intestine-specific hormone sensitive lipase-null mice.

Retinyl ester hydrolases and their roles in vitamin A homeostasis.

ATGL-mediated fat catabolism regulates cardiac mitochondrial function via PPAR-α and PGC-1.

Monoglyceride lipase deficiency in mice impairs lipolysis and attenuates diet-induced insulin resistance.

Cholesteryl ester hydrolase activity is abolished in HSL-/- macrophages but unchanged in macrophages lacking KIAA1363.

Adipose triglyceride lipase plays a key role in the supply of the working muscle with fatty acids.

Esterase 22 and beta-glucuronidase hydrolyze retinoids in mouse liver.

Adipose triglyceride lipase and hormone-sensitive lipase are the major enzymes in adipose tissue triacylglycerol catabolism.

Enhanced bridging function and augmented monocyte adhesion by lipoprotein lipase N9: insights into increased risk of coronary artery disease in N9 carriers.

Immunohistochemical evidence for the myeloperoxidase/H2O2/halide system in human atherosclerotic lesions: colocalization of myeloperoxidase and hypochlorite-modified proteins.

Peer review (3 reviews for 3 publications/grants)