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Bin Geng - One of the best experts on this subject based on the ideXlab platform.
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sulfhydration of Perilipin 1 is involved in the inhibitory effects of cystathionine gamma lyase hydrogen sulfide on adipocyte lipolysis
Biochemical and Biophysical Research Communications, 2020Co-Authors: Yajun Ding, Huamin Wang, Bin GengAbstract:Hydrogen sulfide (H2S) is a novel adipokine mediating glucose uptake, lipid storage and mobilization, thus contributing to the genesis of obesity and associated diseases. Our previous work demonstrated that H2S inhibited isoproterenol-stimulated lipolysis by reducing the phosphorylation of Perilipin 1 (plin-1), a lipid-droplet protein blocking lipase access. How H2S modulates plin-1 phosphorylation is still unclear. Our present study found that an H2S donor slightly increased adipose tissue weight and reduced lipolysis in mice; by contrast, deleting the key H2S generation enzyme cystathionine gamma lyase (CSE) in adipocytes lowered adipose accumulation and enhanced lipolysis. Intriguingly, an H2S donor induced sulfhydration of plin-1 but not hormone-sensitive lipase, and CSE deletion abolished the post-translational modification of plin-1. During isoproterenol-stimulated lipolysis, plin-1 sulfhydration was associated with reduced phosphorylation, and removing sulfhydration by dithiothreitol recovered the phosphorylation. Finally, plin-1 knockout abolished the effect of H2S on lipolysis, which indicates that plin-1 sulfhydration is a major direct target of H2S in lipolysis. We have identified a new post-translation modification, sulfhydration (direct action by H2S) of plin-1, causing reduced phosphorylation then decreased lipolysis. This finding also highlights a novel molecular regulatory mechanism of lipolysis.
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Sulfhydration of Perilipin 1 is involved in the inhibitory effects of cystathionine gamma lyase/hydrogen sulfide on adipocyte lipolysis.
Biochemical and biophysical research communications, 2019Co-Authors: Yajun Ding, Huamin Wang, Bin GengAbstract:Hydrogen sulfide (H2S) is a novel adipokine mediating glucose uptake, lipid storage and mobilization, thus contributing to the genesis of obesity and associated diseases. Our previous work demonstrated that H2S inhibited isoproterenol-stimulated lipolysis by reducing the phosphorylation of Perilipin 1 (plin-1), a lipid-droplet protein blocking lipase access. How H2S modulates plin-1 phosphorylation is still unclear. Our present study found that an H2S donor slightly increased adipose tissue weight and reduced lipolysis in mice; by contrast, deleting the key H2S generation enzyme cystathionine gamma lyase (CSE) in adipocytes lowered adipose accumulation and enhanced lipolysis. Intriguingly, an H2S donor induced sulfhydration of plin-1 but not hormone-sensitive lipase, and CSE deletion abolished the post-translational modification of plin-1. During isoproterenol-stimulated lipolysis, plin-1 sulfhydration was associated with reduced phosphorylation, and removing sulfhydration by dithiothreitol recovered the phosphorylation. Finally, plin-1 knockout abolished the effect of H2S on lipolysis, which indicates that plin-1 sulfhydration is a major direct target of H2S in lipolysis. We have identified a new post-translation modification, sulfhydration (direct action by H2S) of plin-1, causing reduced phosphorylation then decreased lipolysis. This finding also highlights a novel molecular regulatory mechanism of lipolysis.
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Spontaneous development of hepatosteatosis in Perilipin-1 null mice with adipose tissue dysfunction.
Biochimica et biophysica acta. Molecular and cell biology of lipids, 2017Co-Authors: Suning Wei, Shangxin Liu, Weiyi Wang, Jingna Deng, Ying Lyu, Bin GengAbstract:Fatty liver features triglyceride accumulation in hepatocytes and often occurs with obesity and lipodystrophy in humans. Here, we investigated the mechanism of maladaptive hepatosteatosis with adipose-tissue dysfunction. Perilipin 1 (Plin1) did not exist in hepatocytes but was expressed exclusively in adipocytes as a dual modulator for regulating two principal adipose-tissue functions, triglyceride storage and breakdown. Plin1-/- mice showed decreased fat storage but increased lipolysis and efflux of fatty acids from adipose tissue, and hepatosteatosis spontaneously developed without altered circulating inflammatory adipocytokine levels. Plin1-/- adipose dysfunction impaired insulin sensitivity and hepatic glucose metabolism, which might inhibit gluconeogenesis to produce more intermediates for hepatic lipid synthesis. Indeed, the livers of Plin1-/- mice exhibited upregulated mRNA and protein expression of key enzymes and transcriptional factors for the uptake and transport of fatty acids and for de novo synthesis of triglycerides, but the expression of key enzymes and transcriptional factors for fatty-acid oxidation was downregulated. Biochemical assays in Plin1-/- mice confirmed increased fatty acid synthase activity but decreased activity of mitochondrial carnitine palmitoyltransferase 1 and [3H]-palmitate oxidation in the liver. We concluded that dysregulation of two principal functions, adipose storage and hydrolysis, had deleterious consequences on the hepatic lipid metabolism and thereby caused maladaptive hepatosteatosis. This mouse model might mimic and explain the pathogenesis of hepatosteatosis occurring in two typical disorders of adipose tissue dysfunction, obesity and lipodystrophy, particularly in lipodystrophic patients with Plin1 mutation.
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Spontaneous hypertension occurs with adipose tissue dysfunction in Perilipin-1 null mice.
Biochimica et biophysica acta, 2015Co-Authors: Liangqiang Zou, Shangxin Liu, Weiyi Wang, Xiaojing Zhao, Ying Lyv, Bin GengAbstract:Perilipin-1 (Plin1) coats lipid droplets exclusively in adipocytes and regulates two principle functions of adipose tissue, triglyceride storage and hydrolysis, which are disrupted upon Plin1 deficiency. In the present study, we investigated the alterations in systemic metabolites and hormones, vascular function and adipose function in spontaneous hypertensive mice lacking Perilipin-1 (Plin1-/-). Plin1-/- mice developed spontaneous hypertension without obvious alterations in systemic metabolites and hormones. Plin1 expressed only in adipose cells but not in vascular cells, so its ablation would have no direct effect in situ on blood vessels. Instead, Plin1-/- mice showed dysfunctions of perivascular adipose tissue (PVAT), a fat depot that anatomically surrounds systemic arteries and has an anticontractile effect. In Plin1-/- mice, aortic and mesenteric PVAT were reduced in mass and adipocyte derived relaxing factor secretion, but increased in basal lipolysis, angiotensin II secretion, macrophage infiltration and oxidative stress. Such multiple culprits impaired the anticontractile effect of PVAT to promote vasoconstriction of aortic and mesenteric arteries of Plin1-/- mice. Furthermore, arterial vessels of Plin1-/- mice showed increasing angiotensin II receptor type 1, monocyte chemotactic protein-1 and interlukin-6 expression, structural damage of endothelial and smooth muscle cells, along with impaired endothelium-dependent relaxation. Hypertension in Plin1-/- mice might occur as a deleterious consequence of PVAT dysfunction. This finding provides the direct evidence that links dysfunctional PVAT to vascular dysfunction and hypertension, particularly in pathophysiological states. This hypertensive mouse model might mimic and explain the hypertension occurring in patients with adipose tissue dysfunction, particularly with Plin1 mutations.
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Perilipin1 deficiency in whole body or bone marrow-derived cells attenuates lesions in atherosclerosis-prone mice.
PloS one, 2015Co-Authors: Xiaojing Zhao, Bin Geng, Liangqiang Zou, Ying Lyu, Mingming Gao, Ling Zhang, George LiuAbstract:Aims The objective of this study is to determine the role of Perilipin 1 (Plin1) in whole body or bone marrow-derived cells on atherogenesis.
Rami N Alrohil - One of the best experts on this subject based on the ideXlab platform.
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the utility of Perilipin in liposarcomas plin1 differentiates round cell liposarcoma from other round cell sarcomas
Applied Immunohistochemistry & Molecular Morphology, 2020Co-Authors: Margaret L Compton, Rami N AlrohilAbstract:Liposarcoma is the most common soft tissue sarcoma in adults; however, accurate diagnosis often depends on the use of ancillary molecular testing which can be time consuming and expensive. Myxoid/round cell liposarcoma may be a diagnostic challenge due to the morphologic similarities with other nonadipocytic sarcomas with round cell morphology. Immunohistochemistry may be a helpful adjunct to appropriately triage cases for molecular testing. Perilipin 1 (PLIN1) and Perilipin 2 (adipophilin) (PLIN2) are intracellular proteins involved in lipid droplet formation, which we hypothesized may be useful as immunohistochemical markers for liposarcoma. Using archival tumor tissue, we assessed pattern of PLIN1 and PLIN2 expression in 46 adipocytic tumors and 36 nonadipocytic sarcomas. PLIN1 was expressed in 88% of liposarcomas, including 100% of myxoid/round cell liposarcomas, and did not have any expression in nonadipocytic sarcomas. PLIN1 was not expressed in dedifferentiated liposarcoma. Although PLIN2 demonstrates increased sensitivity for liposarcoma, including expression in dedifferentiated liposarcoma, it is not specific for adipocytic differentiation and is expressed in other nonadipocytic sarcomas. Furthermore, PLIN2 is not expressed in lipoma-like well-differentiated liposarcoma, and as such has limited diagnostic utility.
Ying Lyu - One of the best experts on this subject based on the ideXlab platform.
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Spontaneous development of hepatosteatosis in Perilipin-1 null mice with adipose tissue dysfunction.
Biochimica et biophysica acta. Molecular and cell biology of lipids, 2017Co-Authors: Suning Wei, Shangxin Liu, Weiyi Wang, Jingna Deng, Ying Lyu, Bin GengAbstract:Fatty liver features triglyceride accumulation in hepatocytes and often occurs with obesity and lipodystrophy in humans. Here, we investigated the mechanism of maladaptive hepatosteatosis with adipose-tissue dysfunction. Perilipin 1 (Plin1) did not exist in hepatocytes but was expressed exclusively in adipocytes as a dual modulator for regulating two principal adipose-tissue functions, triglyceride storage and breakdown. Plin1-/- mice showed decreased fat storage but increased lipolysis and efflux of fatty acids from adipose tissue, and hepatosteatosis spontaneously developed without altered circulating inflammatory adipocytokine levels. Plin1-/- adipose dysfunction impaired insulin sensitivity and hepatic glucose metabolism, which might inhibit gluconeogenesis to produce more intermediates for hepatic lipid synthesis. Indeed, the livers of Plin1-/- mice exhibited upregulated mRNA and protein expression of key enzymes and transcriptional factors for the uptake and transport of fatty acids and for de novo synthesis of triglycerides, but the expression of key enzymes and transcriptional factors for fatty-acid oxidation was downregulated. Biochemical assays in Plin1-/- mice confirmed increased fatty acid synthase activity but decreased activity of mitochondrial carnitine palmitoyltransferase 1 and [3H]-palmitate oxidation in the liver. We concluded that dysregulation of two principal functions, adipose storage and hydrolysis, had deleterious consequences on the hepatic lipid metabolism and thereby caused maladaptive hepatosteatosis. This mouse model might mimic and explain the pathogenesis of hepatosteatosis occurring in two typical disorders of adipose tissue dysfunction, obesity and lipodystrophy, particularly in lipodystrophic patients with Plin1 mutation.
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Perilipin1 deficiency in whole body or bone marrow-derived cells attenuates lesions in atherosclerosis-prone mice.
PloS one, 2015Co-Authors: Xiaojing Zhao, Bin Geng, Liangqiang Zou, Ying Lyu, Mingming Gao, Ling Zhang, George LiuAbstract:Aims The objective of this study is to determine the role of Perilipin 1 (Plin1) in whole body or bone marrow-derived cells on atherogenesis.
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Defective Differentiation of Adipose Precursor Cells from Lipodystrophic Mice Lacking Perilipin 1
PloS one, 2015Co-Authors: Ying Lyu, Shangxin Liu, Liangqiang Zou, Suning Wei, Jingna Deng, Xiaojing Zhao, Bin GengAbstract:Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation.
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Development of hypertrophic cardiomyopathy in Perilipin-1 null mice with adipose tissue dysfunction
Cardiovascular research, 2014Co-Authors: Shangxin Liu, Bin Geng, Liangqiang Zou, Suning Wei, Weiyi Wang, Jingna Deng, Xiaojing Zhao, Ying LyuAbstract:Aims Perilipin-1 (Plin1), exclusively located on the surface of lipid droplets in adipocytes, regulates the storage and hydrolysis of adipose triglycerides. Plin1 deficiency primarily causes low adiposity and aberrant lipolysis in rodents and humans. Here, we investigated whether adipose tissue dysfunction in Perilipin-1 null ( Plin1−/− ) mice has maladaptive consequences for the heart and an association with hypertrophic cardiomyopathy. Methods and results Perilipin-1 was expressed specifically in adipocytes but was undetectable in cardiomyocytes. Plin1−/− mice were histologically lipodystrophic, with reduced body fat. Paradoxically, the adipocytes of Plin1−/− mice, like those of obese and diabetic mammals, showed robust basal lipolysis and fatty acid efflux to the plasma. Such adipose tissue dysfunctions accounted for the ectopic lipid accumulation and enhanced fatty acid transport and oxidation in Plin1−/− mouse hearts. Excessive fatty acid β-oxidation and lipotoxicity induced excessive production of reactive oxygen species and oxidative stress because antioxidative capacity was reduced in cardiomyocytes, These malefactors injured the myocardial structure and function, as evidenced by disorganized myofilaments as well as irregular and swollen mitochondria with disrupted cristae. Finally, Plin1−/− mice showed grossly visible cardiac hypertrophy, with progressively up-regulated expression of hypertrophy and dysfunction marker genes, leading to heart failure, particularly with left ventricular diastolic dysfunction at 20 weeks of age. Conclusions Adipose tissue dysfunction may have deleterious effects on the heart and contribute to the development of hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy in Plin1−/− mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans, lipodystrophy and obesity.
Shangxin Liu - One of the best experts on this subject based on the ideXlab platform.
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Spontaneous development of hepatosteatosis in Perilipin-1 null mice with adipose tissue dysfunction.
Biochimica et biophysica acta. Molecular and cell biology of lipids, 2017Co-Authors: Suning Wei, Shangxin Liu, Weiyi Wang, Jingna Deng, Ying Lyu, Bin GengAbstract:Fatty liver features triglyceride accumulation in hepatocytes and often occurs with obesity and lipodystrophy in humans. Here, we investigated the mechanism of maladaptive hepatosteatosis with adipose-tissue dysfunction. Perilipin 1 (Plin1) did not exist in hepatocytes but was expressed exclusively in adipocytes as a dual modulator for regulating two principal adipose-tissue functions, triglyceride storage and breakdown. Plin1-/- mice showed decreased fat storage but increased lipolysis and efflux of fatty acids from adipose tissue, and hepatosteatosis spontaneously developed without altered circulating inflammatory adipocytokine levels. Plin1-/- adipose dysfunction impaired insulin sensitivity and hepatic glucose metabolism, which might inhibit gluconeogenesis to produce more intermediates for hepatic lipid synthesis. Indeed, the livers of Plin1-/- mice exhibited upregulated mRNA and protein expression of key enzymes and transcriptional factors for the uptake and transport of fatty acids and for de novo synthesis of triglycerides, but the expression of key enzymes and transcriptional factors for fatty-acid oxidation was downregulated. Biochemical assays in Plin1-/- mice confirmed increased fatty acid synthase activity but decreased activity of mitochondrial carnitine palmitoyltransferase 1 and [3H]-palmitate oxidation in the liver. We concluded that dysregulation of two principal functions, adipose storage and hydrolysis, had deleterious consequences on the hepatic lipid metabolism and thereby caused maladaptive hepatosteatosis. This mouse model might mimic and explain the pathogenesis of hepatosteatosis occurring in two typical disorders of adipose tissue dysfunction, obesity and lipodystrophy, particularly in lipodystrophic patients with Plin1 mutation.
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Spontaneous hypertension occurs with adipose tissue dysfunction in Perilipin-1 null mice.
Biochimica et biophysica acta, 2015Co-Authors: Liangqiang Zou, Shangxin Liu, Weiyi Wang, Xiaojing Zhao, Ying Lyv, Bin GengAbstract:Perilipin-1 (Plin1) coats lipid droplets exclusively in adipocytes and regulates two principle functions of adipose tissue, triglyceride storage and hydrolysis, which are disrupted upon Plin1 deficiency. In the present study, we investigated the alterations in systemic metabolites and hormones, vascular function and adipose function in spontaneous hypertensive mice lacking Perilipin-1 (Plin1-/-). Plin1-/- mice developed spontaneous hypertension without obvious alterations in systemic metabolites and hormones. Plin1 expressed only in adipose cells but not in vascular cells, so its ablation would have no direct effect in situ on blood vessels. Instead, Plin1-/- mice showed dysfunctions of perivascular adipose tissue (PVAT), a fat depot that anatomically surrounds systemic arteries and has an anticontractile effect. In Plin1-/- mice, aortic and mesenteric PVAT were reduced in mass and adipocyte derived relaxing factor secretion, but increased in basal lipolysis, angiotensin II secretion, macrophage infiltration and oxidative stress. Such multiple culprits impaired the anticontractile effect of PVAT to promote vasoconstriction of aortic and mesenteric arteries of Plin1-/- mice. Furthermore, arterial vessels of Plin1-/- mice showed increasing angiotensin II receptor type 1, monocyte chemotactic protein-1 and interlukin-6 expression, structural damage of endothelial and smooth muscle cells, along with impaired endothelium-dependent relaxation. Hypertension in Plin1-/- mice might occur as a deleterious consequence of PVAT dysfunction. This finding provides the direct evidence that links dysfunctional PVAT to vascular dysfunction and hypertension, particularly in pathophysiological states. This hypertensive mouse model might mimic and explain the hypertension occurring in patients with adipose tissue dysfunction, particularly with Plin1 mutations.
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Defective Differentiation of Adipose Precursor Cells from Lipodystrophic Mice Lacking Perilipin 1
PloS one, 2015Co-Authors: Ying Lyu, Shangxin Liu, Liangqiang Zou, Suning Wei, Jingna Deng, Xiaojing Zhao, Bin GengAbstract:Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation.
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Development of hypertrophic cardiomyopathy in Perilipin-1 null mice with adipose tissue dysfunction
Cardiovascular research, 2014Co-Authors: Shangxin Liu, Bin Geng, Liangqiang Zou, Suning Wei, Weiyi Wang, Jingna Deng, Xiaojing Zhao, Ying LyuAbstract:Aims Perilipin-1 (Plin1), exclusively located on the surface of lipid droplets in adipocytes, regulates the storage and hydrolysis of adipose triglycerides. Plin1 deficiency primarily causes low adiposity and aberrant lipolysis in rodents and humans. Here, we investigated whether adipose tissue dysfunction in Perilipin-1 null ( Plin1−/− ) mice has maladaptive consequences for the heart and an association with hypertrophic cardiomyopathy. Methods and results Perilipin-1 was expressed specifically in adipocytes but was undetectable in cardiomyocytes. Plin1−/− mice were histologically lipodystrophic, with reduced body fat. Paradoxically, the adipocytes of Plin1−/− mice, like those of obese and diabetic mammals, showed robust basal lipolysis and fatty acid efflux to the plasma. Such adipose tissue dysfunctions accounted for the ectopic lipid accumulation and enhanced fatty acid transport and oxidation in Plin1−/− mouse hearts. Excessive fatty acid β-oxidation and lipotoxicity induced excessive production of reactive oxygen species and oxidative stress because antioxidative capacity was reduced in cardiomyocytes, These malefactors injured the myocardial structure and function, as evidenced by disorganized myofilaments as well as irregular and swollen mitochondria with disrupted cristae. Finally, Plin1−/− mice showed grossly visible cardiac hypertrophy, with progressively up-regulated expression of hypertrophy and dysfunction marker genes, leading to heart failure, particularly with left ventricular diastolic dysfunction at 20 weeks of age. Conclusions Adipose tissue dysfunction may have deleterious effects on the heart and contribute to the development of hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy in Plin1−/− mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans, lipodystrophy and obesity.
Roland Moll - One of the best experts on this subject based on the ideXlab platform.
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Perilipin 1 is a highly specific marker for adipocytic differentiation in sarcomas with intermediate sensitivity
Journal of Cancer Research and Clinical Oncology, 2017Co-Authors: Christina C. Westhoff, Janice Mrozinski, Ina Riedel, Hans W. Heid, Roland MollAbstract:Purpose Liposarcomas are the most common soft tissue sarcomas of adults. The identification of lipoblastic cells in soft tissue sarcomas is mandatory for the diagnosis of most subtypes of liposarcomas but may be difficult in conventional histology. The present study focuses on the expression and possible diagnostic impact of two PAT family proteins, Perilipin 1/Perilipin and Perilipin 2/adipophilin in human liposarcomas. Methods Eighty-seven cases of liposarcomas and 30 cases of non-lipomatous sarcomas were investigated immunohistochemically for Perilipin 1 and 2 using entire tissue sections. Statistical analyses were performed using appropriate tests. Results Most liposarcomas and non-lipomatous sarcomas displayed positivity for Perilipin 2. In contrast, while more than two-thirds of liposarcomas presented Perilipin 1 positivity, all non-lipomatous sarcomas studied were negative for this marker, with statistical significance ( p
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Perilipin 1 is a highly specific marker for adipocytic differentiation in sarcomas with intermediate sensitivity.
Journal of cancer research and clinical oncology, 2016Co-Authors: Christina C. Westhoff, Janice Mrozinski, Ina Riedel, Hans Heid, Roland MollAbstract:Purpose Liposarcomas are the most common soft tissue sarcomas of adults. The identification of lipoblastic cells in soft tissue sarcomas is mandatory for the diagnosis of most subtypes of liposarcomas but may be difficult in conventional histology. The present study focuses on the expression and possible diagnostic impact of two PAT family proteins, Perilipin 1/Perilipin and Perilipin 2/adipophilin in human liposarcomas.