Lipolysis: cellular mechanisms for lipid mobilization from fat stores

Grabner, G; Xie, Hao; Schweiger, Martina; Zechner, Rudolf

doi:10.1038/s42255-021-00493-6

Cited by 317 publications

(229 citation statements)

References 376 publications

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“…A recent study has suggested that LD-related lipotoxicity participates in PD pathology [ 26 ]. Perilipin family members (PLIN1-5), the surrounding proteins of LDs, are regarded as the most important regulator of LDs, facilitating LD movement and cellular signalling interactions [ 27 , 28 ]. We have previously reported that the PLIN4/LD/mitophagy axis has a crucial role in neurodegeneration owing to MPTP/MPP + insult, indicating PLIN4/LDs as a potential biomarker and therapeutic target for PD [ 21 ].…”

Section: Resultsmentioning

confidence: 99%

Neuronal SH2B1 attenuates apoptosis in an MPTP mouse model of Parkinson's disease via promoting PLIN4 degradation

et al. 2022

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Section: Resultsmentioning

confidence: 99%

Neuronal SH2B1 attenuates apoptosis in an MPTP mouse model of Parkinson's disease via promoting PLIN4 degradation

et al. 2022

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“…To compensate for this imbalance, white adipocytes undergo lipolysis, wherein triacylglycerides (TAG) stored in lipid droplets are sequentially hydrolyzed in a series of enzymatic reactions mediated by adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), and monoacylglycerol lipase (MGL) to produce and secrete non-esterified free fatty acids into the blood for delivery to tissues. The regulation of lipolysis occurs at the transcriptional, post-translational, and neuroendocrine levels in processes that have recently been reviewed [ 19 , 20 , 21 , 22 ]. The lipolytic process is summarized in the following section and Figure 1 A.…”

Section: Flexible Adipose Tissuementioning

confidence: 99%

“…This sequence is summarized in the Figure 1 A insert. The authors acknowledge that alternative lipases contribute to lipolysis (reviewed elsewhere—[ 19 , 20 , 21 , 22 ]) but have chosen to focus on the canonical ATGL and HSL, as they have been shown to be responsible for nearly 90% of TAG hydrolysis [ 41 ].…”

Section: Flexible Adipose Tissuementioning

confidence: 99%

Adipocyte Phenotype Flexibility and Lipid Dysregulation

Preston

Scalia

Autieri

2022

Cells

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The prevalence of obesity and associated cardiometabolic diseases continues to rise, despite efforts to improve global health. The adipose tissue is now regarded as an endocrine organ since its multitude of secretions, lipids chief among them, regulate systemic functions. The loss of normal adipose tissue phenotypic flexibility, especially related to lipid homeostasis, appears to trigger cardiometabolic pathogenesis. The goal of this manuscript is to review lipid balance maintenance by the lean adipose tissue’s propensity for phenotype switching, obese adipose tissue’s narrower range of phenotype flexibility, and what initial factors account for the waning lipid regulatory capacity. Metabolic, hypoxic, and inflammatory factors contribute to the adipose tissue phenotype being made rigid. A better grasp of normal adipose tissue function provides the necessary context for recognizing the extent of obese adipose tissue dysfunction and gaining insight into how pathogenesis evolves.

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“…The catabolism of neutral lipids stored in the LD core is achieved by two major mechanisms, lipolysis and lipophagy ( Figure 1A ). During lipolysis, TAG lipases localized at the LD surface, such as Adipose Triglyceride Lipase (ATGL), liberate free fatty acids and diacylglycerol ( Grabner et al, 2021 ). Diacylglycerol can be further hydrolyzed to produce additional free fatty acids by the sequential action of Hormone Sensitive Lipase (HSL) and Monoacylglycerol Lipase (MAGL).…”

Section: Introductionmentioning

confidence: 99%

Functions of Stress-Induced Lipid Droplets in the Nervous System

Islimye

Girard

Gould

2022

Front. Cell Dev. Biol.

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Lipid droplets are highly dynamic intracellular organelles that store neutral lipids such as cholesteryl esters and triacylglycerols. They have recently emerged as key stress response components in many different cell types. Lipid droplets in the nervous system are mostly observed in vivo in glia, ependymal cells and microglia. They tend to become more numerous in these cell types and can also form in neurons as a consequence of ageing or stresses involving redox imbalance and lipotoxicity. Abundant lipid droplets are also a characteristic feature of several neurodegenerative diseases. In this minireview, we take a cell-type perspective on recent advances in our understanding of lipid droplet metabolism in glia, neurons and neural stem cells during health and disease. We highlight that a given lipid droplet subfunction, such as triacylglycerol lipolysis, can be physiologically beneficial or harmful to the functions of the nervous system depending upon cellular context. The mechanistic understanding of context-dependent lipid droplet functions in the nervous system is progressing apace, aided by new technologies for probing the lipid droplet proteome and lipidome with single-cell type precision.

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Lipolysis: cellular mechanisms for lipid mobilization from fat stores

Cited by 317 publications

References 376 publications

Neuronal SH2B1 attenuates apoptosis in an MPTP mouse model of Parkinson's disease via promoting PLIN4 degradation

Neuronal SH2B1 attenuates apoptosis in an MPTP mouse model of Parkinson's disease via promoting PLIN4 degradation

Adipocyte Phenotype Flexibility and Lipid Dysregulation

Functions of Stress-Induced Lipid Droplets in the Nervous System

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