Journal articles: 'Lipophagie'

1

Zelickson, B. D., and R. K. Winkelmann. "Lipophagic panniculitis in re-excision specimens." Acta Dermato-Venereologica 71, no. 1 (January 1, 1991): 59–61. http://dx.doi.org/10.2340/00015555715961.

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Lipophagic panniculitis consists of a macrophage infiltrate in the subcutaneous tissue. The macrophages transform into foam cells within the panniculus they replace lipocytes and may form giant cells. Although those pathologic features have been described as diagnostic of Weber-Christian disease, we report the occurrence of lipophagic panniculitis in re-excision specimens. Among 252 re-excision specimens from previously biopsied skin tumors, 5 cases in which masses of lipophages were infiltrating and replacing the subcutaneous tissue were found. The infiltrate was localized to the deep dermis and superficial subcutaneous tissue below and beside the initial biopsy site. In 3 cases, suture or hair was detected within the tissue, and granulation tissue with foreign body giant cells was observed along the dermal suture line. In 4 cases there was evidence of phlebitis within or close to areas of infiltration. None of these patients developed symptomatic panniculitis. Lipophagia can be a normal response of wound healing in some patients.

2

Schott, Micah B., Shaun G. Weller, Ryan J. Schulze, Eugene W. Krueger, Kristina Drizyte-Miller, Carol A. Casey, and Mark A. McNiven. "Lipid droplet size directs lipolysis and lipophagy catabolism in hepatocytes." Journal of Cell Biology 218, no. 10 (August 7, 2019): 3320–35. http://dx.doi.org/10.1083/jcb.201803153.

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Lipid droplet (LD) catabolism in hepatocytes is mediated by a combination of lipolysis and a selective autophagic mechanism called lipophagy, but the relative contributions of these seemingly distinct pathways remain unclear. We find that inhibition of lipolysis, lipophagy, or both resulted in similar overall LD content but dramatic differences in LD morphology. Inhibition of the lipolysis enzyme adipose triglyceride lipase (ATGL) resulted in large cytoplasmic LDs, whereas lysosomal inhibition caused the accumulation of numerous small LDs within the cytoplasm and degradative acidic vesicles. Combined inhibition of ATGL and LAL resulted in large LDs, suggesting that lipolysis targets these LDs upstream of lipophagy. Consistent with this, ATGL was enriched in larger-sized LDs, whereas lipophagic vesicles were restricted to small LDs as revealed by immunofluorescence, electron microscopy, and Western blot of size-separated LDs. These findings provide new evidence indicating a synergistic relationship whereby lipolysis targets larger-sized LDs to produce both size-reduced and nascently synthesized small LDs that are amenable for lipophagic internalization.

3

Jonas, Wenke, Kristin Schwerbel, Lisa Zellner, Markus Jähnert, Pascal Gottmann, and Annette Schürmann. "Alterations of Lipid Profile in Livers with Impaired Lipophagy." International Journal of Molecular Sciences 23, no. 19 (October 6, 2022): 11863. http://dx.doi.org/10.3390/ijms231911863.

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Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Various mechanisms such as an increased uptake in fatty acids or de novo synthesis contribute to the development of steatosis and progression to more severe stages. Furthermore, it has been shown that impaired lipophagy, the degradation of lipids by autophagic processes, contributes to NAFLD. Through an unbiased lipidome analysis of mouse livers in a genetic model of impaired lipophagy, we aimed to determine the resulting alterations in the lipidome. Observed changes overlap with those of the human disease. Overall, the entire lipid content and in particular the triacylglycerol concentration increased under conditions of impaired lipophagy. In addition, we detected a reduction in long-chain polyunsaturated fatty acids (PUFAs) and an increased ratio of n-6 PUFAs to n-3 PUFAs, which was due to the depletion of n-3 PUFAs. Although the abundance of major phospholipid classes was reduced, the ratio of phosphatidylcholines to phosphatidylethanolamines was not affected. In conclusion, this study demonstrates that impaired lipophagy contributes to the pathology of NAFLD and is associated with an altered lipid profile. However, the lipid pattern does not appear to be specific for lipophagic alterations, as it resembles mainly that described in relation to fatty liver disease.

4

Alexandrides, C. "Lipophagic Granuloma." Acta Medica Scandinavica 154, S312 (April 24, 2009): 449–60. http://dx.doi.org/10.1111/j.0954-6820.1956.tb17036.x.

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5

Peng, Peng, Wensheng Liu, Adam Utley, Colin Chavel, Louise Carlson, Scott H. Olejniczak, and Kelvin P. Lee. "CD28 Induces Autophagy in Plasma Cells to Enhance Mitochondrial Respiration and Survival." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 71.2. http://dx.doi.org/10.4049/jimmunol.204.supp.71.2.

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Abstract Durable humoral immunity relies on the persistence of long-lived plasma cells (LLPC) that continuously produce protective antibodies. The prototypical T cell costimulatory molecule CD28, that is also expressed on LLPC, is critical to their survival but the mechanisms involved remain unclear. We found CD28 activation enhances autophagy in LLPC/multiple myeloma as evidenced by increased level of autophagy marker LC3II, elevated autophagosome numbers and decreased level of autophagic cargo receptor P62. Inhibition of autophagy by 3MA or BafA abolished CD28’s pro-survival effects. Mechanistically, CD28 activation increased the protein level of ATG5, a critical autophagy regulator, even with translation blockade, but this was abrogated by proteasome inhibition. Knocking down atg5 eliminated CD28’s pro-survival effects, suggesting CD28 signaling regulates ATG5 degradation to sustain pro-survival autophagy. CD28 activation significantly increased mitochondrial respiration and blocking autophagy prevented this. Free fatty acids (FFA) can be degraded from cellular lipid droplets (LD) by lipophage, a selective form of autophagy, to fuel mitochondrial respiration. We found CD28 activation decreased LD staining and blocking autophagy prevented this. Blocking lipophagic lipase by lalistat eliminated CD28-induced oxidative phosphorylation and pro-survival effects. Addition of FFA (oleic and palmitic acids) boosted oxidative phosphorylation and restored survival with autophagy inhibition but not with fatty acid oxidation blockade. These data suggest CD28 signaling regulates ATG5 protein degradation to enhance autophagy and this in return produces FFA to sustain mitochondrial respiration and support LLPC survival.

6

Kumar, Ravinder, Muhammad Arifur Rahman, and Taras Y. Nazarko. "Nitrogen Starvation and Stationary Phase Lipophagy Have Distinct Molecular Mechanisms." International Journal of Molecular Sciences 21, no. 23 (November 29, 2020): 9094. http://dx.doi.org/10.3390/ijms21239094.

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In yeast, the selective autophagy of intracellular lipid droplets (LDs) or lipophagy can be induced by either nitrogen (N) starvation or carbon limitation (e.g., in the stationary (S) phase). We developed the yeast, Komagataella phaffii (formerly Pichia pastoris), as a new lipophagy model and compared the N-starvation and S-phase lipophagy in over 30 autophagy-related mutants using the Erg6-GFP processing assay. Surprisingly, two lipophagy pathways had hardly overlapping stringent molecular requirements. While the N-starvation lipophagy strictly depended on the core autophagic machinery (Atg1-Atg9, Atg18, and Vps15), vacuole fusion machinery (Vam7 and Ypt7), and vacuolar proteolysis (proteinases A and B), only Atg6 and proteinases A and B were essential for the S-phase lipophagy. The rest of the proteins were only partially required in the S-phase. Moreover, we isolated the prl1 (for the positive regulator of lipophagy 1) mutant affected in the S-phase lipophagy, but not N-starvation lipophagy. The prl1 defect was at a stage of delivery of the LDs from the cytoplasm to the vacuole, further supporting the mechanistically different nature of the two lipophagy pathways. Taken together, our results suggest that N-starvation and S-phase lipophagy have distinct molecular mechanisms.

7

Levy, Jack, Mark E. Burnett, and Cynthia M. Magro. "Lipophagic Panniculitis of Childhood." American Journal of Dermatopathology 39, no. 3 (March 2017): 217–24. http://dx.doi.org/10.1097/dad.0000000000000721.

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8

UMBERT, I. J., and R. K. WINKELMANN. "Adult lipophagic atrophic panniculitis." British Journal of Dermatology 124, no. 3 (March 1991): 291–95. http://dx.doi.org/10.1111/j.1365-2133.1991.tb00578.x.

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9

Winkelmann, R. K., Marian T. McEvoy, and Margot S. Peters. "Lipophagic panniculitis of childhood." Journal of the American Academy of Dermatology 21, no. 5 (November 1989): 971–78. http://dx.doi.org/10.1016/s0190-9622(89)70285-1.

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10

Juneja, Manish, Pankaj Raut, Milind Lohkare, Harshawardhan Ramteke, Vaishnavi Walke, and Sakshi Bhatia. "Effects of Lipophagy on Atherosclerosis." Central India Journal of Medical Research 2, no. 01 (May 15, 2023): 17–25. http://dx.doi.org/10.58999/cijmr.v2i01.44.

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An excess build-up of lipids in the arterial wall might result into Atherosclerosis. Lipophagy is the autophagic degradation of lipids that regulates the lipid metabolism in various kinds of cells. Lipophagy replaces intracellular lipid which makes it vital for development and progression of atherosclerosis. This review focuses on advances in lipid metabolism through lipophagy. The role of lipophagy in vascular endothelial cell injury, macrophage lipid accumulation and vascular smooth muscle cells phenotypic shift has been explained by specifying the lipophagy– atherosclerosis relationship. Novel therapeutic choices can be discovered by understanding the significance of lipophagy in these processes which could be a breakthrough in treatment of atherosclerosis.

11

Kumar, Ravinder, Ankit Shroff, and Taras Y. Nazarko. "Komagataella phaffii Cue5 Piggybacks on Lipid Droplets for Its Vacuolar Degradation during Stationary Phase Lipophagy." Cells 11, no. 2 (January 10, 2022): 215. http://dx.doi.org/10.3390/cells11020215.

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Recently, we developed Komagataella phaffii (formerly Pichia pastoris) as a model for lipophagy, the selective autophagy of lipid droplets (LDs). We found that lipophagy pathways induced by acute nitrogen (N) starvation and in stationary (S) phase have different molecular mechanisms. Moreover, both types of lipophagy are independent of Atg11, the scaffold protein that interacts with most autophagic receptors and, therefore, is essential for most types of selective autophagy in yeast. Since yeast aggrephagy, the selective autophagy of ubiquitinated protein aggregates, is also independent of Atg11 and utilizes the ubiquitin-binding receptor, Cue5, we studied the relationship of K. phaffii Cue5 with differentially induced LDs and lipophagy. While there was no relationship of Cue5 with LDs and lipophagy under N-starvation conditions, Cue5 accumulated on LDs in S-phase and degraded together with LDs via S-phase lipophagy. The accumulation of Cue5 on LDs and its degradation by S-phase lipophagy strongly depended on the ubiquitin-binding CUE domain and Prl1, the positive regulator of lipophagy 1. However, unlike Prl1, which is required for S-phase lipophagy, Cue5 was dispensable for it suggesting that Cue5 is rather a new substrate of this pathway. We propose that a similar mechanism (Prl1-dependent accumulation on LDs) might be employed by Prl1 to recruit another ubiquitin-binding protein that is essential for S-phase lipophagy.

12

Wu, Yujia, Zhenlin Wu, Qiying Jin, Jinyuan Liu, and Peiping Xu. "Identification and Analysis of Biomarkers Associated with Lipophagy and Therapeutic Agents for COVID-19." Viruses 16, no. 6 (June 7, 2024): 923. http://dx.doi.org/10.3390/v16060923.

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Background: Lipids, as a fundamental cell component, play an regulating role in controlling the different cellular biological processes involved in viral infections. A notable feature of coronavirus disease 2019 (COVID-19) is impaired lipid metabolism. The function of lipophagy-related genes in COVID-19 is unknown. The present study aimed to investigate biomarkers and drug targets associated with lipophagy and lipophagy-based therapeutic agents for COVID-19 through bioinformatics analysis. Methods: Lipophagy-related biomarkers for COVID-19 were identified using machine learning algorithms such as random forest, Support Vector Machine-Recursive Feature Elimination, Generalized Linear Model, and Extreme Gradient Boosting in three COVID-19-associated GEO datasets: scRNA-seq (GSE145926) and bulk RNA-seq (GSE183533 and GSE190496). The cMAP database was searched for potential COVID-19 medications. Results: The lipophagy pathway was downregulated, and the lipid droplet formation pathway was upregulated, resulting in impaired lipid metabolism. Seven lipophagy-related genes, including ACADVL, HYOU1, DAP, AUP1, PRXAB2, LSS, and PLIN2, were used as biomarkers and drug targets for COVID-19. Moreover, lipophagy may play a role in COVID-19 pathogenesis. As prospective drugs for treating COVID-19, seven potential downregulators (phenoxybenzamine, helveticoside, lanatoside C, geldanamycin, loperamide, pioglitazone, and trichostatin A) were discovered. These medication candidates showed remarkable binding energies against the seven biomarkers. Conclusions: The lipophagy-related genes ACADVL, HYOU1, DAP, AUP1, PRXAB2, LSS, and PLIN2 can be used as biomarkers and drug targets for COVID-19. Seven potential downregulators of these seven biomarkers may have therapeutic effects for treating COVID-19.

13

Li, Xi, Yangjun Yang, Yi Sun, and Shuzhe Ding. "Research Progress on Lipophagy-Mediated Exercise Intervention in Non-Alcoholic Fatty Liver Disease." International Journal of Molecular Sciences 25, no. 6 (March 9, 2024): 3153. http://dx.doi.org/10.3390/ijms25063153.

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Lipophagy is a cellular pathway targeting the lysosomal degradation of lipid droplets, playing a role in promoting lipid turnover and renewal. Abnormal lipophagy processes can lead to the occurrence and development of non-alcoholic fatty liver disease (NAFLD), characterized by the deposition of lipid droplets (LDs) in the liver. The importance of exercise training in preventing and improving NAFLD has been well-established, but the exact mechanisms remain unclear. Recent research findings suggest that lipophagy may serve as a crucial hub for liver lipid turnover under exercise conditions. Exercise may alleviate hepatic lipid accumulation and mitigate inflammatory responses and fibrosis through lipophagy, thereby improving the onset and progression of NAFLD.

14

H. Al-Shebeb, T., and H. S. Al-Nassir. "A HISTOCHEMICAL STUDY ON THE CIRCULATING LIPOPHAGES IN CHOLESTEROL FED GUINEA PIGS." Iraqi Journal of Veterinary Medicine 14, no. 1 (December 28, 1990): 44–51. http://dx.doi.org/10.30539/ijvm.v14i1.1627.

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The postulation that circulating lipophages in cholesterol-fed guinea pigs may originate from lipidladen splenic macrophages was tested. The experimental animals were allocated in two groups: high-cholesterol (HC) and control (C) groups. Wright-Giemsa, Oil-red 0, non specific estrase and Perl's prussian blue stains were. performed on peripheral blood films on both day-30 and 60 of the experiment. Vacuolated leukocytes were demonstrated by day 60 in the HC group and proven to be lipid-laden monocytes. No hemosiderin residue was detected in the circulating lipophages. Our data suggest that lipophages are unlikely to be splenic origin.

15

Xiao, Fei, Chuan Chen, Wuxiao Zhang, Jiawei Wang, and Kun Wu. "FOXO3/Rab7-Mediated Lipophagy and Its Role in Zn-Induced Lipid Metabolism in Yellow Catfish (Pelteobagrus fulvidraco)." Genes 15, no. 3 (March 4, 2024): 334. http://dx.doi.org/10.3390/genes15030334.

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Lipophagy is a selective autophagy that regulates lipid metabolism and reduces hepatic lipid deposition. However, the underlying mechanism has not been understood in fish. In this study, we used micronutrient zinc (Zn) as a regulator of autophagy and lipid metabolism and found that Ras-related protein 7 (rab7) was involved in Zn-induced lipophagy in hepatocytes of yellow catfish Pelteobagrus pelteobagrus. We then characterized the rab7 promoter and identified binding sites for a series of transcription factors, including Forkhead box O3 (FOXO3). Site mutation experiments showed that the −1358/−1369 bp FOXO3 binding site was responsible for Zn-induced transcriptional activation of rab7. Further studies showed that inhibition of rab7 significantly inhibited Zn-induced lipid degradation by lipophagy. Moreover, rab7 inhibitor also mitigated the Zn-induced increase of cpt1α and acadm expression. Our results suggested that Zn exerts its lipid-lowering effect partly through rab7-mediated lipophagy and FA β-oxidation in hepatocytes. Overall, our findings provide novel insights into the FOXO3/rab7 axis in lipophagy regulation and enhance the understanding of lipid metabolism by micronutrient Zn, which may help to reduce excessive lipid accumulation in fish.

16

Liu, Qing, Yuan-Mei Wang, and Hong-Feng Gu. "Lipophagy in atherosclerosis." Clinica Chimica Acta 511 (December 2020): 208–14. http://dx.doi.org/10.1016/j.cca.2020.10.025.

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17

Chen, Wen-Feng, Hong-Fang Wang, Ying Wang, Zhen-Guo Liu, and Bao-Hua Xu. "AmAtg2B-Mediated Lipophagy Regulates Lipolysis of Pupae in Apis mellifera." International Journal of Molecular Sciences 24, no. 3 (January 20, 2023): 2096. http://dx.doi.org/10.3390/ijms24032096.

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Lipophagy plays an important role in regulating lipid metabolism in mammals. The exact function of autophagy-related protein 2 (Atg2) has been investigated in mammals, but research on the existence and functions of Atg2 in Apis mellifera (AmAtg2) is still limited. Here, autophagy occurred in honeybee pupae, which targeted lipid droplets (LDs) in fat body, namely lipophagy, which was verified by co-localization of LDs with microtubule-associated protein 1A/1B light chain 3 beta (LC3). Moreover, AmAtg2 homolog B (AmAtg2B) was expressed specifically in pupal fat body, which indicated that AmAtg2B might have special function in fat body. Further, AmAtg2B antibody neutralization and AmAtg2B knock-down were undertaken to verify the functions in pupae. Results showed that low expression of AmAtg2B at the protein and transcriptional levels led to lipophagy inhibition, which down-regulated the expression levels of proteins and genes related to lipolysis. Altogether, results in this study systematically revealed that AmAtg2B interfered with lipophagy and then caused abnormal lipolysis in the pupal stage.

18

Wang, Chao-Wen, Yu-Hsuan Miao, and Yi-Shun Chang. "A sterol-enriched vacuolar microdomain mediates stationary phase lipophagy in budding yeast." Journal of Cell Biology 206, no. 3 (July 28, 2014): 357–66. http://dx.doi.org/10.1083/jcb.201404115.

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Stationary phase (stat-phase) is a poorly understood physiological state under which cells arrest proliferation and acquire resistance to multiple stresses. Lipid droplets (LDs), organelles specialized for cellular lipid homeostasis, increase in size and number at the onset of stat-phase. However, little is known about the dynamics of LDs under this condition. In this paper, we reveal the passage of LDs from perinuclear endoplasmic reticulum association to entry into vacuoles during the transition to stat-phase. We show that the process requires the core autophagy machinery and a subset of autophagy-related (Atg) proteins involved in selective autophagy. Notably, the process that we term stat-phase lipophagy is mediated through a sterol-enriched vacuolar microdomain whose formation and integrity directly affect LD translocation. Intriguingly, cells defective in stat-phase lipophagy showed disrupted vacuolar microdomains, implying that LD contents, likely sterol esters, contribute to the maintenance of vacuolar microdomains. Together, we propose a feed-forward loop in which lipophagy stimulates vacuolar microdomain formation, which in turn promotes lipophagy during stat-phase.

19

Lin, Hongkun, Xiaoping Guo, Jingjing Liu, Peiyi Liu, Guibin Mei, Hongxia Li, Dan Li, et al. "Improving Lipophagy by Restoring Rab7 Cycle: Protective Effects of Quercetin on Ethanol-Induced Liver Steatosis." Nutrients 14, no. 3 (February 4, 2022): 658. http://dx.doi.org/10.3390/nu14030658.

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Chronic alcohol consumption retards lipophagy, which contributes to the pathogenesis of liver steatosis. Lipophagy-related Rab7 has been presumed as a crucial regulator in the progression of alcohol liver disease despite elusive mechanisms. More importantly, whether or not hepatoprotective quercetin targets Rab7-associated lipophagy disorder is unknown. Herein, alcoholic fatty liver induced by chronic-plus-single-binge ethanol feeding to male C57BL/6J mice was manifested by hampering autophagosomes formation with lipid droplets and fusion with lysosomes compared with the normal control, which was normalized partially by quercetin. The GST-RILP pulldown assay of Rab7 indicated an improved GTP-Rab7 as the quercetin treatment for ethanol-feeding mice. HepG2 cells transfected with CYP2E1 showed similar lipophagy dysfunction when exposed to ethanol, which was blocked when cells were transfected with siRNA-Rab7 in advance. Ethanol-induced steatosis and autophagic flux disruption were aggravated by the Rab7-specific inhibitor CID1067700 while alleviated by transfecting with the Rab7Wt plasmid, which was visualized by immunofluorescence co-localization analysis and mCherry-GFP-LC3 transfection. Furthermore, TBC1D5, a Rab GTPase-activating protein for the subsequent normal circulation of Rab7, was downregulated after alcohol administration but regained by quercetin. Rab7 circulation retarded by ethanol and corrected by quercetin was further revealed by fluorescence recovery after photobleaching (FRAP). Altogether, quercetin attenuates hepatic steatosis by normalizing ethanol-imposed Rab7 turnover disorders and subsequent lipophagy disturbances, highlighting a novel mechanism and the promising prospect of quercetin-like phytochemicals against the crucial first hit from alcohol.

20

Pizato, Kiffer, Luzete, Assumpção, Correa, Melo, Sant’Ana, Ito, and Magalhães. "Omega 3-DHA and Delta-Tocotrienol Modulate Lipid Droplet Biogenesis and Lipophagy in Breast Cancer Cells: the Impact in Cancer Aggressiveness." Nutrients 11, no. 6 (May 28, 2019): 1199. http://dx.doi.org/10.3390/nu11061199.

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Omega 3-docosahexaenoic acid (DHA) and vitamin E Delta-tocotrienol (Delta-T3) are extensively studied as protective nutrients against cancer development. Little is known about the biological mechanisms targeted by these bioactive molecules on lipid droplet (LD) biogenesis, an important breast cancer aggressiveness marker, and the occurrence of lipophagy in breast cancer cells. The aim of this study was to investigate the effect of DHA, Delta-T3 and DHA plus Delta-T3 co-treatment in LD biogenesis and lipophagy process in triple negative breast cancer cell line MDA-MB-231. Cells were treated with 50 μM DHA and/or 5 μM Delta-T3. Our results demonstrated that DHA can trigger an increase in LD biogenesis and co-treatment with Delta-T3 was able to reduce this LD biogenesis. In addition, we showed that a higher cytoplasmic LD content is associated with a higher breast cancer cells malignance and proliferation. Reduction of cytoplasmic LD content by silencing ADRP (adipose differentiation-related protein), a structural LD protein, also decreased cell proliferation in MDA-MB-231 cells. Treatment with DHA and Delta-T3 alone or co-treatment did not reduce cell viability. Moreover, we showed here that DHA can trigger lipophagy in MDA-MB-231 cells and DHA plus Delta-T3 co-treatment was able to enhance this lipophagy process. Our findings demonstrated that co-treatment with DHA plus Delta-T3 in MDA-MB-231 cells could reduce LD biogenesis and potentiate lipophagy in these cells, possibly having a positive impact to inhibit breast cancer malignancy. Therefore, suitable doses of DHA and Delta-T3 vitamin E isoform supplementation can be a prominent tool in therapeutic treatments against breast cancer.

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Yin, Haimeng, Ying Shan, Tian Xia, Yan Ji, Ling Yuan, Yiwen You, and Bo You. "Emerging Roles of Lipophagy in Cancer Metastasis." Cancers 14, no. 18 (September 19, 2022): 4526. http://dx.doi.org/10.3390/cancers14184526.

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Obesity is a prominent risk factor for certain types of tumor progression. Adipocytes within tumor stroma contribute to reshaping tumor microenvironment (TME) and the metabolism and metastasis of tumors through the production of cytokines and adipokines. However, the crosstalk between adipocytes and tumor cells remains a major gap in this field. Known as a subtype of selective autophagy, lipophagy is thought to contribute to lipid metabolism by breaking down intracellular lipid droplets (LDs) and generating free fatty acids (FAs). The metastatic potential of cancer cells closely correlates with the lipid degradation mechanisms, which are required for energy generation, signal transduction, and biosynthesis of membranes. Here, we discuss the recent advance in the understanding of lipophagy with tumor lipid metabolism and review current studies on the roles of lipoghagy in the metastasis of certain human malignancies. Additionally, the novel candidate drugs targeting lipophagy are integrated for effective treatment strategies.

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Singh, Rajat, and Ana Maria Cuervo. "Lipophagy: Connecting Autophagy and Lipid Metabolism." International Journal of Cell Biology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/282041.

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Lipid droplets (LDs), initially considered “inert” lipid deposits, have gained during the last decade the classification of cytosolic organelles due to their defined composition and the multiplicity of specific cellular functions in which they are involved. The classification of LD as organelles brings along the need for their regulated turnover and recent findings support the direct contribution of autophagy to this turnover through a process now described as lipophagy. This paper focuses on the characteristics of this new type of selective autophagy and the cellular consequences of the mobilization of intracellular lipids through this process. Lipophagy impacts the cellular energetic balance directly, through lipid breakdown and, indirectly, by regulating food intake. Defective lipophagy has been already linked to important metabolic disorders such as fatty liver, obesity and atherosclerosis, and the age-dependent decrease in autophagy could underline the basis for the metabolic syndrome of aging.

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Bu, Kyung-Bin, Min Kim, Min Kyoung Shin, Seung-Ho Lee, and Jung-Suk Sung. "Regulation of Benzo[a]pyrene-Induced Hepatic Lipid Accumulation through CYP1B1-Induced mTOR-Mediated Lipophagy." International Journal of Molecular Sciences 25, no. 2 (January 22, 2024): 1324. http://dx.doi.org/10.3390/ijms25021324.

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Metabolic dysfunction-associated steatotic liver disease (MASLD) is caused by lipid accumulation within the liver. The pathogenesis underlying its development is poorly understood. Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and a group 1 carcinogen. The aryl hydrocarbon receptor activation by B[a]P induces cytochrome P450 (CYP) enzymes, contributing to hepatic lipid accumulation. However, the molecular mechanism through which the B[a]P-mediated induction of CYP enzymes causes hepatic lipid accumulation is unknown. This research was conducted to elucidate the role of CYP1B1 in regulating B[a]P-induced lipid accumulation within hepatocytes. B[a]P increased hepatic lipid accumulation, which was mitigated by CYP1B1 knockdown. An increase in the mammalian target of rapamycin (mTOR) by B[a]P was specifically reduced by CYP1B1 knockdown. The reduction of mTOR increased the expression of autophagic flux-related genes and promoted phagolysosome formation. Both the expression and translocation of TFE3, a central regulator of lipophagy, were induced, along with the expression of lipophagy-related genes. Conversely, enhanced mTOR activity reduced TFE3 expression and translocation, which reduced the expression of lipophagy-related genes, diminished phagolysosome production, and increased lipid accumulation. Our results indicate that B[a]P-induced hepatic lipid accumulation is caused by CYP1B1-induced mTOR and the reduction of lipophagy, thereby introducing novel targets and mechanisms to provide insights for understanding B[a]P-induced MASLD.

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Daniele, Joseph R., Ryo Higuchi-Sanabria, Jenni Durieux, Samira Monshietehadi, Vidhya Ramachandran, Sarah U. Tronnes, Naame Kelet, et al. "UPRER promotes lipophagy independent of chaperones to extend life span." Science Advances 6, no. 1 (January 2020): eaaz1441. http://dx.doi.org/10.1126/sciadv.aaz1441.

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Longevity is dictated by a combination of environmental and genetic factors. One of the key mechanisms to regulate life-span extension is the induction of protein chaperones for protein homeostasis. Ectopic activation of the unfolded protein response of the endoplasmic reticulum (UPRER) specifically in neurons is sufficient to enhance organismal stress resistance and extend life span. Here, we find that this activation not only promotes chaperones but also facilitates ER restructuring and ER function. This restructuring is concomitant with lipid depletion through lipophagy. Activation of lipophagy is distinct from chaperone induction and is required for the life-span extension found in this paradigm. Last, we find that overexpression of the lipophagy component, ehbp-1, is sufficient to deplete lipids, remodel ER, and promote life span. Therefore, UPR induction in neurons triggers two distinct programs in the periphery: the proteostasis arm through protein chaperones and metabolic changes through lipid depletion mediated by EH domain binding protein 1 (EHBP-1).

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Singh, Rajat. "Hypothalamic lipophagy and energetic balance." Aging 3, no. 10 (October 23, 2011): 934–42. http://dx.doi.org/10.18632/aging.100393.

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Wang, Chao-Wen. "Lipid droplets, lipophagy, and beyond." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1861, no. 8 (August 2016): 793–805. http://dx.doi.org/10.1016/j.bbalip.2015.12.010.

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Ji, Chonghao, Zhanwei Zhang, Xin Xu, Dawei Song, and Dongjiao Zhang. "Hyperlipidemia impacts osteogenesis via lipophagy." Bone 167 (February 2023): 116643. http://dx.doi.org/10.1016/j.bone.2022.116643.

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Lee, Ara, Meng Li, Young Ho Ko, Sanghwang Park, Jongcheol Seo, Kyeng Min Park, and Kimoon Kim. "Visualization of lipophagy using a supramolecular FRET pair." Chemical Communications 57, no. 91 (2021): 12179–82. http://dx.doi.org/10.1039/d1cc04779e.

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29

Taeg Oh, Goo, Se Jin Jeong, and Sinai Kim. "Peroxiredoxin1 normalizes macrophage lipophagic flux via regulates oxidative stress." Atherosclerosis 263 (August 2017): e88. http://dx.doi.org/10.1016/j.atherosclerosis.2017.06.287.

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Park, Miey, Anshul Sharma, Hana Baek, Jin-Young Han, Junho Yu, and Hae-Jeung Lee. "Stevia and Stevioside Attenuate Liver Steatosis through PPARα-Mediated Lipophagy in db/db Mice Hepatocytes." Antioxidants 11, no. 12 (December 19, 2022): 2496. http://dx.doi.org/10.3390/antiox11122496.

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Lipophagy, a type of autophagy that breaks down lipid droplets, is essential in the regulation of intracellular lipid accumulation and intracellular free fatty acid levels in numerous organisms and metabolic conditions. We investigated the effects of Stevia rebaudiana Bertoni (S), a low-calorie sweetener, and stevioside (SS) on hepatic steatosis and autophagy in hepatocytes, as well as in db/db mice. S and SS reduced the body and liver weight and levels of serum triglyceride, total cholesterol, and hepatic lipogenic proteins. In addition, S and SS increased the levels of fatty acid oxidase, peroxisome proliferator-activated receptor alpha (PPARα), and microtubule-associated protein light chain 3 B but decreased that of sequestosome 1 (p62) in the liver of db/db mice. Additionally, Beclin 1, lysosomal associated membrane protein 1, and phosphorylated adenosine monophosphate-activated protein kinase protein expression was augmented following S and SS treatment of db/db mice. Furthermore, the knockdown of PPARα blocked lipophagy in response to SS treatment in HepG2 cells. These outcomes indicate that PPARα-dependent lipophagy is involved in hepatic steatosis in the db/db mouse model and that SS, a PPARα agonist, represents a new therapeutic option for managing associated diseases.

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Rahman, Muhammad Arifur, Ravinder Kumar, Enrique Sanchez, and Taras Y. Nazarko. "Lipid Droplets and Their Autophagic Turnover via the Raft-Like Vacuolar Microdomains." International Journal of Molecular Sciences 22, no. 15 (July 29, 2021): 8144. http://dx.doi.org/10.3390/ijms22158144.

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Although once perceived as inert structures that merely serve for lipid storage, lipid droplets (LDs) have proven to be the dynamic organelles that hold many cellular functions. The LDs’ basic structure of a hydrophobic core consisting of neutral lipids and enclosed in a phospholipid monolayer allows for quick lipid accessibility for intracellular energy and membrane production. Whereas formed at the peripheral and perinuclear endoplasmic reticulum, LDs are degraded either in the cytosol by lipolysis or in the vacuoles/lysosomes by autophagy. Autophagy is a regulated breakdown of dysfunctional, damaged, or surplus cellular components. The selective autophagy of LDs is called lipophagy. Here, we review LDs and their degradation by lipophagy in yeast, which proceeds via the micrometer-scale raft-like lipid domains in the vacuolar membrane. These vacuolar microdomains form during nutrient deprivation and facilitate internalization of LDs via the vacuolar membrane invagination and scission. The resultant intra-vacuolar autophagic bodies with LDs inside are broken down by vacuolar lipases and proteases. This type of lipophagy is called microlipophagy as it resembles microautophagy, the type of autophagy when substrates are sequestered right at the surface of a lytic compartment. Yeast microlipophagy via the raft-like vacuolar microdomains is a great model system to study the role of lipid domains in microautophagic pathways.

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Mastoridou, Eleftheria M., Anna C. Goussia, Panagiotis Kanavaros, and Antonia V. Charchanti. "Involvement of Lipophagy and Chaperone-Mediated Autophagy in the Pathogenesis of Non-Alcoholic Fatty Liver Disease by Regulation of Lipid Droplets." International Journal of Molecular Sciences 24, no. 21 (November 2, 2023): 15891. http://dx.doi.org/10.3390/ijms242115891.

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Non-alcoholic fatty liver disease (NAFLD) is defined as the accumulation of lipids in the form of lipid droplets in more than 5% of hepatocytes. It is regarded as a range of diverse pathologies, including simple steatosis and steatohepatitis. The structural characteristics of lipid droplets, along with their protein composition, mainly including perilipins, have been implicated in the etiology of the disease. These proteins have garnered increasing attention as a pivotal regulator since their levels and distinct expression appear to be associated with the progression from simple steatosis to steatohepatitis. Perilipins are target proteins of chaperone-mediated autophagy, and their degradation is a prerequisite for lipolysis and lipophagy to access the lipid core. Both lipophagy and chaperone-mediated autophagy have significant implications on the development of the disease, as evidenced by their upregulation during the initial phases of simple steatosis and their subsequent downregulation once steatosis is established. On the contrary, during steatohepatitis, the process of chaperone-mediated autophagy is enhanced, although lipophagy remains suppressed. Evidently, the reduced levels of autophagic pathways observed in simple steatosis serve as a defensive mechanism against lipotoxicity. Conversely, in steatohepatitis, chaperone-mediated autophagy fails to compensate for the continuous generation of small lipid droplets and thus cannot protect hepatocytes from lipotoxicity.

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Maan, Meenu, Jeffrey M. Peters, Mainak Dutta, and Andrew D. Patterson. "Lipid metabolism and lipophagy in cancer." Biochemical and Biophysical Research Communications 504, no. 3 (October 2018): 582–89. http://dx.doi.org/10.1016/j.bbrc.2018.02.097.

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Bai, Yuansong, Lingjun Meng, Leng Han, Yuanyuan Jia, Yanan Zhao, Huan Gao, Rui Kang, Xiaofeng Wang, Daolin Tang, and Enyong Dai. "Lipid storage and lipophagy regulates ferroptosis." Biochemical and Biophysical Research Communications 508, no. 4 (January 2019): 997–1003. http://dx.doi.org/10.1016/j.bbrc.2018.12.039.

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Weidberg, Hilla, Elena Shvets, and Zvulun Elazar. "Lipophagy: Selective Catabolism Designed for Lipids." Developmental Cell 16, no. 5 (May 2009): 628–30. http://dx.doi.org/10.1016/j.devcel.2009.05.001.

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Yang, Yangjun, Xi Li, Zonghan Liu, Xinyu Ruan, Huihui Wang, Qiang Zhang, Lu Cao, Luchen Song, Yinghong Chen, and Yi Sun. "Moderate Treadmill Exercise Alleviates NAFLD by Regulating the Biogenesis and Autophagy of Lipid Droplet." Nutrients 14, no. 22 (November 20, 2022): 4910. http://dx.doi.org/10.3390/nu14224910.

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Lipid droplet is a dynamic organelle that undergoes periods of biogenesis and degradation under environmental stimuli. The excessive accumulation of lipid droplets is the major characteristic of non-alcoholic fatty liver disease (NAFLD). Moderate aerobic exercise is a powerful intervention protecting against the progress of NAFLD. However, its impact on lipid droplet dynamics remains ambiguous. Mice were fed with 15 weeks of high-fat diet in order to induce NAFLD. Meanwhile, the mice performed 15 weeks of treadmill exercise. Our results showed that 15 weeks of regular moderate treadmill exercise alleviated obesity, insulin intolerance, hyperlipidemia, and hyperglycemia induced by HFD. Importantly, exercise improved histological phenotypes of NAFLD, including hepatic steatosis, inflammation, and locular ballooning, as well as prevented liver fat deposition and liver injury induced by HFD. Exercise reduced hepatic lipid droplet size, and moreover, it reduced PLIN2 protein level and increased PLIN3 protein level in the liver of HFD mice. Interestingly, our results showed that exercise did not significantly affect the gene expressions of DGAT1, DGAT2, or SEIPIN, which were involved in TG synthesis. However, it did reduce the expressions of FITM2, CIDEA, and FSP27, which were major involved in lipid droplet growth and budding, and lipid droplet expansion. In addition, exercise reduced ATGL protein level in HFD mice, and regulated lipophagy-related markers, including increasing ATG5, LAMP1, LAMP2, LAL, and CTSD, decreasing LC3II/I and p62, and promoting colocalization of LAMP1 with LDs. In summary, our data suggested that 15 weeks of moderate treadmill exercise was beneficial for regulating liver lipid droplet dynamics in HFD mice by inhibiting abnormal lipid droplets expansion and enhancing clearance of lipid droplets by lysosomes during the lipophagic process, which might provide highly flexible turnover for lipid mobilization and metabolism. Abbreviations: β-actin: actin beta; ATG5: autophagy related 5; LAMP2: lysosomal-associated membrane protein 2; LAMP1: lysosomal-associated membrane protein 1; SQSTM1/p62: sequestosome 1; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; ATGL: adipose triglyceride lipase; CSTD: cathepsin D; LAL: lysosomal acid lipase; DGAT1: diacylglycerol-o-acyltransferase 1; DGAT2: diacylglycerol-o-acyltransferase 2; CIDEA: cell death inducing dffa-like effector a; CIDEC/FSP27: cell death inducing dffa-like effector c; FITM2: fat storage-inducing transmembrane protein 2; PLIN2: adipose differentiation related protein; PLN3: tail-interacting protein 47; HSP90: heat shock protein 90; SREBP1c: sterol regulatory element binding protein-1c; chREBP: carbohydrate response element binding protein.

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Griffin, John D., Eloy Bejarano, Xiang-Dong Wang, and Andrew S. Greenberg. "Integrated Action of Autophagy and Adipose Tissue Triglyceride Lipase Ameliorates Diet-Induced Hepatic Steatosis in Liver-Specific PLIN2 Knockout Mice." Cells 10, no. 5 (April 25, 2021): 1016. http://dx.doi.org/10.3390/cells10051016.

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An imbalance in the storage and breakdown of hepatic lipid droplet (LD) triglyceride (TAG) leads to hepatic steatosis, a defining feature of non-alcoholic fatty liver disease (NAFLD). The two primary cellular pathways regulating hepatic TAG catabolism are lipolysis, initiated by adipose triglyceride lipase (ATGL), and lipophagy. Each of these processes requires access to the LD surface to initiate LD TAG catabolism. Ablation of perilipin 2 (PLIN2), the most abundant lipid droplet-associated protein in steatotic liver, protects mice from diet-induced NAFLD. However, the mechanisms underlaying this protection are unclear. We tested the contributions of ATGL and lipophagy mediated lipolysis to reduced hepatic TAG in mice with liver-specific PLIN2 deficiency (PLIN2LKO) fed a Western-type diet for 12 weeks. We observed enhanced autophagy in the absence of PLIN2, as determined by ex vivo p62 flux, as well as increased p62- and LC3-positive autophagic vesicles in PLIN2LKO livers and isolated primary hepatocytes. Increased levels of autophagy correlated with significant increases in cellular fatty acid (FA) oxidation in PLIN2LKO hepatocytes. We observed that inhibition of either autophagy or ATGL blunted the increased FA oxidation in PLIN2LKO hepatocytes. Additionally, combined inhibition of ATGL and autophagy reduced FA oxidation to the same extent as treatment with either inhibitor alone. In sum, these studies show that protection against NAFLD in the absence of hepatic PLIN2 is driven by the integrated actions of both ATGL and lipophagy.

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Irungbam, Karuna, Yuri Churin, Tomomitsu Matono, Jakob Weglage, Matthias Ocker, Dieter Glebe, Martin Hardt, Alica Koeppel, Martin Roderfeld, and Elke Roeb. "Cannabinoid receptor 1 knockout alleviates hepatic steatosis by downregulating perilipin 2." Laboratory Investigation 100, no. 3 (September 30, 2019): 454–65. http://dx.doi.org/10.1038/s41374-019-0327-5.

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Abstract The endocannabinoid (EC) system has been implicated in the pathogenesis of several metabolic diseases, including nonalcoholic fatty liver disease (NAFLD). With the current study we aimed to verify the modulatory effect of endocannabinoid receptor 1 (CB1)-signaling on perilipin 2 (PLIN2)-mediated lipophagy. Here, we demonstrate that a global knockout of the cannabinoid receptor 1 gene (CB1−/−) reduced the expression of the lipid droplet binding protein PLIN2 in the livers of CB1−/− and hepatitis B surface protein (HBs)-transgenic mice, which spontaneously develop hepatic steatosis. In addition, the pharmacologic activation and antagonization of CB1 in cell culture also caused an induction or reduction of PLIN2, respectively. The decreased PLIN2 expression was associated with suppressed lipogenesis and triglyceride (TG) synthesis and enhanced autophagy as shown by increased colocalization of LC3B with lysosomal-associated membrane protein 1 (LAMP1) in HBs/CB1−/− mice. The induction of autophagy was further supported by the increased expression of LAMP1 in CB1−/− and HBs/CB1−/− mice. LAMP1 and PLIN2 were co-localized in HBs/CB1−/− indicating autophagy of cytoplasmic lipid droplets (LDs) i.e., lipophagy. Lipolysis of lipid droplets was additionally indicated by elevated expression of lysosomal acid lipase. In conclusion, these results suggest that loss of CB1 signaling leads to reduced PLIN2 abundance, which triggers lipophagy. Our new findings about the association between CB1 signaling and PLIN2 may stimulate translational studies analyzing new diagnostic and therapeutic options for NAFLD.

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Sun, Jian, Yan Chen, Tao Wang, Waseem Ali, Yonggang Ma, Zongping Liu, and Hui Zou. "Role of Mitochondrial Reactive Oxygen Species-Mediated Chaperone-Mediated Autophagy and Lipophagy in Baicalin and N-Acetylcysteine Mitigation of Cadmium-Induced Lipid Accumulation in Liver." Antioxidants 13, no. 1 (January 17, 2024): 115. http://dx.doi.org/10.3390/antiox13010115.

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Cadmium (Cd) is a major health concern globally and can accumulate and cause damage in the liver for which there is no approved treatment. Baicalin and N-acetylcysteine (NAC) have been found to have protective effects against a variety of liver injuries, but it is not clear whether their combined use is effective in preventing and treating Cd-induced lipid accumulation. The study found that Cd increased the production of mitochondrial reactive oxygen species (mROS) and elevated the level of chaperone-mediated autophagy (CMA). Interestingly, mROS-mediated CMA exacerbates the Cd-induced inhibition of lipophagy. Baicalin and NAC counteracted inhibition of lipophagy by attenuating Cd-induced CMA, suggesting an interplay between CMA elevation, mitochondrial destruction, and mROS formation. Maintaining the stability of mitochondrial structure and function is essential for alleviating Cd-induced lipid accumulation in the liver. Choline is an essential component of the mitochondrial membrane and is responsible for maintaining its structure and function. Mitochondrial transcriptional factor A (TFAM) is involved in mitochondrial DNA transcriptional activation and replication. Our study revealed that the combination of baicalin and NAC can regulate choline metabolism through TFAM and thereby maintain mitochondrial structure and functionality. In summary, the combination of baicalin and NAC plays a more beneficial role in alleviating Cd-induced lipid accumulation than the drug alone, and the combination of baicalin and NAC can stabilize mitochondrial structure and function and inhibit mROS-mediated CMA through TFAM-choline, thereby promoting lipophagy to alleviate Cd-induced lipid accumulation.

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Ward, Carl, Nuria Martinez-Lopez, Elsje G. Otten, Bernadette Carroll, Dorothea Maetzel, Rajat Singh, Sovan Sarkar, and Viktor I. Korolchuk. "Autophagy, lipophagy and lysosomal lipid storage disorders." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1861, no. 4 (April 2016): 269–84. http://dx.doi.org/10.1016/j.bbalip.2016.01.006.

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Angelini, Corrado, Anna Chiara Nascimbeni, Giovanna Cenacchi, and Elisabetta Tasca. "Lipolysis and lipophagy in lipid storage myopathies." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1862, no. 7 (July 2016): 1367–73. http://dx.doi.org/10.1016/j.bbadis.2016.04.008.

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Carotti, Simone, Katia Aquilano, Francesco Valentini, Sergio Ruggiero, Francesca Alletto, Sergio Morini, Antonio Picardi, Raffaele Antonelli-Incalzi, Daniele Lettieri-Barbato, and Umberto Vespasiani-Gentilucci. "An overview of deregulated lipid metabolism in nonalcoholic fatty liver disease with special focus on lysosomal acid lipase." American Journal of Physiology-Gastrointestinal and Liver Physiology 319, no. 4 (October 1, 2020): G469—G480. http://dx.doi.org/10.1152/ajpgi.00049.2020.

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Obesity and type 2 diabetes are frequently complicated by excess fat accumulation in the liver, which is known as nonalcoholic fatty liver disease (NAFLD). In this context, liver steatosis develops as a result of the deregulation of pathways controlling de novo lipogenesis and fat catabolism. Recent evidences suggest the clinical relevance of a reduction in the activity of lysosomal acid lipase (LAL), which is a key enzyme for intracellular fat disposal, in patients with NAFLD. In this review, we provided a comprehensive overview of the critical steps in hepatic fat metabolism and alterations in these pathways in NAFLD, with a special focus on lipophagy and LAL activity. During NAFLD, hepatic fat metabolism is impaired at several levels, which is significantly contributed to by impaired lipophagy, in which reduced LAL activity may play an important role. For further research and intervention in NAFLD, targeting LAL activity may provide interesting perspectives.

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Lee, Haesu, Mi Hye Kim, Seong Chul Jin, Jae Min Han, Jun Hyuk Park, and Woong Mo Yang. "Lipolytic and Lipophagic Effects of Pinellia ternata Pharmacopuncture on Localized Adiposity." Evidence-Based Complementary and Alternative Medicine 2021 (January 6, 2021): 1–9. http://dx.doi.org/10.1155/2021/7347639.

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Localized adiposity is not only a common aesthetic issue but also a health risk factor. Pharmacopuncture can be a therapeutic option for the imbalance of regional fat distribution. The tuber of Pinellia ternata has been prescribed as antitussive and expectorant as a traditional Korean medicine. This study investigated the effects of pharmacopuncture with P. ternata water extract (PT) on localized adiposity. Male C57BL/6J mice were fed on a high-fat diet (HFD) for 6 weeks. 100 μL of 10 mg/mL of PT was injected into the left-side inguinal fat pad, while saline was injected into the right-side inguinal fat pad as self-control. Treatments were performed 3 times per week for 4 weeks. The inguinal fat weight was analyzed by dual-energy X-ray absorptiometry. PT pharmacopuncture significantly decreased the weight of the inguinal fat pad. The adipocyte size was reduced with increases of lipolytic enzymes and lipophagy-related factors by PT pharmacopuncture. There was marked inhibition of lipid accumulation content in 3T3-L1 adipocytes by PT treatment. The expressions of adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), autophagy-related gene (ATG) 5, ATG7, and LC3 were markedly increased by PT treatments in vivo and in vitro. This study suggests that pharmacopuncture of Pinellia ternata has ameliorative effects on adiposity by lipid catabolic effects via activating both lipolysis and lipophagy in a localized region.

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Li, Zhipeng, Ryan J. Schulze, Shaun G. Weller, Eugene W. Krueger, Micah B. Schott, Xiaodong Zhang, Carol A. Casey, et al. "A novel Rab10-EHBP1-EHD2 complex essential for the autophagic engulfment of lipid droplets." Science Advances 2, no. 12 (December 2016): e1601470. http://dx.doi.org/10.1126/sciadv.1601470.

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The autophagic digestion of lipid droplets (LDs) through lipophagy is an essential process by which most cells catabolize lipids as an energy source. However, the cellular machinery used for the envelopment of LDs during autophagy is poorly understood. We report a novel function for a small Rab guanosine triphosphatase (GTPase) in the recruitment of adaptors required for the engulfment of LDs by the growing autophagosome. In hepatocytes stimulated to undergo autophagy, Rab10 activity is amplified significantly, concomitant with its increased recruitment to nascent autophagic membranes at the LD surface. Disruption of Rab10 function by small interfering RNA knockdown or expression of a GTPase-defective variant leads to LD accumulation. Finally, Rab10 activation during autophagy is essential for LC3 recruitment to the autophagosome and stimulates its increased association with the adaptor protein EHBP1 (EH domain binding protein 1) and the membrane-deforming adenosine triphosphatase EHD2 (EH domain containing 2) that, together, are essential in driving the activated “engulfment” of LDs during lipophagy in hepatocytes.

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Thomes, Paul G., Karuna Rasineni, Li Yang, Terrence M. Donohue, Jacy L. Kubik, Mark A. McNiven, and Carol A. Casey. "Ethanol withdrawal mitigates fatty liver by normalizing lipid catabolism." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 4 (April 1, 2019): G509—G518. http://dx.doi.org/10.1152/ajpgi.00376.2018.

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We are investigating the changes in hepatic lipid catabolism that contribute to alcohol-induced fatty liver. Following chronic ethanol (EtOH) exposure, abstinence from alcohol resolves steatosis. Here, we investigated the hepatocellular events that lead to this resolution by quantifying specific catabolic parameters that returned to control levels after EtOH was withdrawn. We hypothesized that, after its chronic consumption, EtOH withdrawal reactivates lipid catabolic processes that restore lipostasis. Male Wistar rats were fed control and EtOH liquid diets for 6 wk. Randomly chosen EtOH-fed rats were then fed control diet for 7 days. Liver triglycerides (TG), lipid peroxides, key markers of fatty acid (FA) metabolism, lipophagy, and autophagy were quantified. Compared with controls, EtOH-fed rats had higher hepatic triglycerides, lipid peroxides, and serum free fatty acids (FFA). The latter findings were associated with higher levels of FA transporters (FATP 2, 4, and 5) but lower quantities of peroxisome proliferator-activated receptor-α (PPAR-α), which governs FA oxidation. EtOH-fed animals also had lower nuclear levels of the autophagy-regulating transcription factor EB (TFEB), associated with lower hepatic lipophagy and autophagy. After EtOH-fed rats were refed control diet for 7 days, their serum FFA levels and those of FATPs fell to control (normal) levels, whereas PPAR-α levels rose to normal. Hepatic TG and malondialdehyde levels in EtOH-withdrawn rats declined to near control levels. EtOH withdrawal restored nuclear TFEB content, hepatic lipophagy, and autophagy activity to control levels. EtOH withdrawal reversed aberrant FA metabolism and restored lysosomal function to promote resolution of alcohol-induced fatty liver. NEW & NOTEWORTHY Here, using an animal model, we show mechanisms of reversal of fatty liver and injury following EtOH withdrawal. Our data indicate that reactivation of autophagy and lysosome function through the restoration of transcription factor EB contribute to reversal of fatty liver and injury following EtOH withdrawal.

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Martinez-Lopez, Nuria, and Rajat Singh. "Telemetric control of peripheral lipophagy by hypothalamic autophagy." Autophagy 12, no. 8 (June 24, 2016): 1404–5. http://dx.doi.org/10.1080/15548627.2016.1185578.

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Liu, K., and M. J. Czaja. "Regulation of lipid stores and metabolism by lipophagy." Cell Death & Differentiation 20, no. 1 (May 18, 2012): 3–11. http://dx.doi.org/10.1038/cdd.2012.63.

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Wang, Jing, Si-Lan Han, Ling-Yu Li, Dong-Liang Lu, Samwel Mchele Limbu, Dong-Liang Li, Mei-Ling Zhang, and Zhen-Yu Du. "Lipophagy is essential for lipid metabolism in fish." Science Bulletin 63, no. 14 (July 2018): 879–82. http://dx.doi.org/10.1016/j.scib.2018.05.026.

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Schulze, Ryan J., Aishwarya Sathyanarayan, and Douglas G. Mashek. "Breaking fat: The regulation and mechanisms of lipophagy." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1862, no. 10 (October 2017): 1178–87. http://dx.doi.org/10.1016/j.bbalip.2017.06.008.

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Leopold, Christina, Douglas Mashek, and Dagmar Kratky. "The role of lipophagy in hepatic energy metabolism." Atherosclerosis 263 (August 2017): e13-e14. http://dx.doi.org/10.1016/j.atherosclerosis.2017.06.071.

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Journal articles on the topic 'Lipophagie'

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