Acyl-CoA-Binding Protein Is a Lipogenic Factor that Triggers Food Intake and Obesity

Pedro, José Manuel Bravo-San; Sica, Valentina; Martins, Isabelle; Pol, Jonathan; Loos, Friedemann; Maiuri, Maria Chiara; Durand, Sylvère; Bossut, Noëlie; Aprahamian, Fanny; Anagnostopoulos, Gerasimos; Niso-Santano, Mireia; Aranda, Fernando; Ramírez‐Pardo, Ignacio; Lallement, Justine; Denom, Jessica; Boedec, Erwan; Gorwood, Philip; Ramoz, Nicolás; Clément, Karine; Pelloux, Véronique; Alili, Rohia; Pattou, François; Raverdy, Violeta; Caïazzo, Robert; Denis, Raphaël; Boya, Patricia; Galluzzi, Lorenzo; Madeo, Frank; Migrenne-Li, Stéphanie; Cruciani-Guglielmacci, Céline; Tavernarakis, Nektarios; López-Otı́n, Carlos; Magnan, Christophe; Kroemer, Guido

doi:10.1016/j.cmet.2019.07.010

Cited by 73 publications

(173 citation statements)

References 52 publications

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“…The cells respond by exporting functionally active antioxidants and Acb1. Although Acb1 is not known as an antioxidant, it is emerging as an important lipogenic signaling factor secreted upon starvation in metazoans (Bravo-San Pedro et al, 2019; Ryuda et al, 2011). We suggest ROS produced during starvation acts as a signal to release a variety of proteins that include antioxidants in order to maintain cells in a metabolically active, but otherwise dormant form (e.g., sporulation in yeast and Dictyostelium discoideum ; Charmpilas et al, 2020; Duran et al, 2010; Kinseth et al, 2007; Manjithaya et al, 2010), until their return to normal growth conditions.…”

Section: Resultsmentioning

confidence: 99%

“…The secreted Acb1 in lower eukaryotes, such as yeast and slime mold, functions in signaling and regulating the starvation-induced cell differentiation program of sporulation (Anjard et al, 1998; Charmpilas et al, 2020; Kinseth et al, 2007; Manjithaya et al, 2010). In the human brain, the Acb1 orthologue ACBP (also known as Diazepam binding inhibitor) modulates GABA (γ-Aminobutyric Acid) receptor signaling, and, more recently in whole animals, ACBP has been identified as an important lipogenic signaling factor (Costa and Guidotti, 1991; Gandolfo et al, 2001; Bravo-San Pedro et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

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Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1

Cruz-García

Brouwers

Malhotra

et al. 2020

Journal of Cell Biology

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Nutrient deprivation triggers the release of signal-sequence–lacking Acb1 and the antioxidant superoxide dismutase 1 (SOD1). We now report that secreted SOD1 is functionally active and accompanied by export of other antioxidant enzymes such as thioredoxins (Trx1 and Trx2) and peroxiredoxin Ahp1 in a Grh1-dependent manner. Our data reveal that starvation leads to production of nontoxic levels of reactive oxygen species (ROS). Treatment of cells with N-acetylcysteine (NAC), which sequesters ROS, prevents antioxidants and Acb1 secretion. Starved cells lacking Grh1 are metabolically active, but defective in their ability to regrow upon return to growth conditions. Treatment with NAC restored the Grh1-dependent effect of starvation on cell growth. In sum, starvation triggers ROS production and cells respond by secreting antioxidants and the lipogenic signaling protein Acb1. We suggest that starvation-specific unconventional secretion of antioxidants and Acb1-like activities maintain cells in a form necessary for growth upon their eventual return to normal conditions.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1

Cruz-García

Brouwers

Malhotra

et al. 2020

Journal of Cell Biology

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“…ACBP can modulate dietary behavior by regulating the glucose level and lipid metabolism in the body [44]. A recent study has shown that by inserting monoclonal anti-ACBP antibodies into mice to neutralize the extracellular pool of ACBP, the food intake of mice after starvation was reduced, and the plasma glucose levels were significantly increased.…”

Section: The Influence Of Acbp On Obesitymentioning

confidence: 99%

“…A recent study has shown that by inserting monoclonal anti-ACBP antibodies into mice to neutralize the extracellular pool of ACBP, the food intake of mice after starvation was reduced, and the plasma glucose levels were significantly increased. Furthermore, when tamoxifen (a method that is based on TAM induced ACBP excision) was injected into mice to remove ACBP in vivo, researchers found that the mice could still maintain normal blood glucose levels in the cells and that the metabolic changes in the plasma and brown adipose tissue were similar to those of normal mice after starvation [44]. Some research has reported that hunger causes the autophagy-dependent release of ACBP from cells, thereby leading to an increase in plasma ACBP concentrations.…”

Section: The Influence Of Acbp On Obesitymentioning

confidence: 99%

“…For example, the ACBP family proteins in A. oryzae and yeast can combine a variety of different acyl-CoA esters, which play an important role in the normal physiological function of the cell [68]. The unconventional secretion of ACBP exists in A. oryzae, yeast, and some mammals, but its potential mechanism remains to be explored [44,54,69]. ACBP in M. rubers can affect MPs synthesis; however, the mechanism remains to be explored [13].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

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Advances in Understanding the Acyl-CoA-Binding Protein in Plants, Mammals, Yeast, and Filamentous Fungi

Qiu

Zeng

2020

JoF

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Acyl-CoA-binding protein (ACBP) is an important protein with a size of about 10 kDa. It has a high binding affinity for C12–C22 acyl-CoA esters and participates in lipid metabolism. ACBP and its family of proteins have been found in all eukaryotes and some prokaryotes. Studies have described the function and structure of ACBP family proteins in mammals (such as humans and mice), plants (such as Oryza sativa, Arabidopsis thaliana, and Hevea brasiliensis) and yeast. However, little information on the structure and function of the proteins in filamentous fungi has been reported. This article concentrates on recent advances in the research of the ACBP family proteins in plants and mammals, especially in yeast, filamentous fungi (such as Monascus ruber and Aspergillus oryzae), and fungal pathogens (Aspergillus flavus, Cryptococcus neoformans). Furthermore, we discuss some problems in the field, summarize the binding characteristics of the ACBP family proteins in filamentous fungi and yeast, and consider the future of ACBP development.

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The role of autophagy in bone homeostasis

Guo

Yang

et al. 2021

Journal Cellular Physiology

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Autophagy is an evolutionarily conserved intracellular process and is considered one of the main catabolism pathways. In the process of autophagy, cells are digested nonselectively or selectively to recover nutrients and energy, so it is regarded as an antiaging process. In addition to the essential role of autophagy in cellular homeostasis, autophagy is a stress response mechanism for cell survival. Here, we review recent literature describing the pathway of autophagy and its role in different bone cell types, including osteoblasts, osteoclasts, and osteocytes. Also discussed is the mechanism of autophagy in bone diseases associated with bone homeostasis, including osteoporosis and Paget's disease. Finally, we discuss the application of autophagy regulators in bone diseases. This review aims to introduce autophagy, summarize the understanding of its relevance in bone physiology, and discuss its role and therapeutic potential in the pathogenesis of bone diseases such as osteoporosis.

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Acyl-CoA-Binding Protein Is a Lipogenic Factor that Triggers Food Intake and Obesity

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Cited by 73 publications

References 52 publications

Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1

Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1

Advances in Understanding the Acyl-CoA-Binding Protein in Plants, Mammals, Yeast, and Filamentous Fungi

The role of autophagy in bone homeostasis

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