Liver ACOX1 regulates levels of circulating lipids that promote metabolic health through adipose remodeling

The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-med...

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Published inNature communications Vol. 15; no. 1; pp. 4214 - 16
Main Authors Lu, Dongliang, He, Anyuan, Tan, Min, Mrad, Marguerite, El Daibani, Amal, Hu, Donghua, Liu, Xuejing, Kleiboeker, Brian, Che, Tao, Hsu, Fong-Fu, Bambouskova, Monika, Semenkovich, Clay F., Lodhi, Irfan J.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 17.05.2024
Nature Publishing Group
Nature Portfolio
Subjects
13
13/31
14
14/19
38/91
631/443/319/1642/393
631/443/319/2723
631/80/86/2365
64/60
692/4017
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Acyl-CoA Oxidase - genetics
Acyl-CoA Oxidase - metabolism
Adipocytes
Adipose tissue
Adipose Tissue - metabolism
Animals
Biogenesis
Body fat
Browning
Coenzyme A
Coenzymes
Diet, High-Fat
Energy Metabolism
Enzymes
Fatty acids
Fatty Acids - metabolism
Gene expression
Homeostasis
Humanities and Social Sciences
Insulin
Insulin Resistance
Lipid Metabolism
Lipids
Liver
Liver - metabolism
Male
Metabolic disorders
Metabolic rate
Metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
multidisciplinary
Obesity
Obesity - genetics
Obesity - metabolism
Oxidation
Oxidation-Reduction
Physiology
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Science
Science (multidisciplinary)
Substrates
Translocation
Online AccessGet full text

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Abstract The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 ( Acox1 -LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1 -LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω−3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders. The peroxisomal β-oxidation enzyme ACOX1 increases in liver with obesity, but the physiological significance is unclear. Here, the authors show that liver-specific knockout of Acox1 leads to accumulation of omega-3 VLCFAs that promote metabolic health through activation of GPR120 in adipose tissue.
AbstractList The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 ( Acox1 -LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1 -LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω−3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders. The peroxisomal β-oxidation enzyme ACOX1 increases in liver with obesity, but the physiological significance is unclear. Here, the authors show that liver-specific knockout of Acox1 leads to accumulation of omega-3 VLCFAs that promote metabolic health through activation of GPR120 in adipose tissue.
The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1-LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω-3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.
The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1-LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω-3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1-LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω-3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.
Abstract The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 ( Acox1 -LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1 -LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω−3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.
Abstract The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1-LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω−3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.
The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1-LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω−3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.The peroxisomal β-oxidation enzyme ACOX1 increases in liver with obesity, but the physiological significance is unclear. Here, the authors show that liver-specific knockout of Acox1 leads to accumulation of omega-3 VLCFAs that promote metabolic health through activation of GPR120 in adipose tissue.
ArticleNumber 4214
Author Che, Tao
Liu, Xuejing
Lodhi, Irfan J.
Lu, Dongliang
Tan, Min
El Daibani, Amal
Kleiboeker, Brian
He, Anyuan
Bambouskova, Monika
Hu, Donghua
Mrad, Marguerite
Hsu, Fong-Fu
Semenkovich, Clay F.
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0000-0002-6246-9862
0000-0002-1620-3027
0000-0002-3196-1803
0000-0002-8022-4092
0000-0003-1163-1871
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11101658/
PMID 38760332
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crossref_primary_10_1038_s41467_024_48471_2
pubmed_primary_38760332
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PublicationCentury 2000
PublicationDate 2024-05-17
PublicationDateYYYYMMDD 2024-05-17
PublicationDate_xml – month: 05
  year: 2024
  text: 2024-05-17
  day: 17
PublicationDecade 2020
PublicationPlace London
PublicationPlace_xml – name: London
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PublicationTitle Nature communications
PublicationTitleAbbrev Nat Commun
PublicationTitleAlternate Nat Commun
PublicationYear 2024
Publisher Nature Publishing Group UK
Nature Publishing Group
Nature Portfolio
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
– name: Nature Portfolio
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Snippet The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA),...
Abstract The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids...
Abstract The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids...
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StartPage 4214
SubjectTerms 13
13/31
14
14/19
38/91
631/443/319/1642/393
631/443/319/2723
631/80/86/2365
64/60
692/4017
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96/95
Acyl-CoA Oxidase - genetics
Acyl-CoA Oxidase - metabolism
Adipocytes
Adipose tissue
Adipose Tissue - metabolism
Animals
Biogenesis
Body fat
Browning
Coenzyme A
Coenzymes
Diet, High-Fat
Energy Metabolism
Enzymes
Fatty acids
Fatty Acids - metabolism
Gene expression
Homeostasis
Humanities and Social Sciences
Insulin
Insulin Resistance
Lipid Metabolism
Lipids
Liver
Liver - metabolism
Male
Metabolic disorders
Metabolic rate
Metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
multidisciplinary
Obesity
Obesity - genetics
Obesity - metabolism
Oxidation
Oxidation-Reduction
Physiology
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Science
Science (multidisciplinary)
Substrates
Translocation
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Title Liver ACOX1 regulates levels of circulating lipids that promote metabolic health through adipose remodeling
URI https://link.springer.com/article/10.1038/s41467-024-48471-2
https://www.ncbi.nlm.nih.gov/pubmed/38760332
https://www.proquest.com/docview/3056069741
https://www.proquest.com/docview/3056670202/abstract/
https://pubmed.ncbi.nlm.nih.gov/PMC11101658
https://doaj.org/article/b6905b9dcfe54890b07750ac3d66d2a7
Volume 15
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