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Hyötyläinen, TuuliaORCID iD iconorcid.org/0000-0002-4382-4355
Publications (10 of 104) Show all publications
Salonurmi, T., Nabil, H., Ronkainen, J., Hyötyläinen, T., Hautajärvi, H., Savolainen, M. J., . . . Hukkanen, J. (2020). 4β-Hydroxycholesterol Signals From the Liver to Regulate Peripheral Cholesterol Transporters.. Frontiers in Pharmacology, 11, Article ID 361.
Open this publication in new window or tab >>4β-Hydroxycholesterol Signals From the Liver to Regulate Peripheral Cholesterol Transporters.
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2020 (English)In: Frontiers in Pharmacology, ISSN 1663-9812, E-ISSN 1663-9812, Vol. 11, article id 361Article in journal (Refereed) Published
Abstract [en]

Activation of pregnane X receptor (PXR) elevates circulating 4β-hydroxycholesterol (4βHC), an agonist of liver X receptor (LXR). PXR may also regulate 25-hydroxycholesterol and 27-hydroxycholesterol. Our aim was to elucidate the roles of PXR and oxysterols in the regulation of cholesterol transporters. We measured oxysterols in serum of volunteers dosed with PXR agonist rifampicin 600 mg/day versus placebo for a week and analyzed the expression of cholesterol transporters in mononuclear cells. The effect of 4βHC on the transport of cholesterol and the expression of cholesterol transporters was studied in human primary monocyte-derived macrophages and foam cells in vitro. The expression of cholesterol transporters was measured also in rat tissues after dosing with a PXR agonist. The levels of 4βHC were elevated, while 25-hydroxycholesterol and 27-hydroxycholesterol remained unchanged in volunteers dosed with rifampicin. The expression of ATP binding cassette transporter A1 (ABCA1) was induced in human mononuclear cells in vivo. The influx of cholesterol was repressed by 4βHC, as was the expression of influx transporter lectin-like oxidized LDL receptor-1 in vitro. The cholesterol efflux and the expression of efflux transporters ABCA1 and ABCG1 were induced. The expression of inducible degrader of the LDL receptor was induced. In rats, PXR agonist increased circulating 4βHC and expression of LXR targets in peripheral tissues, especially ABCA1 and ABCG1 in heart. In conclusion, PXR activation-elevated 4βHC is a signaling molecule that represses cholesterol influx and induces efflux. The PXR-4βHC-LXR pathway could link the hepatic xenobiotic exposure and the regulation of cholesterol transport in peripheral tissues.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2020
Keywords
4β-hydroxycholesterol, ATP binding cassette transporter A1, ATP binding cassette transporter G1, inducible degrader of the LDL receptor, lectin-like oxidized LDL receptor-1, liver X receptor, pregnane X receptor
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:oru:diva-81158 (URN)10.3389/fphar.2020.00361 (DOI)000525643900001 ()32292343 (PubMedID)2-s2.0-85083268495 (Scopus ID)
Funder
Novo Nordisk, NNF14OC0010653 NNF15OC0015846
Note

Funding Agencies:

Academy of Finland 286743 276747

Duodecim Society of Oulu  

Finnish Medical Foundation  

Finnish Foundation for Cardiovascular Research  

Northern Finland Health Care Support Foundation  

Diabetes Research Foundation 

Available from: 2020-04-16 Created: 2020-04-16 Last updated: 2020-04-24Bibliographically approved
Luukkonen, P. K., Tukiainen, T., Juuti, A., Sammalkorpi, H., Haridas, P. A., Niemelä, O., . . . Yki-Järvinen, H. (2020). Hydroxysteroid 17-β dehydrogenase 13 variant increases phospholipids and protects against fibrosis in nonalcoholic fatty liver disease. JCI Insight, 5(5), Article ID 132158.
Open this publication in new window or tab >>Hydroxysteroid 17-β dehydrogenase 13 variant increases phospholipids and protects against fibrosis in nonalcoholic fatty liver disease
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2020 (English)In: JCI Insight, ISSN 2379-3708, Vol. 5, no 5, article id 132158Article in journal (Refereed) Published
Abstract [en]

Carriers of the hydroxysteroid 17-β dehydrogenase 13 (HSD17B13) gene variant (rs72613567:TA) have a reduced risk of NASH and cirrhosis but not steatosis. We determined its effect on liver histology, lipidome, and transcriptome using ultra performance liquid chromatography-mass spectrometry and RNA-seq. In carriers and noncarriers of the gene variant, we also measured pathways of hepatic fatty acids (de novo lipogenesis [DNL] and adipose tissue lipolysis [ATL] using 2H2O and 2H-glycerol) and insulin sensitivity using 3H-glucose and euglycemic-hyperinsulinemic clamp) and plasma cytokines. Carriers and noncarriers had similar age, sex and BMI. Fibrosis was significantly less frequent while phospholipids, but not other lipids, were enriched in the liver in carriers compared with noncarriers. Expression of 274 genes was altered in carriers compared with noncarriers, consisting predominantly of downregulated inflammation-related gene sets. Plasma IL-6 concentrations were lower, but DNL, ATL and hepatic insulin sensitivity were similar between the groups. In conclusion, carriers of the HSD17B13 variant have decreased fibrosis and expression of inflammation-related genes but increased phospholipids in the liver. These changes are not secondary to steatosis, DNL, ATL, or hepatic insulin sensitivity. The increase in phospholipids and decrease in fibrosis are opposite to features of choline-deficient models of liver disease and suggest HSD17B13 as an attractive therapeutic target.

Place, publisher, year, edition, pages
American Society for Clinical Investigation, 2020
Keywords
Fibrosis, Genetic variation, Hepatitis, Hepatology, Metabolism
National Category
Medical Genetics
Identifiers
urn:nbn:se:oru:diva-80607 (URN)10.1172/jci.insight.132158 (DOI)000519997400006 ()32161197 (PubMedID)2-s2.0-85082739096 (Scopus ID)
Funder
Novo Nordisk
Note

Funding Agencies:

Elucidating Pathways of Steatohepatitis consortium - Horizon 2020 Framework Program of the European Union 634413

Innovative Medicines Initiative 2 Joint Undertaking 777377

European Union (EU)

European Federation of Pharmaceutical Industries and Associations  

Academy of Finland

EVO  

Sigrid Juselius Foundation

Ministry of Education, Universities and Research  

Italian National Research Council

British Heart Foundation Senior Fellowship in Basic Science  FS/15/56/31645

Jalmari and Rauha Ahokas Foundation  

Paulo Foundation 

Available from: 2020-03-13 Created: 2020-03-13 Last updated: 2020-05-12Bibliographically approved
Thomas, I., Dickens, A. M., Posti, J. P., Mohammadian, M., Ledig, C., Takala, R. S. K., . . . Oresic, M. (2020). Integrative Analysis of Circulating Metabolite Profiles and Magnetic Resonance Imaging Metrics in Patients with Traumatic Brain Injury. International Journal of Molecular Sciences, 21(4), Article ID E1395.
Open this publication in new window or tab >>Integrative Analysis of Circulating Metabolite Profiles and Magnetic Resonance Imaging Metrics in Patients with Traumatic Brain Injury
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2020 (English)In: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 21, no 4, article id E1395Article in journal (Refereed) Published
Abstract [en]

Recent evidence suggests that patients with traumatic brain injuries (TBIs) have a distinct circulating metabolic profile. However, it is unclear if this metabolomic profile corresponds to changes in brain morphology as observed by magnetic resonance imaging (MRI). The aim of this study was to explore how circulating serum metabolites, following TBI, relate to structural MRI (sMRI) findings. Serum samples were collected upon admission to the emergency department from patients suffering from acute TBI and metabolites were measured using mass spectrometry-based metabolomics. Most of these patients sustained a mild TBI. In the same patients, sMRIs were taken and volumetric data were extracted (138 metrics). From a pool of 203 eligible screened patients, 96 met the inclusion criteria for this study. Metabolites were summarized as eight clusters and sMRI data were reduced to 15 independent components (ICs). Partial correlation analysis showed that four metabolite clusters had significant associations with specific ICs, reflecting both the grey and white matter brain injury. Multiple machine learning approaches were then applied in order to investigate if circulating metabolites could distinguish between positive and negative sMRI findings. A logistic regression model was developed, comprised of two metabolic predictors (erythronic acid and myo-inositol), which, together with neurofilament light polypeptide (NF-L), discriminated positive and negative sMRI findings with an area under the curve of the receiver-operating characteristic of 0.85 (specificity = 0.89, sensitivity = 0.65). The results of this study show that metabolomic analysis of blood samples upon admission, either alone or in combination with protein biomarkers, can provide valuable information about the impact of TBI on brain structural changes.

Place, publisher, year, edition, pages
MDPI, 2020
Keywords
Blood biomarkers, magnetic resonance imaging, mass spectrometry, metabolomics, traumatic brain injury
National Category
Neurosciences
Identifiers
urn:nbn:se:oru:diva-80215 (URN)10.3390/ijms21041395 (DOI)000522524400222 ()32092929 (PubMedID)2-s2.0-85079887972 (Scopus ID)
Funder
Swedish Research Council, 2018-02629
Note

Funding Agencies:

European Union (EU) 270259

GE-NFL Head Health Challenge I Award 7620

Academy of Finland 17379

Emil Aaltonen Foundation  

Finnish Brain Foundation  

Maire Taponen Foundation 

Available from: 2020-02-27 Created: 2020-02-27 Last updated: 2020-04-20Bibliographically approved
Luukkonen, P. K., Juuti, A., Sammalkorpi, H., Penttilä, A. K., Oresic, M., Hyötyläinen, T., . . . Yki-Järvinen, H. (2020). MARC1 variant rs2642438 increases hepatic phosphatidylcholines and decreases severity of non-alcoholic fatty liver disease in humans [Letter to the editor]. Journal of Hepatology
Open this publication in new window or tab >>MARC1 variant rs2642438 increases hepatic phosphatidylcholines and decreases severity of non-alcoholic fatty liver disease in humans
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2020 (English)In: Journal of Hepatology, ISSN 0168-8278, E-ISSN 1600-0641Article in journal, Letter (Refereed) Epub ahead of print
Place, publisher, year, edition, pages
Elsevier, 2020
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:oru:diva-82232 (URN)10.1016/j.jhep.2020.04.021 (DOI)32471727 (PubMedID)
Available from: 2020-05-31 Created: 2020-05-31 Last updated: 2020-06-04Bibliographically approved
Sen, P., Dickens, A. M., López-Bascón, M. A., Lindeman, T., Kemppainen, E., Lamichhane, S., . . . Oresic, M. (2020). Metabolic alterations in immune cells associate with progression to type 1 diabetes. Diabetologia, 63(5), 1017-1031
Open this publication in new window or tab >>Metabolic alterations in immune cells associate with progression to type 1 diabetes
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2020 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 63, no 5, p. 1017-1031Article in journal (Refereed) Published
Abstract [en]

AIMS/HYPOTHESIS: Previous metabolomics studies suggest that type 1 diabetes is preceded by specific metabolic disturbances. The aim of this study was to investigate whether distinct metabolic patterns occur in peripheral blood mononuclear cells (PBMCs) of children who later develop pancreatic beta cell autoimmunity or overt type 1 diabetes.

METHODS: In a longitudinal cohort setting, PBMC metabolomic analysis was applied in children who (1) progressed to type 1 diabetes (PT1D, n = 34), (2) seroconverted to ≥1 islet autoantibody without progressing to type 1 diabetes (P1Ab, n = 27) or (3) remained autoantibody negative during follow-up (CTRL, n = 10).

RESULTS: During the first year of life, levels of most lipids and polar metabolites were lower in the PT1D and P1Ab groups compared with the CTRL group. Pathway over-representation analysis suggested alanine, aspartate, glutamate, glycerophospholipid and sphingolipid metabolism were over-represented in PT1D. Genome-scale metabolic models of PBMCs during type 1 diabetes progression were developed by using publicly available transcriptomics data and constrained with metabolomics data from our study. Metabolic modelling confirmed altered ceramide pathways, known to play an important role in immune regulation, as specifically associated with type 1 diabetes progression.

CONCLUSIONS/INTERPRETATION: Our data suggest that systemic dysregulation of lipid metabolism, as observed in plasma, may impact the metabolism and function of immune cells during progression to overt type 1 diabetes.

DATA AVAILABILITY: The GEMs for PBMCs have been submitted to BioModels (www.ebi.ac.uk/biomodels/), under accession number MODEL1905270001. The metabolomics datasets and the clinical metadata generated in this study were submitted to MetaboLights (https://www.ebi.ac.uk/metabolights/), under accession number MTBLS1015.

Place, publisher, year, edition, pages
Springer, 2020
Keywords
Birth cohort, Ceramides, Genome-scale metabolic modelling, Lipidomics, Metabolomics, Peripheral blood mononuclear cells, Sphingolipid metabolism, Type 1 diabetes
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:oru:diva-79927 (URN)10.1007/s00125-020-05107-6 (DOI)000516166400001 ()32043185 (PubMedID)2-s2.0-85079460322 (Scopus ID)
Funder
Novo Nordisk, NNF18OC0034506
Note

Funding Agencies:

Juvenile Diabetes Research Foundation 2-SRA-2014-159-Q-R

Academy of Finland 250114

Academy of Finland (Personalised Health 2014 programme project)  292568

FPU scholarship from the Spanish Ministry of Education, Culture and Sport  FPU15/02373

Available from: 2020-02-20 Created: 2020-02-20 Last updated: 2020-05-04Bibliographically approved
Fart, F., Salihovic, S., McGlinchey, A. J., Oresic, M., Halfvarson, J., Hyötyläinen, T. & Schoultz, I. (2020). Per- and polyfluoroalkyl substances (PFAS) are significantly increased in patients with late-onset of ulcerative colitis. Journal of Crohn's & Colitis, 14(Suppl. 1), S138-S139
Open this publication in new window or tab >>Per- and polyfluoroalkyl substances (PFAS) are significantly increased in patients with late-onset of ulcerative colitis
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2020 (English)In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 14, no Suppl. 1, p. S138-S139Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Oxford University Press, 2020
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:oru:diva-81135 (URN)10.1093/ecco-jcc/jjz203.147 (DOI)000518803400149 ()
Available from: 2020-04-14 Created: 2020-04-14 Last updated: 2020-04-14Bibliographically approved
Qadri, S., Lallukka-Brück, S., Luukkonen, P. K., Zhou, Y., Gastaldelli, A., Orho-Melander, M., . . . Yki-Järvinen, H. (2020). The PNPLA3-I148M variant increases polyunsaturated triglycerides in human adipose tissue. Liver international (Print)
Open this publication in new window or tab >>The PNPLA3-I148M variant increases polyunsaturated triglycerides in human adipose tissue
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2020 (English)In: Liver international (Print), ISSN 1478-3223, E-ISSN 1478-3231Article in journal (Refereed) Epub ahead of print
Abstract [en]

BACKGROUND & AIMS: The I148M variant in PNPLA3 is the major genetic risk factor for non-alcoholic fatty liver disease (NAFLD). The liver is enriched with polyunsaturated triglycerides (PUFA-TGs) in PNPLA3-I148M carriers. Gene expression data indicate that PNPLA3 is liver-specific in humans, but whether it functions in adipose tissue (AT) is unknown. We investigated whether PNPLA3-I148M modifies AT metabolism in human NAFLD.

METHODS: Profiling of the AT lipidome and fasting serum non-esterified fatty acid (NEFA) composition were conducted in 125 volunteers (PNPLA3148MM/MI , n=63; PNPLA3148II , n=62). AT fatty acid composition was determined in 50 volunteers homozygous for the variant (PNPLA3148MM , n=25) or lacking the variant (PNPLA3148II , n=25). Whole-body insulin sensitivity of lipolysis was determined using [2 H5 ]glycerol, and PNPLA3 mRNA and protein levels were measured in subcutaneous AT and liver biopsies in a subset of the volunteers.

RESULTS: PUFA-TGs were significantly increased in AT in carriers versus non-carriers of PNPLA3-I148M. The variant did not alter the rate of lipolysis or the composition of fasting serum NEFAs. PNPLA3 mRNA was 33-fold higher in the liver than in AT (p<0.0001). In contrast, PNPLA3 protein levels per tissue protein were 3-fold higher in AT than the liver (p<0.0001) and 9-fold higher when related to whole-body AT and liver tissue masses (p<0.0001).

CONCLUSIONS: Contrary to previous assumptions, PNPLA3 is highly abundant in AT. PNPLA3-I148M locally remodels AT TGs to become polyunsaturated as it does in the liver, without affecting lipolysis or composition of serum NEFAs. Changes in AT metabolism do not contribute to NAFLD in PNPLA3-I148M carriers.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2020
Keywords
Adipose tissue, fatty acids, lipidomics, lipolysis, non-alcoholic fatty liver disease, triglycerides
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:oru:diva-81765 (URN)10.1111/liv.14507 (DOI)000533393400001 ()32386450 (PubMedID)
Funder
Novo Nordisk
Note

Funding Agencies:

European Union (EU) 634413777377-2

British Heart Foundation FS/15/56/31645

Sigrid Juselius Foundation

Academy of Finland 309263

EVO

Available from: 2020-05-11 Created: 2020-05-11 Last updated: 2020-05-29Bibliographically approved
Lamichhane, S., Kemppainen, E., Trošt, K., Siljander, H., Hyöty, H., Ilonen, J., . . . Oresic, M. (2019). Circulating metabolites in progression to islet autoimmunity and type 1 diabetes. Diabetologia, 62(12), 2287-2297
Open this publication in new window or tab >>Circulating metabolites in progression to islet autoimmunity and type 1 diabetes
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2019 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 62, no 12, p. 2287-2297Article in journal (Refereed) Published
Abstract [en]

AIMS/HYPOTHESIS: Metabolic dysregulation may precede the onset of type 1 diabetes. However, these metabolic disturbances and their specific role in disease initiation remain poorly understood. In this study, we examined whether children who progress to type 1 diabetes have a circulatory polar metabolite profile distinct from that of children who later progress to islet autoimmunity but not type 1 diabetes and a matched control group.

METHODS: We analysed polar metabolites from 415 longitudinal plasma samples in a prospective cohort of children in three study groups: those who progressed to type 1 diabetes; those who seroconverted to one islet autoantibody but not to type 1 diabetes; and an antibody-negative control group. Metabolites were measured using two-dimensional GC high-speed time of flight MS.

RESULTS: In early infancy, progression to type 1 diabetes was associated with downregulated amino acids, sugar derivatives and fatty acids, including catabolites of microbial origin, compared with the control group. Methionine remained persistently upregulated in those progressing to type 1 diabetes compared with the control group and those who seroconverted to one islet autoantibody. The appearance of islet autoantibodies was associated with decreased glutamic and aspartic acids.

CONCLUSIONS/INTERPRETATION: Our findings suggest that children who progress to type 1 diabetes have a unique metabolic profile, which is, however, altered with the appearance of islet autoantibodies. Our findings may assist with early prediction of the disease.

Place, publisher, year, edition, pages
Springer, 2019
Keywords
Beta cell autoimmunity, Metabolomics, Type 1 diabetes
National Category
Other Basic Medicine Endocrinology and Diabetes
Identifiers
urn:nbn:se:oru:diva-75892 (URN)10.1007/s00125-019-04980-0 (DOI)000500998600012 ()31444528 (PubMedID)2-s2.0-85070968581 (Scopus ID)
Note

Funding Agencies:

Juvenile Diabetes Research Foundation 4-1998-2744-1999-731 4-2001-4352-SRA-2014-159-Q-R

Special research funds for Oulu University Hospital in Finland  

Special research funds for Tampere University Hospital in Finland  

Special research funds for Turku University Hospital in Finland  

Academy of Finland 250114

Available from: 2019-08-26 Created: 2019-08-26 Last updated: 2019-12-19Bibliographically approved
Lamichhane, S., Ahonen, L., Dyrlund, T. S., Dickens, A. M., Siljander, H., Hyöty, H., . . . Oresic, M. (2019). Cord-Blood Lipidome in Progression to Islet Autoimmunity and Type 1 Diabetes. Biomolecules, 9(1), Article ID E33.
Open this publication in new window or tab >>Cord-Blood Lipidome in Progression to Islet Autoimmunity and Type 1 Diabetes
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2019 (English)In: Biomolecules, E-ISSN 2218-273X, Vol. 9, no 1, article id E33Article in journal (Refereed) Published
Abstract [en]

Previous studies suggest that children who progress to type 1 diabetes (T1D) later in life already have an altered serum lipid molecular profile at birth. Here, we compared cord blood lipidome across the three study groups: children who progressed to T1D (PT1D; n = 30), children who developed at least one islet autoantibody but did not progress to T1D during the follow-up (P1Ab; n = 33), and their age-matched controls (CTR; n = 38). We found that phospholipids, specifically sphingomyelins, were lower in T1D progressors when compared to P1Ab and the CTR. Cholesterol esters remained higher in PT1D when compared to other groups. A signature comprising five lipids was predictive of the risk of progression to T1D, with an area under the receiver operating characteristic curve (AUROC) of 0.83. Our findings provide further evidence that the lipidomic profiles of newborn infants who progress to T1D later in life are different from lipidomic profiles in P1Ab and CTR.

Place, publisher, year, edition, pages
MDPI, 2019
Keywords
Autoimmunity, cord blood, lipidomics, metabolomics, type 1 diabetes
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:oru:diva-71853 (URN)10.3390/biom9010033 (DOI)000458051700033 ()30669674 (PubMedID)2-s2.0-85060365305 (Scopus ID)
Note

Funding Agencies:

JDRF  4-1998-274  4-1999-731 4-2001-435 

Special research funds for Oulu, Tampere and Turku University Hospitals in Finland  

Juvenile Diabetes Research Foundation  2-SRA-2014-159-Q-R 

Academy of Finland (Centre of Excellence in Molecular Systems Immunology and Physiology Research-SyMMyS)  250114 

Available from: 2019-02-12 Created: 2019-02-12 Last updated: 2019-06-19Bibliographically approved
Hernández-Alvarez, M. I., Sebastián, D., Vives, S., Ivanova, S., Bartoccioni, P., Kakimoto, P., . . . Zorzano, A. (2019). Deficient Endoplasmic Reticulum-Mitochondrial Phosphatidylserine Transfer Causes Liver Disease. Cell, 177(4), 881-895.e17
Open this publication in new window or tab >>Deficient Endoplasmic Reticulum-Mitochondrial Phosphatidylserine Transfer Causes Liver Disease
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2019 (English)In: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 177, no 4, p. 881-895.e17Article in journal (Refereed) Published
Abstract [en]

Non-alcoholic fatty liver is the most common liver disease worldwide. Here, we show that the mitochondrial protein mitofusin 2 (Mfn2) protects against liver disease. Reduced Mfn2 expression was detected in liver biopsies from patients with non-alcoholic steatohepatitis (NASH). Moreover, reduced Mfn2 levels were detected in mouse models of steatosis or NASH, and its re-expression in a NASH mouse model ameliorated the disease. Liver-specific ablation of Mfn2 in mice provoked inflammation, triglyceride accumulation, fibrosis, and liver cancer. We demonstrate that Mfn2 binds phosphatidylserine (PS) and can specifically extract PS into membrane domains, favoring PS transfer to mitochondria and mitochondrial phosphatidylethanolamine (PE) synthesis. Consequently, hepatic Mfn2 deficiency reduces PS transfer and phospholipid synthesis, leading to endoplasmic reticulum (ER) stress and the development of a NASH-like phenotype and liver cancer. Ablation of Mfn2 in liver reveals that disruption of ER-mitochondrial PS transfer is a new mechanism involved in the development of liver disease.

Place, publisher, year, edition, pages
Cell Press, 2019
Keywords
MAMs, Mfn2, NASH, mitochondria, phosphatidylserine, phospholipid transfer
National Category
Gastroenterology and Hepatology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:oru:diva-74195 (URN)10.1016/j.cell.2019.04.010 (DOI)000466843000010 ()31051106 (PubMedID)2-s2.0-85064698279 (Scopus ID)
Note

Funding Agencies:

CONACYT, Mexico  

MICINN Spain  

Coordenacao de Aperfeicoamento do Pessoal de Nivel Superior (CAPES)  

MINECO  SAF201675246R 

Generalitat de Catalunya (ICREA Academia)  2014SGR48  2017SGR696 

INFLAMES (ISCIII) PIE-14/00045 

CIBERDEM, ISCIII, INTERREG IV-B-SUDOE-FEDER (DIOMED)  SOE1/P1/E178 

"la Caixa'' Foundation  

Miguel Servet tenure-track program from the Fondo de Investigacion Sanitaria  CP10/00438  CPII16/00008 

ERD  

MINECO through the Centres of Excellence Severo Ochoa Award  

CERCA Programme of the Generalitat de Catalunya 

Available from: 2019-05-13 Created: 2019-05-13 Last updated: 2019-06-19Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0002-4382-4355

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