Adipocyte inflammation is the primary driver of hepatic insulin resistance in a human iPSC-based microphysiological system.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
12 Sep 2024
Historique:
received: 16 01 2024
accepted: 28 08 2024
medline: 13 9 2024
pubmed: 13 9 2024
entrez: 12 9 2024
Statut: epublish

Résumé

Interactions between adipose tissue, liver and immune system are at the center of metabolic dysfunction-associated steatotic liver disease and type 2 diabetes. To address the need for an accurate in vitro model, we establish an interconnected microphysiological system (MPS) containing white adipocytes, hepatocytes and proinflammatory macrophages derived from isogenic human induced pluripotent stem cells. Using this MPS, we find that increasing the adipocyte-to-hepatocyte ratio moderately affects hepatocyte function, whereas macrophage-induced adipocyte inflammation causes lipid accumulation in hepatocytes and MPS-wide insulin resistance, corresponding to initiation of metabolic dysfunction-associated steatotic liver disease. We also use our MPS to identify and characterize pharmacological intervention strategies for hepatic steatosis and systemic insulin resistance and find that the glucagon-like peptide-1 receptor agonist semaglutide improves hepatocyte function by acting specifically on adipocytes. These results establish our MPS modeling the adipose tissue-liver axis as an alternative to animal models for mechanistic studies or drug discovery in metabolic diseases.

Identifiants

pubmed: 39266553
doi: 10.1038/s41467-024-52258-w
pii: 10.1038/s41467-024-52258-w
doi:

Substances chimiques

Glucagon-Like Peptide-1 Receptor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

7991

Subventions

Organisme : U.S. Department of Health & Human Services | National Institutes of Health (NIH)
ID : UG3DK120004
Organisme : NIAMS NIH HHS
ID : R01 AR066735
Pays : United States
Organisme : NIDDK NIH HHS
ID : UG3 DK120004
Pays : United States
Organisme : U.S. Department of Health & Human Services | National Institutes of Health (NIH)
ID : P30DK026743
Organisme : NIDDK NIH HHS
ID : UG3 DK120004
Pays : United States
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : GR 5417/1-1

Informations de copyright

© 2024. The Author(s).

Références

Ogden, C. L. et al. Trends in obesity prevalence by race and hispanic origin—1999-2000 to 2017-2018. JAMA 324, 1208–1210 (2020).
pubmed: 32857101 pmcid: 7455882 doi: 10.1001/jama.2020.14590
Rosen, E. D. & Spiegelman, B. M. What we talk about when we talk about fat. Cell 156, 20–44 (2014).
pubmed: 24439368 pmcid: 3934003 doi: 10.1016/j.cell.2013.12.012
Haffner, S. M. Pre-diabetes, insulin resistance, inflammation and CVD risk. Diabetes Res. Clin. Pract. 61, S9–S18 (2003).
pubmed: 12880690 doi: 10.1016/S0168-8227(03)00122-0
Santoro, A., McGraw, T. E. & Kahn, B. B. Insulin action in adipocytes, adipose remodeling, and systemic effects. Cell Metab. 33, 748–757 (2021).
pubmed: 33826917 pmcid: 8078167 doi: 10.1016/j.cmet.2021.03.019
Birkenfeld, A. L. & Shulman, G. I. Nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes. Hepatology 59, 713–723 (2014).
pubmed: 23929732 doi: 10.1002/hep.26672
Cusi, K. The role of adipose tissue and lipotoxicity in the pathogenesis of type 2 diabetes. Curr. Diabetes Rep. 10, 306–315 (2010).
doi: 10.1007/s11892-010-0122-6
Fabbrini, E., Sullivan, S. & Klein, S. Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology 51, 679–689 (2010).
pubmed: 20041406 doi: 10.1002/hep.23280
Qi, L. et al. Human iPSC‐derived proinflammatory macrophages cause insulin resistance in an isogenic white adipose tissue microphysiological system. Small 19, 2203725 (2023).
Chabowski, A. et al. Fatty acid transporters involved in the palmitate and oleate induced insulin resistance in primary rat hepatocytes. Acta Physiol. 207, 346–357 (2013).
doi: 10.1111/apha.12022
Kozyra, M. et al. Human hepatic 3D spheroids as a model for steatosis and insulin resistance. Sci. Rep. 8, 14297 (2018).
pubmed: 30250238 pmcid: 6155201 doi: 10.1038/s41598-018-32722-6
Müller, F. A. & Sturla, S. J. Human in vitro models of nonalcoholic fatty liver disease. Curr. Opin. Toxicol. 16, 9–16 (2019).
doi: 10.1016/j.cotox.2019.03.001
Senn, J. J., Klover, P. J., Nowak, I. A. & Mooney, R. A. Interleukin-6 induces cellular insulin resistance in hepatocytes. Diabetes 51, 3391–3399 (2002).
pubmed: 12453891 doi: 10.2337/diabetes.51.12.3391
Nov, O. et al. Interleukin-1β may mediate insulin resistance in liver-derived cells in response to adipocyte inflammation. Endocrinology 151, 4247–4256 (2010).
pubmed: 20660063 doi: 10.1210/en.2010-0340
Huang, W. et al. Depletion of liver Kupffer cells prevents the development of diet-induced hepatic steatosis and insulin resistance. Diabetes 59, 347–357 (2010).
pubmed: 19934001 doi: 10.2337/db09-0016
Chen, Z., Yu, R., Xiong, Y., Du, F. & Zhu, S. A vicious circle between insulin resistance and inflammation in nonalcoholic fatty liver disease. Lipids health Dis. 16, 1–9 (2017).
doi: 10.1186/s12944-017-0572-9
Feaver, R. E. et al. Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis. JCI Insight 1, e90954 (2016).
Rennert, K. et al. A microfluidically perfused three dimensional human liver model. Biomaterials 71, 119–131 (2015).
pubmed: 26322723 doi: 10.1016/j.biomaterials.2015.08.043
Du, Y. et al. Mimicking liver sinusoidal structures and functions using a 3D-configured microfluidic chip. Lab Chip. 17, 782–794 (2017).
pubmed: 28112323 doi: 10.1039/C6LC01374K
Prodanov, L. et al. Long‐term maintenance of a microfluidic 3D human liver sinusoid. Biotechnol. Bioeng. 113, 241–246 (2016).
pubmed: 26152452 doi: 10.1002/bit.25700
Li, X., George, S. M., Vernetti, L., Gough, A. H. & Taylor, D. L. A glass-based, continuously zonated and vascularized human liver acinus microphysiological system (vLAMPS) designed for experimental modeling of diseases and ADME/TOX. Lab Chip. 18, 2614–2631 (2018).
pubmed: 30063238 pmcid: 6113686 doi: 10.1039/C8LC00418H
Rogal, J. et al. Autologous human immunocompetent white adipose tissue‐on‐chip. Adv. Sci. 9, 2104451 (2022).
doi: 10.1002/advs.202104451
Rogal, J. et al. WAT-on-a-chip integrating human mature white adipocytes for mechanistic research and pharmaceutical applications. Sci. Rep. 10, 1–12 (2020).
doi: 10.1038/s41598-020-63710-4
Compera, N. et al. Adipose microtissue-on-chip: a 3D cell culture platform for differentiation, stimulation, and proteomic analysis of human adipocytes. Lab Chip. 22, 3172–3186 (2022).
pubmed: 35875914 pmcid: 9400584 doi: 10.1039/D2LC00245K
Gori, M. et al. Investigating nonalcoholic fatty liver disease in a liver-on-a-chip microfluidic device. PLoS ONE 11, e0159729 (2016).
pubmed: 27438262 pmcid: 4954713 doi: 10.1371/journal.pone.0159729
Wiriyakulsit, N., Keawsomnuk, P., Thongin, S., Ketsawatsomkron, P. & Muta, K. A model of hepatic steatosis with declined viability and function in a liver-organ-on-a-chip. Sci. Rep. 13, 17019 (2023).
pubmed: 37813918 pmcid: 10562420 doi: 10.1038/s41598-023-44198-0
Du, K. et al. Modeling nonalcoholic fatty liver disease on a liver lobule chip with dual blood supply. Acta Biomater. 134, 228–239 (2021).
pubmed: 34265474 doi: 10.1016/j.actbio.2021.07.013
McCarron, S. et al. Functional characterization of organoids derived from irreversibly damaged liver of patients with NASH. Hepatology 74, 1825–1844 (2021).
pubmed: 33901295 doi: 10.1002/hep.31857
Kostrzewski, T. et al. Modelling human liver fibrosis in the context of non-alcoholic steatohepatitis using a microphysiological system. Commun. Biol. 4, 1080 (2021).
pubmed: 34526653 pmcid: 8443589 doi: 10.1038/s42003-021-02616-x
Freag, M. S. et al. Human nonalcoholic steatohepatitis on a chip. Hepatol. Commun. 5, 217–233 (2021).
pubmed: 33553970 doi: 10.1002/hep4.1647
Wang, Y. et al. Modeling human nonalcoholic fatty liver disease (NAFLD) with an organoids-on-a-chip system. ACS Biomater. Sci. Eng. 6, 5734–5743 (2020).
pubmed: 33320545 doi: 10.1021/acsbiomaterials.0c00682
Kumar, M. et al. A fully defined matrix to support a pluripotent stem cell derived multi-cell-liver steatohepatitis and fibrosis model. Biomaterials 276, 121006 (2021).
pubmed: 34304139 doi: 10.1016/j.biomaterials.2021.121006
Slaughter, V. L. et al. Validation of an adipose-liver human-on-a-chip model of NAFLD for preclinical therapeutic efficacy evaluation. Sci. Rep. 11, 13159 (2021).
pubmed: 34162924 pmcid: 8222323 doi: 10.1038/s41598-021-92264-2
Baldini, F. et al. Adipocyte-hepatocyte crosstalk in cellular models of obesity: role of soluble factors. Life Sci. 317, 121464 (2023).
pubmed: 36731646 doi: 10.1016/j.lfs.2023.121464
Groeger, M. et al. Modeling and therapeutic targeting of inflammation-induced hepatic insulin resistance using human iPSC-derived hepatocytes and macrophages. Nat. Commun. 14, 3902 (2023).
pubmed: 37400454 pmcid: 10318012 doi: 10.1038/s41467-023-39311-w
Qi, L. et al. Probing insulin sensitivity with metabolically competent human stem cell‐derived white adipose tissue microphysiological systems. Small 18, e2103157 (2021).
Matsuo, K. et al. ACVR1R206H extends inflammatory responses in human induced pluripotent stem cell-derived macrophages. Bone 153, 116129 (2021).
pubmed: 34311122 pmcid: 8803261 doi: 10.1016/j.bone.2021.116129
Lee-Montiel, F. T. et al. Integrated isogenic human induced pluripotent stem cell–based liver and heart microphysiological systems predict unsafe drug–drug interaction. Front. Pharmacol. 12, 667010 (2021).
pubmed: 34025426 pmcid: 8138446 doi: 10.3389/fphar.2021.667010
Hatton, I. A. et al. The human cell count and size distribution. Proc. Natl Acad. Sci. USA 120, e2303077120 (2023).
pubmed: 37722043 pmcid: 10523466 doi: 10.1073/pnas.2303077120
Newsome, P. N. et al. A placebo-controlled trial of subcutaneous semaglutide in nonalcoholic steatohepatitis. N. Engl. J. Med. 384, 1113–1124 (2021).
pubmed: 33185364 doi: 10.1056/NEJMoa2028395
Ejarque, M. et al. Role of adipose tissue GLP-1R expression in metabolic improvement after bariatric surgery in patients with type 2 diabetes. Sci. Rep. 9, 6274 (2019).
pubmed: 31000783 pmcid: 6472499 doi: 10.1038/s41598-019-42770-1
Jiang, Y. et al. GLP-1 improves adipocyte insulin sensitivity following induction of endoplasmic reticulum stress. Front. Pharmacol. 9, 1168 (2018).
pubmed: 30459598 pmcid: 6232689 doi: 10.3389/fphar.2018.01168
Jin, T. & Weng, J. Hepatic functions of GLP-1 and its based drugs: current disputes and perspectives. Am. J. Physiol. Endocrinol. Metab. 311, E620–E627 (2016).
pubmed: 27507553 doi: 10.1152/ajpendo.00069.2016
Duwaerts, C. C. & Maher, J. J. Macronutrients and the adipose-liver axis in obesity and fatty liver. Cell. Mol. Gastroenterol. Hepatol. 7, 749–761 (2019).
pubmed: 30763771 pmcid: 6463203 doi: 10.1016/j.jcmgh.2019.02.001
Du Plessis, J. et al. Pro-inflammatory cytokines but not endotoxin-related parameters associate with disease severity in patients with NAFLD. PloS one 11, e0166048 (2016).
pubmed: 27992443 pmcid: 5167229 doi: 10.1371/journal.pone.0166048
Salans, L. B., Cushman, S. W. & Weismann, R. E. Studies of human adipose tissue adipose cell size and number in nonobese and obese patients. J. Clin. Investig. 52, 929–941 (1973).
pubmed: 4693656 pmcid: 302341 doi: 10.1172/JCI107258
Barbe, P., Millet, L., Galitzky, J., Lafontan, M. & Berlan, M. In situ assessment of the role of the β1, β2‐and β3‐adrenoceptors in the control of lipolysis and nutritive blood flow in human subcutaneous adipose tissue. Br. J. Pharmacol. 117, 907–913 (1996).
pubmed: 8851509 pmcid: 1909425 doi: 10.1111/j.1476-5381.1996.tb15279.x
Benvenuti, S. et al. Rosiglitazone stimulates adipogenesis and decreases osteoblastogenesis in human mesenchymal stem cells. J. Endocrinol. Investig. 30, RC26–RC30 (2007).
doi: 10.1007/BF03350807
Tsurufuji, S., Sugio, K. & Takemasa, F. The role of glucocorticoid receptor and gene expression in the anti-inflammatory action of dexamethasone. Nature 280, 408–410 (1979).
pubmed: 460415 doi: 10.1038/280408a0
Burén, J., Liu, H.-X., Jensen, J. & Eriksson, J. W. Dexamethasone impairs insulin signalling and glucose transport by depletion of insulin receptor substrate-1, phosphatidylinositol 3-kinase and protein kinase B in primary cultured rat adipocytes. Eur. J. Endocrinol. 146, 419–429 (2002).
pubmed: 11888850 doi: 10.1530/eje.0.1460419
Luan, G. et al. Dexamethasone-induced mitochondrial dysfunction and insulin resistance-study in 3T3-L1 adipocytes and mitochondria isolated from mouse liver. Molecules 24, 1982 (2019).
pubmed: 31126054 pmcid: 6572075 doi: 10.3390/molecules24101982
Howell, J. J. et al. Metformin inhibits hepatic mTORC1 signaling via dose-dependent mechanisms involving AMPK and the TSC complex. Cell Metab. 25, 463–471 (2017).
pubmed: 28089566 pmcid: 5299044 doi: 10.1016/j.cmet.2016.12.009
Cao, J. et al. Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK). J. Biol. Chem. 289, 20435–20446 (2014).
pubmed: 24928508 pmcid: 4110255 doi: 10.1074/jbc.M114.567271
Tiikkainen, M. et al. Effects of rosiglitazone and metformin on liver fat content, hepatic insulin resistance, insulin clearance, and gene expression in adipose tissue in patients with type 2 diabetes. Diabetes 53, 2169–2176 (2004).
pubmed: 15277403 doi: 10.2337/diabetes.53.8.2169
Petit, J.-M. & Vergès, B. GLP-1 receptor agonists in NAFLD. Diabetes Metab. 43, 2S28–22S33 (2017).
pubmed: 28431668 doi: 10.1016/S1262-3636(17)30070-8
Bifari, F. et al. Multiple target tissue effects of GLP-1 analogues on non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Pharmacol. Res. 137, 219–229 (2018).
pubmed: 30359962 doi: 10.1016/j.phrs.2018.09.025
Niu, S. et al. Semaglutide ameliorates metabolism and hepatic outcomes in an NAFLD mouse model. Front. Endocrinol. 13, 1046130 (2022).
doi: 10.3389/fendo.2022.1046130
Newsome, P. N. & Ambery, P. Incretins (GLP1 r agonists and dual, triple agonists) and the liver. J. Hepatol. 79, 1557–1565 (2023).
Garvey, W. T. et al. Two-year effects of semaglutide in adults with overweight or obesity: the STEP 5 trial. Nat. Med. 28, 2083–2091 (2022).
pubmed: 36216945 pmcid: 9556320 doi: 10.1038/s41591-022-02026-4
Lee, Y.-S. et al. Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes. Diabetologia 55, 2456–2468 (2012).
pubmed: 22722451 doi: 10.1007/s00125-012-2592-3
Wan, S. & Sun, H. Glucagon‑like peptide‑1 modulates RAW264. 7 macrophage polarization by interfering with the JNK/STAT3 signaling pathway. Exp. Therap. Med. 17, 3573–3579 (2019).
Seino, Y., Fukushima, M. & Yabe, D. GIP and GLP‐1, the two incretin hormones: similarities and differences. J. Diabetes Investig. 1, 8–23 (2010).
pubmed: 24843404 pmcid: 4020673 doi: 10.1111/j.2040-1124.2010.00022.x
Pyke, C. & Knudsen, L. The glucagon-like peptide-1 receptor-or not? Endocrinology 154, 4–8 (2013).
pubmed: 23267050 doi: 10.1210/en.2012-2124
Pyke, C. et al. GLP-1 receptor localization in monkey and human tissue: novel distribution revealed with extensively validated monoclonal antibody. Endocrinology 155, 1280–1290 (2014).
pubmed: 24467746 doi: 10.1210/en.2013-1934
Gamberi, T., Magherini, F., Modesti, A. & Fiaschi, T. Adiponectin signaling pathways in liver diseases. Biomedicines 6, 52 (2018).
pubmed: 29735928 pmcid: 6027295 doi: 10.3390/biomedicines6020052
Yaribeygi, H., Maleki, M., Butler, A. E., Jamialahmadi, T. & Sahebkar, A. The impact of incretin-based medications on lipid metabolism. J. Diabetes Res. 2021, 1815178 (2021).
Chen, Y. et al. Genome-wide association meta-analysis identifies 17 loci associated with nonalcoholic fatty liver disease. Nat. Genet. 55, 1640–1650 (2023).
pubmed: 37709864 pmcid: 10918428 doi: 10.1038/s41588-023-01497-6
Emont, M. P. et al. A single-cell atlas of human and mouse white adipose tissue. Nature 603, 926–933 (2022).
pubmed: 35296864 pmcid: 9504827 doi: 10.1038/s41586-022-04518-2
Kreitzer, F. R. et al. A robust method to derive functional neural crest cells from human pluripotent stem cells. Am. J. stem cells 2, 119 (2013).
pubmed: 23862100 pmcid: 3708511
Knight, C. G. et al. The collagen-binding A-domains of Integrins α1β1 and α2β1recognize the same specific amino acid sequence, GFOGER, in native (triple-helical) collagens. J. Biol. Chem. 275, 35–40 (2000).
pubmed: 10617582 doi: 10.1074/jbc.275.1.35
Weisberg, S. P. et al. Obesity is associated with macrophage accumulation in adipose tissue. J. Clin. Invest 112, 1796–1808 (2003).
pubmed: 14679176 pmcid: 296995 doi: 10.1172/JCI200319246

Auteurs

Lin Qi (L)

Department of Nutritional Science and Toxicology, College of Natural Resources, University of California Berkeley, Berkeley, CA, 94720, USA.

Marko Groeger (M)

Division of Transplant Surgery, Department of Surgery, University of California San Francisco, San Francisco, CA, 94143, USA.
Eli and Edythe Broad Center for Regeneration Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.

Aditi Sharma (A)

Eli and Edythe Broad Center for Regeneration Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.
Division of Endocrinology and Metabolism, Department of Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.
Institute for Human Genetics, University of California San Francisco, San Francisco, CA, 94143, USA.

Ishan Goswami (I)

Department of Bioengineering, College of Engineering, University of California Berkeley, Berkeley, CA, 94720, USA.

Erzhen Chen (E)

Department of Nutritional Science and Toxicology, College of Natural Resources, University of California Berkeley, Berkeley, CA, 94720, USA.

Fenmiao Zhong (F)

Department of Nutritional Science and Toxicology, College of Natural Resources, University of California Berkeley, Berkeley, CA, 94720, USA.

Apsara Ram (A)

Eli and Edythe Broad Center for Regeneration Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.
Division of Endocrinology and Metabolism, Department of Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.
Institute for Human Genetics, University of California San Francisco, San Francisco, CA, 94143, USA.

Kevin Healy (K)

Department of Bioengineering, College of Engineering, University of California Berkeley, Berkeley, CA, 94720, USA.
Department of Materials Science and Engineering, College of Engineering, University of California Berkeley, Berkeley, CA, 94720, USA.

Edward C Hsiao (EC)

Eli and Edythe Broad Center for Regeneration Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.
Division of Endocrinology and Metabolism, Department of Medicine, University of California San Francisco, San Francisco, CA, 94143, USA.
Institute for Human Genetics, University of California San Francisco, San Francisco, CA, 94143, USA.

Holger Willenbring (H)

Division of Transplant Surgery, Department of Surgery, University of California San Francisco, San Francisco, CA, 94143, USA. holger.willenbring@ucsf.edu.
Eli and Edythe Broad Center for Regeneration Medicine, University of California San Francisco, San Francisco, CA, 94143, USA. holger.willenbring@ucsf.edu.
Liver Center, University of California San Francisco, San Francisco, CA, 94143, USA. holger.willenbring@ucsf.edu.

Andreas Stahl (A)

Department of Nutritional Science and Toxicology, College of Natural Resources, University of California Berkeley, Berkeley, CA, 94720, USA. astahl@berkeley.edu.

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