Apolipoprotein CIII Reduction Protects White Adipose Tissues against Obesity-Induced Inflammation and Insulin Resistance in Mice
| Autor: | Recio-López, Patricia, Valladolid-Acebes, Ismael, Berggren, Per-Olof, Juntti-Berggren, Lisa |
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| Rok vydání: | 2021 |
| Předmět: |
Male
diet-induced obesity QH301-705.5 Adipose Tissue White Lipolysis Diet High-Fat Article Mice Adipose Tissue Brown white adipose tissue insulin resistance Adipocytes Animals Insulin Obesity Biology (General) QD1-999 Inflammation Apolipoprotein C-III apolipoprotein CIII food and beverages nutritional and metabolic diseases Thermogenesis Mice Inbred C57BL Chemistry Liver lipids (amino acids peptides and proteins) antisense oligonucleotides |
| Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 23, Iss 62, p 62 (2022) |
| ISSN: | 1422-0067 |
| Popis: | Apolipoprotein CIII (apoCIII) is proinflammatory and increases in high-fat diet (HFD)-induced obesity and insulin resistance. We have previously shown that reducing apoCIII improves insulin sensitivity in vivo by complex mechanisms involving liver and brown adipose tissue. In this study the focus was on subcutaneous (SAT) and visceral (VAT) white adipose tissue (WAT). Mice were either given HFD for 14 weeks and directly from start also treated with antisense oligonucleotide (ASO) against apoCIII or given HFD for 10 weeks and HFD+ASO for an additional 14 weeks. Both groups had animals treated with inactive (Scr) ASO as controls and in parallel chow-fed mice were injected with saline. Preventing an increase or lowering apoCIII in the HFD-fed mice decreased adipocytes’ size, reduced expression of inflammatory cytokines and increased expression of genes related to thermogenesis and beiging. Isolated adipocytes from both VAT and SAT from the ASO-treated mice had normal insulin-induced inhibition of lipolysis compared to cells from Scr-treated mice. In conclusion, the HFD-induced metabolic derangements in WATs can be prevented and reversed by lowering apoCIII. |
| Databáze: | OpenAIRE |
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