Miladinović, Nenad

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Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver

Gligorovska, Ljupka; Teofilović, Ana; Vojnović-Milutinović, Danijela; Miladinović, Nenad; Kovačević, Sanja; Veličković, Nataša; Đorđević, Ana

(Blackwell Publishing Inc., 2021)

TY  - JOUR
AU  - Gligorovska, Ljupka
AU  - Teofilović, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Miladinović, Nenad
AU  - Kovačević, Sanja
AU  - Veličković, Nataša
AU  - Đorđević, Ana
PY  - 2021
UR  - https://onlinelibrary.wiley.com/doi/10.1002/biof.1711
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4148
AB  - Dietary fructose can disturb hepatic lipid metabolism in a way that leads to lipid accumulation and steatosis, which is often accompanied with low-grade inflammation. The macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with important role not only in the regulation of inflammation, but also in the modulation of energy metabolism in the liver. Thus, the aim of this study was to investigate the role of Mif deficiency in fructose-induced disturbances of hepatic lipid metabolism and ectopic lipid accumulation. Wild type (WT) and Mif deficient (MIF−/−) C57Bl/6J mice were used to analyze the effects of 9-week 20% fructose-enriched diet on hepatic lipid metabolism (both lipogenesis and β-oxidation) and histology, inflammatory status and glucocorticoid receptor (GR) signaling. The results showed fructose-induced elevation of lipogenic genes (fatty acid synthase (Fas) and stearoyl-CoA desaturase-1 (Scd1) and transcriptional lipogenic regulators (liver X receptor (LXR), sterol regulatory element binding protein 1c (SREBP1c), and carbohydrate response element-binding protein (ChREBP)). However, microvesicular fatty changes, accompanied with enhanced inflammation, were observable only in fructose-fed Mif deficient animals, and were most likely result of GR activation and facilitated uptake and decreased β-oxidation of FFA, as evidenced by elevated protein level of fatty acid translocase (FAT/CD36) and decreased carnitine palmitoyl transferase 1 (CPT1) level. In conclusion, the results show that Mif deficiency aggravates the effects of energy-rich fructose diet on hepatic lipid accumulation, most likely through enhanced inflammation and activation of GR signaling pathway.
PB  - Blackwell Publishing Inc.
T2  - BioFactors
T1  - Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver
DO  - 10.1002/biof.1711
SP  - biof.1711
ER  - 
@article{
author = "Gligorovska, Ljupka and Teofilović, Ana and Vojnović-Milutinović, Danijela and Miladinović, Nenad and Kovačević, Sanja and Veličković, Nataša and Đorđević, Ana",
year = "2021",
abstract = "Dietary fructose can disturb hepatic lipid metabolism in a way that leads to lipid accumulation and steatosis, which is often accompanied with low-grade inflammation. The macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with important role not only in the regulation of inflammation, but also in the modulation of energy metabolism in the liver. Thus, the aim of this study was to investigate the role of Mif deficiency in fructose-induced disturbances of hepatic lipid metabolism and ectopic lipid accumulation. Wild type (WT) and Mif deficient (MIF−/−) C57Bl/6J mice were used to analyze the effects of 9-week 20% fructose-enriched diet on hepatic lipid metabolism (both lipogenesis and β-oxidation) and histology, inflammatory status and glucocorticoid receptor (GR) signaling. The results showed fructose-induced elevation of lipogenic genes (fatty acid synthase (Fas) and stearoyl-CoA desaturase-1 (Scd1) and transcriptional lipogenic regulators (liver X receptor (LXR), sterol regulatory element binding protein 1c (SREBP1c), and carbohydrate response element-binding protein (ChREBP)). However, microvesicular fatty changes, accompanied with enhanced inflammation, were observable only in fructose-fed Mif deficient animals, and were most likely result of GR activation and facilitated uptake and decreased β-oxidation of FFA, as evidenced by elevated protein level of fatty acid translocase (FAT/CD36) and decreased carnitine palmitoyl transferase 1 (CPT1) level. In conclusion, the results show that Mif deficiency aggravates the effects of energy-rich fructose diet on hepatic lipid accumulation, most likely through enhanced inflammation and activation of GR signaling pathway.",
publisher = "Blackwell Publishing Inc.",
journal = "BioFactors",
title = "Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver",
doi = "10.1002/biof.1711",
pages = "biof.1711"
}
Gligorovska, L., Teofilović, A., Vojnović-Milutinović, D., Miladinović, N., Kovačević, S., Veličković, N.,& Đorđević, A.. (2021). Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver. in BioFactors
Blackwell Publishing Inc.., biof.1711.
https://doi.org/10.1002/biof.1711
Gligorovska L, Teofilović A, Vojnović-Milutinović D, Miladinović N, Kovačević S, Veličković N, Đorđević A. Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver. in BioFactors. 2021;:biof.1711.
doi:10.1002/biof.1711 .
Gligorovska, Ljupka, Teofilović, Ana, Vojnović-Milutinović, Danijela, Miladinović, Nenad, Kovačević, Sanja, Veličković, Nataša, Đorđević, Ana, "Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver" in BioFactors (2021):biof.1711,
https://doi.org/10.1002/biof.1711 . .
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