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3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver.
J Endocrinol. 2012 Feb; 212(2):149-58.JE

Abstract

Recent reports demonstrated that 3,5-diiodo-l-thyronine (T(2)) was able to prevent lipid accumulation in the liver of rats fed a high-fat diet (HFD). In this study, we investigated how the rat liver responds to HFD and T(2) treatment by assessing the transcription profiles of some genes involved in the pathways of lipid metabolism: oxidation, storage and secretion. The mRNA levels of the peroxisome proliferator-activated receptors (PPARα, PPARγ and PPARδ), and of their target enzymes acyl-CoA oxidase and stearoyl-CoA desaturase were evaluated by real-time RT-PCR. Moreover, the expression of the adipose triglyceride lipase involved in lipid mobilisation, of the main PAT proteins acting in lipid droplet (LD) turnover, and of apoprotein B (apo B), the major protein component of very low-density lipoproteins (VLDLs) were analysed. Overall, our data demonstrated that T(2) administration to HFD rats counteracts most of the hepatic transcriptional changes that occurred in response to the excess exogenous fat. In particular, our results suggest that T(2) may prevent the pathways leading to lipid storage in LDs, promote the processes of lipid mobilisation from LDs and secretion as VLDL, in addition to the stimulation of pathways of lipid oxidation. In conclusion, our findings might give an insight into the mechanisms underlying the anti-steatotic ability of T(2) and help to define the potential therapeutic role of T(2) for preventing or treating liver steatosis.

Authors+Show Affiliations

DIPTERIS, Università di Genova, Genova, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22107956

Citation

Grasselli, Elena, et al. "3,5-Diiodo-L-thyronine Modulates the Expression of Genes of Lipid Metabolism in a Rat Model of Fatty Liver." The Journal of Endocrinology, vol. 212, no. 2, 2012, pp. 149-58.
Grasselli E, Voci A, Demori I, et al. 3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver. J Endocrinol. 2012;212(2):149-58.
Grasselli, E., Voci, A., Demori, I., Canesi, L., De Matteis, R., Goglia, F., Lanni, A., Gallo, G., & Vergani, L. (2012). 3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver. The Journal of Endocrinology, 212(2), 149-58. https://doi.org/10.1530/JOE-11-0288
Grasselli E, et al. 3,5-Diiodo-L-thyronine Modulates the Expression of Genes of Lipid Metabolism in a Rat Model of Fatty Liver. J Endocrinol. 2012;212(2):149-58. PubMed PMID: 22107956.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver. AU - Grasselli,Elena, AU - Voci,Adriana, AU - Demori,Ilaria, AU - Canesi,Laura, AU - De Matteis,Rita, AU - Goglia,Fernando, AU - Lanni,Antonia, AU - Gallo,Gabriella, AU - Vergani,Laura, Y1 - 2011/11/22/ PY - 2011/11/24/entrez PY - 2011/11/24/pubmed PY - 2012/3/1/medline SP - 149 EP - 58 JF - The Journal of endocrinology JO - J Endocrinol VL - 212 IS - 2 N2 - Recent reports demonstrated that 3,5-diiodo-l-thyronine (T(2)) was able to prevent lipid accumulation in the liver of rats fed a high-fat diet (HFD). In this study, we investigated how the rat liver responds to HFD and T(2) treatment by assessing the transcription profiles of some genes involved in the pathways of lipid metabolism: oxidation, storage and secretion. The mRNA levels of the peroxisome proliferator-activated receptors (PPARα, PPARγ and PPARδ), and of their target enzymes acyl-CoA oxidase and stearoyl-CoA desaturase were evaluated by real-time RT-PCR. Moreover, the expression of the adipose triglyceride lipase involved in lipid mobilisation, of the main PAT proteins acting in lipid droplet (LD) turnover, and of apoprotein B (apo B), the major protein component of very low-density lipoproteins (VLDLs) were analysed. Overall, our data demonstrated that T(2) administration to HFD rats counteracts most of the hepatic transcriptional changes that occurred in response to the excess exogenous fat. In particular, our results suggest that T(2) may prevent the pathways leading to lipid storage in LDs, promote the processes of lipid mobilisation from LDs and secretion as VLDL, in addition to the stimulation of pathways of lipid oxidation. In conclusion, our findings might give an insight into the mechanisms underlying the anti-steatotic ability of T(2) and help to define the potential therapeutic role of T(2) for preventing or treating liver steatosis. SN - 1479-6805 UR - https://www.unboundmedicine.com/medline/citation/22107956/35_Diiodo_L_thyronine_modulates_the_expression_of_genes_of_lipid_metabolism_in_a_rat_model_of_fatty_liver_ L2 - https://joe.bioscientifica.com/doi/10.1530/JOE-11-0288 DB - PRIME DP - Unbound Medicine ER -