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Start Over Author "Demori I" Journal journal of endocrinology
4 results on '"Demori I"'

1. 3,5-Diiodo-l-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver

Author

Grasselli E, Voci A, Demori I, Canesi L, De Matteis R, Goglia F, Gallo G, Vergani L. J. E.n.d.o.c.r.i.n.o.l. 2012 Feb, 212:149 58, LANNI, Antonia, Grasselli, E, Voci, A, Demori, I, Canesi, L, De Matteis, R, Goglia, F, Lanni, Antonia, Gallo, G, 2012 Feb, Vergani L. J. E. n. d. o. c. r. i. n. o. l., and 212:149, 58

Subjects
Male, Very low-density lipoprotein, OVERWEIGHT RATS, Apolipoprotein B, Diiodothyronines, Endocrinology, Diabetes and Metabolism, Peroxisome Proliferator-Activated Receptors, Vesicular Transport Proteins, Muscle Proteins, Lipoproteins, VLDL, HEPATOCYTES, Random Allocation, Endocrinology, Lipid droplet, Protein Isoforms, Receptor, IN-VIVO, Anti-Inflammatory Agents, Non-Steroidal, Fatty liver, Intracellular Signaling Peptides and Proteins, Liver, ACTIVATED-RECEPTOR-GAMMA, SKELETAL-MUSCLE, lipids (amino acids, peptides, and proteins), PPAR-GAMMA, ADIPOSE TRIGLYCERIDE LIPASE, Stearoyl-CoA Desaturase, medicine.medical_specialty, Biology, Perilipin-5, Perilipin-2, Perilipin-3, Lipid oxidation, Internal medicine, medicine, Animals, HEPATIC STEATOSIS, PAT-FAMILY, ALPHA, RNA, Messenger, Rats, Wistar, Apolipoproteins B, Membrane Proteins, Lipid metabolism, Lipase, Lipid Metabolism, medicine.disease, Rats, Fatty Liver, Gene Expression Regulation, Adipose triglyceride lipase, biology.protein, Acyl-CoA Oxidase
Abstract

Recent reports demonstrated that 3,5-diiodo-l-thyronine (T2) 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 T2treatment 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 T2administration 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 T2may 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 T2and help to define the potential therapeutic role of T2for preventing or treating liver steatosis.

Published
2011

4. 3,5-Diiodo-L-thyronine modulates the expression of genes of lipid metabolism in a rat model of fatty liver.

Author

Grasselli E, Voci A, Demori I, Canesi L, De Matteis R, Goglia F, Lanni A, Gallo G, and Vergani L

Subjects
Acyl-CoA Oxidase genetics, Acyl-CoA Oxidase metabolism, Animals, Apolipoproteins B genetics, Apolipoproteins B metabolism, Fatty Liver immunology, Fatty Liver pathology, Intracellular Signaling Peptides and Proteins genetics, Intracellular Signaling Peptides and Proteins metabolism, Lipase genetics, Lipase metabolism, Lipoproteins, VLDL metabolism, Liver immunology, Liver metabolism, Liver pathology, Male, Membrane Proteins genetics, Membrane Proteins metabolism, Muscle Proteins genetics, Muscle Proteins metabolism, Perilipin-2, Perilipin-3, Perilipin-5, Peroxisome Proliferator-Activated Receptors genetics, Peroxisome Proliferator-Activated Receptors metabolism, Protein Isoforms genetics, Protein Isoforms metabolism, RNA, Messenger metabolism, Random Allocation, Rats, Rats, Wistar, Stearoyl-CoA Desaturase genetics, Stearoyl-CoA Desaturase metabolism, Vesicular Transport Proteins genetics, Vesicular Transport Proteins metabolism, Anti-Inflammatory Agents, Non-Steroidal therapeutic use, Diiodothyronines therapeutic use, Fatty Liver metabolism, Fatty Liver prevention & control, Gene Expression Regulation drug effects, Lipid Metabolism drug effects, Liver drug effects
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.

Published
2012
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