Non-Alcoholic Fatty Liver Disease (NAFLD) is nowadays considered one of the most diffused pathologic conditions affecting the liver especially in the Western world. The pathological mechanisms that induce the development of NAFLD are so far not completely clarified, even if now most researchers believe that an important condition that has to be satisfied is a significant accumulation of lipids inside the hepatocyte, principally as triglycerides. In the liver, such a lipid accumulation leads to an impairment of insulin signaling, which typically results in a failed phosphorylation of Akt, inducing the onset of insulin resistance. In the last years many researchers and clinicians focused their attention on the role played by fructose in metabolic diseases, such as obesity, type 2 diabetes, metabolic syndrome, as well as in liver specific pathologies, such as NAFLD. This huge debate about the role of fructose probably rose as a consequence of the recent increased diffusion of sweetened foods and beverages. In this context, the aim of this work was to develop an in vitro model for NAFLD, with particular reference to the role played by oleic acid and fructose in the onset of steatosis and insulin resistance. Moreover, we tested the effects of 3,5-diiodothyronine on steatosis and insulin resistance, trying to assess the potential mechanisms of action involved, considering the increasing interest about its role as a biologically active molecule. Our results show that, differently to oleic acid, fructose per se, in the range of physiological concentrations, is not able to induce neither triglycerides accumulation nor insulin resistance. Moreover we demonstrated that 3,5-diiodothyronine, at physiological levels, reduces triglycerides content and stimulates phosphorylation of Akt.

Gnocchi D, Massimi M, Alisi A, Incerpi S, & Bruscalupi G (2014). Effect of Fructose and 3,5- Diiodothyronine (3,5-T2) on Lipid Accumulation and Insulin Signaling in Non- Alcoholic Fatty Liver Disease (NAFLD)-Like Rat Primary Hepatocytes. HORMONE AND METABOLIC RESEARCH, 46, 333-340 [10.1055/s-0034-1371858].

Effect of Fructose and 3,5- Diiodothyronine (3,5-T2) on Lipid Accumulation and Insulin Signaling in Non- Alcoholic Fatty Liver Disease (NAFLD)-Like Rat Primary Hepatocytes

INCERPI, Sandra;
2014

Abstract

Non-Alcoholic Fatty Liver Disease (NAFLD) is nowadays considered one of the most diffused pathologic conditions affecting the liver especially in the Western world. The pathological mechanisms that induce the development of NAFLD are so far not completely clarified, even if now most researchers believe that an important condition that has to be satisfied is a significant accumulation of lipids inside the hepatocyte, principally as triglycerides. In the liver, such a lipid accumulation leads to an impairment of insulin signaling, which typically results in a failed phosphorylation of Akt, inducing the onset of insulin resistance. In the last years many researchers and clinicians focused their attention on the role played by fructose in metabolic diseases, such as obesity, type 2 diabetes, metabolic syndrome, as well as in liver specific pathologies, such as NAFLD. This huge debate about the role of fructose probably rose as a consequence of the recent increased diffusion of sweetened foods and beverages. In this context, the aim of this work was to develop an in vitro model for NAFLD, with particular reference to the role played by oleic acid and fructose in the onset of steatosis and insulin resistance. Moreover, we tested the effects of 3,5-diiodothyronine on steatosis and insulin resistance, trying to assess the potential mechanisms of action involved, considering the increasing interest about its role as a biologically active molecule. Our results show that, differently to oleic acid, fructose per se, in the range of physiological concentrations, is not able to induce neither triglycerides accumulation nor insulin resistance. Moreover we demonstrated that 3,5-diiodothyronine, at physiological levels, reduces triglycerides content and stimulates phosphorylation of Akt.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11590/137638
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