Non-alcoholic fatty liver disease(NAFLD) is a common clinicopathological condition, encompassing a range of conditions caused by lipid deposition within liver cells. To date, no approved drugs are available for the tr...Non-alcoholic fatty liver disease(NAFLD) is a common clinicopathological condition, encompassing a range of conditions caused by lipid deposition within liver cells. To date, no approved drugs are available for the treatment of NAFLD, despite the fact that it represents a serious and growing clinical problem in the Western world. Identification of the molecular mechanisms leading to NAFLD-related fat accumulation, mitochondrial dysfunction and oxidative balance impairment facilitates the development of specific interventions aimed at preventing the progression of hepatic steatosis. In this review, we focus our attention on the role of dysfunctions in mitochondrial bioenergetics in the pathogenesis of fatty liver. Major data from the literature about the mitochondrial targeting of some antioxidant molecules as a potential treatment for hepatic steatosis are described and critically analysed. There is ample evidence of the positive effects of several classes of antioxidants, such as polyphenols(i.e., resveratrol, quercetin, coumestrol, anthocyanins, epigallocatechin gallate and curcumin), carotenoids(i.e., lycopene, astaxanthin and fucoxanthin) and glucosinolates(i.e., glucoraphanin, sulforaphane, sinigrin and allyl-isothiocyanate), on the reversion of fatty liver. Although the mechanism of action is not yet fully elucidated, in some cases an indirect interaction with mitochondrial metabolism is expected. We believe that such knowledge will eventually translate into the development of novel therapeutic approaches for fatty liver.展开更多
Non-alcoholic fatty liver disease(NAFLD)describes a range of conditions caused by fat deposition within liver cells.Liver fat content reflects the equilibrium between several metabolic pathways involved in triglycerid...Non-alcoholic fatty liver disease(NAFLD)describes a range of conditions caused by fat deposition within liver cells.Liver fat content reflects the equilibrium between several metabolic pathways involved in triglyceride synthesis and disposal,such as lipolysis in adipose tissue and de novo lipogenesis,triglyceride esterification,fatty acid oxidation and very-low-density lipoprotein synthesis/secretion in hepatic tissue.In particular,it has been demonstrated that hepatic de novo lipogenesis plays a significant role in NAFLD pathogenesis.It is widely known that the fatty acid composition of the diet influences hepatic lipogenesis along with other metabolic pathways.Therefore,dietary fat may not only be involved in the pathogenesis of hepatic steatosis,but may also prevent and/or reverse hepatic fat accumulation.In this review,major data from the literature about the role of some dietary fats as a potential cause of hepatic fat accumulation or as a potential treatment for NAFLD are described.Moreover,biochemical mechanisms responsible for an increase or decrease in hepatic lipid content are critically analyzed.It is noteworthy that both quantitative and qualitative aspects of dietary fat influence triglyceride deposition in the liver.A high-fat diet or the dietary administration of conjugated linoleic acids induced hepatic steatosis.In contrast,supplementation of the diet with krill oil or pine nut oil helped in the prevention and/or in the treatment of steatotic liver.Quite interesting is the"case"of olive oil,since several studies have often provided different and or conflicting results in animal models.展开更多
文摘Non-alcoholic fatty liver disease(NAFLD) is a common clinicopathological condition, encompassing a range of conditions caused by lipid deposition within liver cells. To date, no approved drugs are available for the treatment of NAFLD, despite the fact that it represents a serious and growing clinical problem in the Western world. Identification of the molecular mechanisms leading to NAFLD-related fat accumulation, mitochondrial dysfunction and oxidative balance impairment facilitates the development of specific interventions aimed at preventing the progression of hepatic steatosis. In this review, we focus our attention on the role of dysfunctions in mitochondrial bioenergetics in the pathogenesis of fatty liver. Major data from the literature about the mitochondrial targeting of some antioxidant molecules as a potential treatment for hepatic steatosis are described and critically analysed. There is ample evidence of the positive effects of several classes of antioxidants, such as polyphenols(i.e., resveratrol, quercetin, coumestrol, anthocyanins, epigallocatechin gallate and curcumin), carotenoids(i.e., lycopene, astaxanthin and fucoxanthin) and glucosinolates(i.e., glucoraphanin, sulforaphane, sinigrin and allyl-isothiocyanate), on the reversion of fatty liver. Although the mechanism of action is not yet fully elucidated, in some cases an indirect interaction with mitochondrial metabolism is expected. We believe that such knowledge will eventually translate into the development of novel therapeutic approaches for fatty liver.
文摘Non-alcoholic fatty liver disease(NAFLD)describes a range of conditions caused by fat deposition within liver cells.Liver fat content reflects the equilibrium between several metabolic pathways involved in triglyceride synthesis and disposal,such as lipolysis in adipose tissue and de novo lipogenesis,triglyceride esterification,fatty acid oxidation and very-low-density lipoprotein synthesis/secretion in hepatic tissue.In particular,it has been demonstrated that hepatic de novo lipogenesis plays a significant role in NAFLD pathogenesis.It is widely known that the fatty acid composition of the diet influences hepatic lipogenesis along with other metabolic pathways.Therefore,dietary fat may not only be involved in the pathogenesis of hepatic steatosis,but may also prevent and/or reverse hepatic fat accumulation.In this review,major data from the literature about the role of some dietary fats as a potential cause of hepatic fat accumulation or as a potential treatment for NAFLD are described.Moreover,biochemical mechanisms responsible for an increase or decrease in hepatic lipid content are critically analyzed.It is noteworthy that both quantitative and qualitative aspects of dietary fat influence triglyceride deposition in the liver.A high-fat diet or the dietary administration of conjugated linoleic acids induced hepatic steatosis.In contrast,supplementation of the diet with krill oil or pine nut oil helped in the prevention and/or in the treatment of steatotic liver.Quite interesting is the"case"of olive oil,since several studies have often provided different and or conflicting results in animal models.