腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK)是一种广泛参与多种代谢调节的激酶,是主要的细胞"能量感受器"。AMPK通过α亚基的Thr172发生磷酸化而激活,通过抑制脂质合成相关转录因子以及肝脏糖异生来控制脂质合...腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK)是一种广泛参与多种代谢调节的激酶,是主要的细胞"能量感受器"。AMPK通过α亚基的Thr172发生磷酸化而激活,通过抑制脂质合成相关转录因子以及肝脏糖异生来控制脂质合成以及血糖稳定。肝脏糖异生的调控过程中,通过激素及转录因子如Fox O1、CREB、TORC2、HNF-4α、PGC-1α等的参与,最后将信号传达至糖异生的2个关键性限速酶基因PECK与G6Pase,起到调控作用。激活的AMPK能抑制糖异生转录因子及相关关键酶的有效表达,阻止肝脏发生糖异生,进而下降血糖浓度。本文旨在讨论与总结AMPK在肝脏糖脂代谢中的作用,重点分析AMPK与肝脏糖异生信号通路转录因子之间的联系。展开更多
The World Health Organization recommends that the daily intake of added sugars should make up no more than 10% of total energy.The consumption of sugarsweetened beverages is the main source of added sugars.Fructose,to...The World Health Organization recommends that the daily intake of added sugars should make up no more than 10% of total energy.The consumption of sugarsweetened beverages is the main source of added sugars.Fructose,together with glucose,as a component of high fructose corn syrups or as a component of the sucrose molecule,is one of the main sweeteners present in this kind of beverages.Data from prospective and intervention studies clearly point to high fructose consumption,mainly in the form of sweetened beverages,as a risk factor for several metabolic diseases in humans.The incidence of hypertension,nonalcoholic fatty liver disease(NAFLD),dyslipidemia(mainly hypertriglyceridemia),insulin resistance,type 2 diabetes mellitus,obesity,and the cluster of many of these pathologies in the form of metabolic syndrome is higher in human population segments that show high intake of fructose.Adolescent and young adults from lowincome families are especially at risk.We recently reviewed evidence from experimental animals and human data that confirms the deleterious effect of fructose on lipid and glucose metabolism.In this present review we update the information generated in the past 2 years about high consumption of fructose-enriched beverages and the occurrence of metabolic disturbances,especially NAFLD,type 2 diabetes mellitus,and metabolic syndrome.We have explored recent data from observational and experimental human studies,as well as experimental data from animal and cell models.Finally,using information generated in our laboratory and others,we provide a view of the molecular mechanisms that may be specifically involved in the development of liver lipid and glucose metabolic alterations after fructose consumption in liquid form.展开更多
This work aimed at investigating whether the liver glucose metabolism could have a role in any change of glucose homeostasis that might exist in the reduced-litter rat at the age of 60 days. Additionally, post-weaning...This work aimed at investigating whether the liver glucose metabolism could have a role in any change of glucose homeostasis that might exist in the reduced-litter rat at the age of 60 days. Additionally, post-weaning caloric restriction and its hepatic effects were explored, as this intervention is reported as a useful measure against obesity and its related disturbances. The animals were raised in litters of nine （control, CG） or three pups during lactation. These small-litter pups were FG （fed freely） or subjected to 30% RG （caloric restriction） after weaning until 60 days of age. The increased adiposity induced by lactational overfeeding was not reversed by caloric restriction. Hepatocyte glucose metabolism and glucose tolerance test were not affected by litter size, but caloric restriction increased liver basal glucose release, diminished gluconeogenesis and retarded the glycemic decay during the insulin tolerance test. Liver glucose metabolism of young adult rats was not affected by lactational overfeeding. Up to this age, however, moderate caloric restriction had a potent influence that might compromise whole-body glucose homeostasis and prompt to insulin resistance.展开更多
文摘腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK)是一种广泛参与多种代谢调节的激酶,是主要的细胞"能量感受器"。AMPK通过α亚基的Thr172发生磷酸化而激活,通过抑制脂质合成相关转录因子以及肝脏糖异生来控制脂质合成以及血糖稳定。肝脏糖异生的调控过程中,通过激素及转录因子如Fox O1、CREB、TORC2、HNF-4α、PGC-1α等的参与,最后将信号传达至糖异生的2个关键性限速酶基因PECK与G6Pase,起到调控作用。激活的AMPK能抑制糖异生转录因子及相关关键酶的有效表达,阻止肝脏发生糖异生,进而下降血糖浓度。本文旨在讨论与总结AMPK在肝脏糖脂代谢中的作用,重点分析AMPK与肝脏糖异生信号通路转录因子之间的联系。
基金Supported by Fundació Privada Catalana de Nutrició i Lípids and Grant SAF2010-15664 from the Spanish Ministry of Sci ence and Innovation
文摘The World Health Organization recommends that the daily intake of added sugars should make up no more than 10% of total energy.The consumption of sugarsweetened beverages is the main source of added sugars.Fructose,together with glucose,as a component of high fructose corn syrups or as a component of the sucrose molecule,is one of the main sweeteners present in this kind of beverages.Data from prospective and intervention studies clearly point to high fructose consumption,mainly in the form of sweetened beverages,as a risk factor for several metabolic diseases in humans.The incidence of hypertension,nonalcoholic fatty liver disease(NAFLD),dyslipidemia(mainly hypertriglyceridemia),insulin resistance,type 2 diabetes mellitus,obesity,and the cluster of many of these pathologies in the form of metabolic syndrome is higher in human population segments that show high intake of fructose.Adolescent and young adults from lowincome families are especially at risk.We recently reviewed evidence from experimental animals and human data that confirms the deleterious effect of fructose on lipid and glucose metabolism.In this present review we update the information generated in the past 2 years about high consumption of fructose-enriched beverages and the occurrence of metabolic disturbances,especially NAFLD,type 2 diabetes mellitus,and metabolic syndrome.We have explored recent data from observational and experimental human studies,as well as experimental data from animal and cell models.Finally,using information generated in our laboratory and others,we provide a view of the molecular mechanisms that may be specifically involved in the development of liver lipid and glucose metabolic alterations after fructose consumption in liquid form.
文摘This work aimed at investigating whether the liver glucose metabolism could have a role in any change of glucose homeostasis that might exist in the reduced-litter rat at the age of 60 days. Additionally, post-weaning caloric restriction and its hepatic effects were explored, as this intervention is reported as a useful measure against obesity and its related disturbances. The animals were raised in litters of nine （control, CG） or three pups during lactation. These small-litter pups were FG （fed freely） or subjected to 30% RG （caloric restriction） after weaning until 60 days of age. The increased adiposity induced by lactational overfeeding was not reversed by caloric restriction. Hepatocyte glucose metabolism and glucose tolerance test were not affected by litter size, but caloric restriction increased liver basal glucose release, diminished gluconeogenesis and retarded the glycemic decay during the insulin tolerance test. Liver glucose metabolism of young adult rats was not affected by lactational overfeeding. Up to this age, however, moderate caloric restriction had a potent influence that might compromise whole-body glucose homeostasis and prompt to insulin resistance.
