About 30% of patients with cirrhosis have diabetes mellitus(DM).Nowadays,it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease.DM...About 30% of patients with cirrhosis have diabetes mellitus(DM).Nowadays,it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease.DM,which develops as a complication of cirrhosis,is known as "hepatogenous diabetes".Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease.An impaired response of the islet β-cells of the pancreas and hepatic insulin resistance are also contributory factors.Non-alcoholic fatty liver disease,alcoholic cirrhosis,chronic hepatitis C(CHC) and hemochromatosis are more frequently associated with DM.Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis.DM in cirrhotic patients may be subclinical.Hepatogenous diabetes is clinically different from that of type 2 DM,since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis.DM increases the mortality of cirrhotic patients.Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs.This manuscript will review evidence that exists in relation to:type 2 DM alone or as part of the metabolic syndrome in the development of liver disease;factors involved in the genesis of hepatogenous diabetes;the impact of DM on the clinical outcome of liver disease;the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.展开更多
Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress...Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM.展开更多
给9日龄 SD 雌性大鼠注射丙酸睾丸酮造成雄激素致不孕大鼠(ASR),分别观察卵巢形态、血液及组织匀浆激素含量、糖耐量和血胰岛素水平以及卵泡膜和卵巢间质细胞在体外不同刺激状态下(空白、加胰岛素、加 hCG、加胰岛素+hCG)的 T 含量。结...给9日龄 SD 雌性大鼠注射丙酸睾丸酮造成雄激素致不孕大鼠(ASR),分别观察卵巢形态、血液及组织匀浆激素含量、糖耐量和血胰岛素水平以及卵泡膜和卵巢间质细胞在体外不同刺激状态下(空白、加胰岛素、加 hCG、加胰岛素+hCG)的 T 含量。结果发现:(1)卵巢体积缩小,呈多囊性改变,无黄体;(2)垂体 LH 含量比对照组降低(P<0.01),肾上腺及卵巢中 T、E_2 含量明显升高(分别为P<0.05及P<0.01);(3)糖耐量下降,胰岛素水平显著升高(分别为 P<0.01及 P<0.05);(4)卵泡膜和卵巢间质细胞体外培养 T 含量明显高于对照组(P<0.001),在 hCG 协同作用下胰岛素可使 ASR 及正常大鼠卵巢 T 含量明显增加(P<0.01)。提示雄激素致不孕大鼠可作为高胰岛素和高雄激素性无排卵的动物模型。展开更多
文摘About 30% of patients with cirrhosis have diabetes mellitus(DM).Nowadays,it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease.DM,which develops as a complication of cirrhosis,is known as "hepatogenous diabetes".Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease.An impaired response of the islet β-cells of the pancreas and hepatic insulin resistance are also contributory factors.Non-alcoholic fatty liver disease,alcoholic cirrhosis,chronic hepatitis C(CHC) and hemochromatosis are more frequently associated with DM.Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis.DM in cirrhotic patients may be subclinical.Hepatogenous diabetes is clinically different from that of type 2 DM,since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis.DM increases the mortality of cirrhotic patients.Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs.This manuscript will review evidence that exists in relation to:type 2 DM alone or as part of the metabolic syndrome in the development of liver disease;factors involved in the genesis of hepatogenous diabetes;the impact of DM on the clinical outcome of liver disease;the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.
文摘Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM.
文摘给9日龄 SD 雌性大鼠注射丙酸睾丸酮造成雄激素致不孕大鼠(ASR),分别观察卵巢形态、血液及组织匀浆激素含量、糖耐量和血胰岛素水平以及卵泡膜和卵巢间质细胞在体外不同刺激状态下(空白、加胰岛素、加 hCG、加胰岛素+hCG)的 T 含量。结果发现:(1)卵巢体积缩小,呈多囊性改变,无黄体;(2)垂体 LH 含量比对照组降低(P<0.01),肾上腺及卵巢中 T、E_2 含量明显升高(分别为P<0.05及P<0.01);(3)糖耐量下降,胰岛素水平显著升高(分别为 P<0.01及 P<0.05);(4)卵泡膜和卵巢间质细胞体外培养 T 含量明显高于对照组(P<0.001),在 hCG 协同作用下胰岛素可使 ASR 及正常大鼠卵巢 T 含量明显增加(P<0.01)。提示雄激素致不孕大鼠可作为高胰岛素和高雄激素性无排卵的动物模型。
