BACKGROUND Autonomous cortisol secretion(ACS)is linked to a higher prevalence of metabolic abnormalities and an increased risk of major adverse cardiovascular events.AIM To evaluate glucose and bone metabolism in pati...BACKGROUND Autonomous cortisol secretion(ACS)is linked to a higher prevalence of metabolic abnormalities and an increased risk of major adverse cardiovascular events.AIM To evaluate glucose and bone metabolism in patients with ACS using a continuous glucose monitoring system(CGMS)and dual-energy X-ray absorptiometry(DXA).METHODS Patients diagnosed with ACS,including Cushing syndrome,mild ACS(MACS),and nonfunctional adrenal incidentaloma(NFAI),were recruited for this study.Glucose variability and glycemic status were assessed using CGMS.Regional bone mineral content(BMC),bone mineral density(BMD),and bone area(BA)were evaluated using DXA.CGMS-and DXA-derived parameters were compared across the subgroups of ACS.Correlation analysis was performed to examine relationships between varying degrees of cortisol secretion,measured by cortisol after 1 mg overnight dexamethasone suppression test(DST)or 24-hour urine free cortisol(24h UFC),and CGMS-or DXA-derived parameters.RESULTS A total of 64 patients with ACS were included in this study:19 with Cushing syndrome,11 with MACS,and 34 with NFAI.Glucose variability,time above range(TAR),and time in range(TIR)along with specific areal BMC,BMD,and BA,differed significantly between groups of Cushing syndrome and NFAI.A significant positive correlation was observed between glucose variability or TAR and cortisol after 1 mg overnight DST or 24h UFC.By contrast,TIR,along with regional BMC,BMD,and BA,were negatively correlated with varying degrees of cortisol secretion.CONCLUSION Glucose and bone metabolism impairments are on a continuum alteration from NFAI to MACS and Cushing syndrome.Prompt attention should be given to these patients with ACS,especially those with mild hormone secretion.Parameters of glucose variability and glycemic status along with bone condition in regions rich in cancellous bone will provide valuable information.展开更多
DNAJC12基因编码DNAJC12蛋白,后者为热休克蛋白40(DnaJ heat shock protein family,HSP40)家族成员,该家族功能是帮助热休克蛋白70(heat shock protein 70,HSP70)维持蛋白质稳态。DNAJC12双等位基因突变可导致患者出现血苯丙氨酸浓度升...DNAJC12基因编码DNAJC12蛋白,后者为热休克蛋白40(DnaJ heat shock protein family,HSP40)家族成员,该家族功能是帮助热休克蛋白70(heat shock protein 70,HSP70)维持蛋白质稳态。DNAJC12双等位基因突变可导致患者出现血苯丙氨酸浓度升高、智力障碍、帕金森、肌张力异常及精神行为异常等临床表现;DNAJC12基因的表达异常与肿瘤、抑郁症等疾病的发生和进展有关。本文就DNAJC12双等位基因突变及表达异常与疾病关系的最新研究进展进行综述。展开更多
Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reporte...Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine. Homocysteine induces necrosis of endothelium, proliferation of vascular smooth muscle cells, proliferation and activation of vascular fibroblast cells and mitochondrial structural destruction and dysfunction of myocardium cells. Taurine, an end metabolic product of homocysteine, obviously reduces cardiovascular injury induced by homocysteine. The possible mechanism of antagonism by reducing oxidative stress and endoplasmic reticulum stress has been proved. Hydrogen sulfide, another end metabolic product of homocysteine, obviously reducing cardiovascular injury of homocysteine by scavenging oxidative radicals has been found. Metallothionein a derivant production of homocysteine metabolism, antagonism to homocysteine injury to cardiovascular system been discussed. Homocysteine, taurine, hydrogen sulfide and metallothionein, as a metabolic product of methionine, interactive antagonism and interactive biological influence have been reviewed. Induced endogenous or exogenous supply of taurine, hydrogen sulfide and metallothionein might resist cardiovascular injury induced by hyperhomocysteinemia. According to the methionine metabolic cycle, using endogenous antagonistic substances might be a new clinical preventive and treatment target of homocystinemia.展开更多
基金Supported by National Natural Science Foundation of China(General Program),No.82073909Four‘Batches’Innovation Project of Invigorating Medical through Science and Technology of Shanxi Province,No.2023XM022The Shanxi Provincial Central Leading Local Science and Technology Development Fund Project,No.YDZJSX2022A059 and No.YDZJSX20231A059。
文摘BACKGROUND Autonomous cortisol secretion(ACS)is linked to a higher prevalence of metabolic abnormalities and an increased risk of major adverse cardiovascular events.AIM To evaluate glucose and bone metabolism in patients with ACS using a continuous glucose monitoring system(CGMS)and dual-energy X-ray absorptiometry(DXA).METHODS Patients diagnosed with ACS,including Cushing syndrome,mild ACS(MACS),and nonfunctional adrenal incidentaloma(NFAI),were recruited for this study.Glucose variability and glycemic status were assessed using CGMS.Regional bone mineral content(BMC),bone mineral density(BMD),and bone area(BA)were evaluated using DXA.CGMS-and DXA-derived parameters were compared across the subgroups of ACS.Correlation analysis was performed to examine relationships between varying degrees of cortisol secretion,measured by cortisol after 1 mg overnight dexamethasone suppression test(DST)or 24-hour urine free cortisol(24h UFC),and CGMS-or DXA-derived parameters.RESULTS A total of 64 patients with ACS were included in this study:19 with Cushing syndrome,11 with MACS,and 34 with NFAI.Glucose variability,time above range(TAR),and time in range(TIR)along with specific areal BMC,BMD,and BA,differed significantly between groups of Cushing syndrome and NFAI.A significant positive correlation was observed between glucose variability or TAR and cortisol after 1 mg overnight DST or 24h UFC.By contrast,TIR,along with regional BMC,BMD,and BA,were negatively correlated with varying degrees of cortisol secretion.CONCLUSION Glucose and bone metabolism impairments are on a continuum alteration from NFAI to MACS and Cushing syndrome.Prompt attention should be given to these patients with ACS,especially those with mild hormone secretion.Parameters of glucose variability and glycemic status along with bone condition in regions rich in cancellous bone will provide valuable information.
文摘DNAJC12基因编码DNAJC12蛋白,后者为热休克蛋白40(DnaJ heat shock protein family,HSP40)家族成员,该家族功能是帮助热休克蛋白70(heat shock protein 70,HSP70)维持蛋白质稳态。DNAJC12双等位基因突变可导致患者出现血苯丙氨酸浓度升高、智力障碍、帕金森、肌张力异常及精神行为异常等临床表现;DNAJC12基因的表达异常与肿瘤、抑郁症等疾病的发生和进展有关。本文就DNAJC12双等位基因突变及表达异常与疾病关系的最新研究进展进行综述。
文摘Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine. Homocysteine induces necrosis of endothelium, proliferation of vascular smooth muscle cells, proliferation and activation of vascular fibroblast cells and mitochondrial structural destruction and dysfunction of myocardium cells. Taurine, an end metabolic product of homocysteine, obviously reduces cardiovascular injury induced by homocysteine. The possible mechanism of antagonism by reducing oxidative stress and endoplasmic reticulum stress has been proved. Hydrogen sulfide, another end metabolic product of homocysteine, obviously reducing cardiovascular injury of homocysteine by scavenging oxidative radicals has been found. Metallothionein a derivant production of homocysteine metabolism, antagonism to homocysteine injury to cardiovascular system been discussed. Homocysteine, taurine, hydrogen sulfide and metallothionein, as a metabolic product of methionine, interactive antagonism and interactive biological influence have been reviewed. Induced endogenous or exogenous supply of taurine, hydrogen sulfide and metallothionein might resist cardiovascular injury induced by hyperhomocysteinemia. According to the methionine metabolic cycle, using endogenous antagonistic substances might be a new clinical preventive and treatment target of homocystinemia.
