BACKGROUND The effect of the sympathetic nervous system on peripheral arteries causes vasoconstriction when smooth muscle cells in the walls of blood vessels contract,which leads to narrowing of arteries and reduction...BACKGROUND The effect of the sympathetic nervous system on peripheral arteries causes vasoconstriction when smooth muscle cells in the walls of blood vessels contract,which leads to narrowing of arteries and reduction of the blood flow.AIM To compare sympathetic vasomotor activation of the brachial arteries in healthy subjects and patients with painful diabetic neuropathy;and therefore,to assess whether there is significant vasomotor dysfunction of medium sized arteries in diabetic neuropathy.METHODS The study included 41 diabetic neuropathy patients and 41 healthy controls.Baseline diameter and flow rate of the brachial arteries were measured.Then,using a bipolar stimulus electrode,a 10 mA,1 Hz electrical stimulus was administered to the median nerve at the wrist level for 5 s.The brachial artery diameter and blood flow rate were re-measured after stimulation.RESULTS In the control group,the median flow rate was 70.0 mL/min prior to stimulation and 35.0 mL/min after stimulation,with a statistically significant decrease(P<0.001),which is consistent with sympathetic nervous system functioning(vasoconstriction).In the diabetic neuropathy group,median flow rate before the stimulation was 35.0 mL/min.After stimulation,the median flow rate was 77.0 mL/min;thus,no significant decrease in the flow rate was detected.In the control group,the median brachial artery diameter,which was 3.6 mm prior to stimulation,decreased to 3.4 mm after stimulation,and this decrease was also statistically significant(P=0.046).In the diabetic neuropathy group,the median brachial artery diameter increased from 3.4 mm to 3.6 mm following nerve stimulation.Once again,no narrowing was observed.CONCLUSION Our research suggests that diabetic neuropathy results in significant vasomotor dysfunction of medium sized peripheral arteries.Physiological vasoconstriction in response to sympathetic activation is impaired in diabetic neuropathy.展开更多
BACKGROUND Time in range(TIR),as a novel metric for glycemic control,has robust relevance with diabetic complications.Diabetic peripheral neuropathy(DPN)is characterized by sudomotor dysfunction.AIM To explore the rel...BACKGROUND Time in range(TIR),as a novel metric for glycemic control,has robust relevance with diabetic complications.Diabetic peripheral neuropathy(DPN)is characterized by sudomotor dysfunction.AIM To explore the relationship between TIR obtained from continuous glucose monitoring(CGM)and sudomotor function detected by SUDOSCAN in subjects with type 2 diabetes.METHODS The research enrolled 466 inpatients with type 2 diabetes.All subjects underwent 3-d CGM and SUDOSCAN.SUDOSCAN was assessed with electrochemical skin conductance in hands(HESC)and feet(FESC).Average feet ESC<60μS was defined as sudomotor dysfunction(+),otherwise it was sudomotor dysfunction(-).TIR refers to the percentage of time when blood glucose is between 3.9-10 mmol/L during 1 d period.RESULTS Among the enrolled subjects,135(28.97%)presented with sudomotor dysfunction.Patients with sudomotor dysfunction(+)showed a decreased level of TIR(P<0.001).Compared to the lowest tertile of TIR,the middle and the highest tertiles of TIR was associated with an obviously lower prevalence of sudomotor dysfunction(20.51%and 21.94%vs 44.52%)(P<0.001).In addition,with the increase of TIR,HESC and FESC increased(P<0.001).Regression analysis demonstrated that TIR was inversely and independently linked with the prevalence of sudomotor dysfunction after adjusting for confounding values(odds ratio=0.979,95%CI:0.971-0.987,P<0.001).CONCLUSION The tight glycemic control assessed by TIR is of vitally protective value for sudomotor dysfunction in type 2 diabetes mellitus.展开更多
Hydrogen sulfide is an antioxidant molecule that has a wide range of biological effects against oxidative stress. Balanced oxidative stress is also vital for maintaining cellular function in biological system, where r...Hydrogen sulfide is an antioxidant molecule that has a wide range of biological effects against oxidative stress. Balanced oxidative stress is also vital for maintaining cellular function in biological system, where reactive oxygen species are the main source of oxidative stress. When the normal redox balance is disturbed, deoxyribonucleic acid, lipid, and protein molecules are oxidized under pathological conditions, like diabetes mellitus that leads to diabetic peripheral neuropathy. In diabetes mellitus-induced diabetic peripheral neuropathy, due to hyperglycemia, pancreatic beta cell(β cell) shows resistance to insulin secretion. As a consequence, glucose metabolism is disturbed in neuronal cells which are distracted from providing proper cell signaling pathway. Not only diabetic peripheral neuropathy but also other central damages occur in brain neuropathy. Neurological studies regarding type 1 diabetes mellitus patients with Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis have shown changes in the central nervous system because high blood glucose levels(HbA1 c) appeared with poor cognitive function. Oxidative stress plays a role in inhibiting insulin signaling that is necessary for brain function. Hydrogen sulfide exhibits antioxidant effects against oxidative stress, where cystathionine β synthase, cystathionine γ lyase, and 3-mercaptopyruvate sulfurtransferase are the endogenous sources of hydrogen sulfide. This review is to explore the pathogenesis of diabetes mellitus-induced diabetic peripheral neuropathy and other neurological comorbid disorders under the oxidative stress condition and the anti-oxidative effects of hydrogen sulfide.展开更多
文摘BACKGROUND The effect of the sympathetic nervous system on peripheral arteries causes vasoconstriction when smooth muscle cells in the walls of blood vessels contract,which leads to narrowing of arteries and reduction of the blood flow.AIM To compare sympathetic vasomotor activation of the brachial arteries in healthy subjects and patients with painful diabetic neuropathy;and therefore,to assess whether there is significant vasomotor dysfunction of medium sized arteries in diabetic neuropathy.METHODS The study included 41 diabetic neuropathy patients and 41 healthy controls.Baseline diameter and flow rate of the brachial arteries were measured.Then,using a bipolar stimulus electrode,a 10 mA,1 Hz electrical stimulus was administered to the median nerve at the wrist level for 5 s.The brachial artery diameter and blood flow rate were re-measured after stimulation.RESULTS In the control group,the median flow rate was 70.0 mL/min prior to stimulation and 35.0 mL/min after stimulation,with a statistically significant decrease(P<0.001),which is consistent with sympathetic nervous system functioning(vasoconstriction).In the diabetic neuropathy group,median flow rate before the stimulation was 35.0 mL/min.After stimulation,the median flow rate was 77.0 mL/min;thus,no significant decrease in the flow rate was detected.In the control group,the median brachial artery diameter,which was 3.6 mm prior to stimulation,decreased to 3.4 mm after stimulation,and this decrease was also statistically significant(P=0.046).In the diabetic neuropathy group,the median brachial artery diameter increased from 3.4 mm to 3.6 mm following nerve stimulation.Once again,no narrowing was observed.CONCLUSION Our research suggests that diabetic neuropathy results in significant vasomotor dysfunction of medium sized peripheral arteries.Physiological vasoconstriction in response to sympathetic activation is impaired in diabetic neuropathy.
基金National Natural Science Foundation of China,No.81774134 and No.81873174Natural Science Foundation of Jiangsu Province of China,No.BK20150558 and No.BK20171331+2 种基金Postdoctoral Foundation of Jiangsu Province of China,No.1501120CJiangsu Province 333 Talent Funding Project,No.BRA2017595Young Medical Key Talents Project of Jiangsu Province,No.QNRC2016902.
文摘BACKGROUND Time in range(TIR),as a novel metric for glycemic control,has robust relevance with diabetic complications.Diabetic peripheral neuropathy(DPN)is characterized by sudomotor dysfunction.AIM To explore the relationship between TIR obtained from continuous glucose monitoring(CGM)and sudomotor function detected by SUDOSCAN in subjects with type 2 diabetes.METHODS The research enrolled 466 inpatients with type 2 diabetes.All subjects underwent 3-d CGM and SUDOSCAN.SUDOSCAN was assessed with electrochemical skin conductance in hands(HESC)and feet(FESC).Average feet ESC<60μS was defined as sudomotor dysfunction(+),otherwise it was sudomotor dysfunction(-).TIR refers to the percentage of time when blood glucose is between 3.9-10 mmol/L during 1 d period.RESULTS Among the enrolled subjects,135(28.97%)presented with sudomotor dysfunction.Patients with sudomotor dysfunction(+)showed a decreased level of TIR(P<0.001).Compared to the lowest tertile of TIR,the middle and the highest tertiles of TIR was associated with an obviously lower prevalence of sudomotor dysfunction(20.51%and 21.94%vs 44.52%)(P<0.001).In addition,with the increase of TIR,HESC and FESC increased(P<0.001).Regression analysis demonstrated that TIR was inversely and independently linked with the prevalence of sudomotor dysfunction after adjusting for confounding values(odds ratio=0.979,95%CI:0.971-0.987,P<0.001).CONCLUSION The tight glycemic control assessed by TIR is of vitally protective value for sudomotor dysfunction in type 2 diabetes mellitus.
基金supported by Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Science,ICT and Future Planning,No.2018R1A2B6001123(to NYJ),No.2018R1D1A1B07040282(to JJ)
文摘Hydrogen sulfide is an antioxidant molecule that has a wide range of biological effects against oxidative stress. Balanced oxidative stress is also vital for maintaining cellular function in biological system, where reactive oxygen species are the main source of oxidative stress. When the normal redox balance is disturbed, deoxyribonucleic acid, lipid, and protein molecules are oxidized under pathological conditions, like diabetes mellitus that leads to diabetic peripheral neuropathy. In diabetes mellitus-induced diabetic peripheral neuropathy, due to hyperglycemia, pancreatic beta cell(β cell) shows resistance to insulin secretion. As a consequence, glucose metabolism is disturbed in neuronal cells which are distracted from providing proper cell signaling pathway. Not only diabetic peripheral neuropathy but also other central damages occur in brain neuropathy. Neurological studies regarding type 1 diabetes mellitus patients with Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis have shown changes in the central nervous system because high blood glucose levels(HbA1 c) appeared with poor cognitive function. Oxidative stress plays a role in inhibiting insulin signaling that is necessary for brain function. Hydrogen sulfide exhibits antioxidant effects against oxidative stress, where cystathionine β synthase, cystathionine γ lyase, and 3-mercaptopyruvate sulfurtransferase are the endogenous sources of hydrogen sulfide. This review is to explore the pathogenesis of diabetes mellitus-induced diabetic peripheral neuropathy and other neurological comorbid disorders under the oxidative stress condition and the anti-oxidative effects of hydrogen sulfide.
