Diabetic kidney disease(DKD) is one of the most common diabetic complications, as well as the leading cause of chronic kidney disease and end-stage renal disease around the world. To prevent the dreadful consequence, ...Diabetic kidney disease(DKD) is one of the most common diabetic complications, as well as the leading cause of chronic kidney disease and end-stage renal disease around the world. To prevent the dreadful consequence, development of new assays for diagnostic of DKD has always been the priority in the research field of diabetic complications. At present, urinary albumin-to-creatinine ratio and estimated glomerular filtration rate(eG FR) are the standard methods for assessing glomerular damage and renal function changes in clinical practice. However, due to diverse tissue involvement in different individuals, the so-called "non-albuminuric renal impairment" is not uncommon, especially in patients with type 2 diabetes. On the other hand, the precision of creatinine-based GFR estimates is limited in hyperfiltration status. These facts make albuminuria and eG FR less reliable indicators for early-stage DKD. In recent years, considerable progress has been made in the understanding of the pathogenesis of DKD, along with the elucidation of its genetic profiles and phenotypic expression of different molecules. With the help of ever-evolving technologies, it has gradually become plausible to apply the thriving information in clinical practice. The strength and weakness of several novel biomarkers, genomic, proteomic and metabolomic signatures in assisting the early diagnosis of DKD will be discussed in this article.展开更多
Diabetic complications including diabetic nephropathy,retinopathy,and neuropathy are as major causes of morbidity and mortality in diabetes individuals worldwide and current therapies are still unsatisfactory.One of t...Diabetic complications including diabetic nephropathy,retinopathy,and neuropathy are as major causes of morbidity and mortality in diabetes individuals worldwide and current therapies are still unsatisfactory.One of the reasons for failure to develop effective treatment is the lack of fundamental understanding for underlying mechanisms.Genetic studies are powerful tools to dissect disease mechanism.The heritability(h2) was estimated to be 0.3-0.44 for diabetic nephropathy and 0.25-0.50 for diabetic retinopathy respectively.Previous linkage studies for diabetic nephropathy have identified overlapped linkage regions in 1q43-44,3q21-23,3q26,10p12-15,18q22-23,19q13,22q11-12.3 in multiple ethnic groups.Genome-wide association studies(GWAS) of diabetic nephropathy have been conducted in several populations.However,most of the identified risk loci could not be replicated by independent studies with a few exceptions including those in ELMO1,FRMD3,CARS,MYO16/IRS2,and APOL3-MYH9 genes.Functional studies of these genes revealed the involvement of cytoskeleton reorganization(especially non-muscle type myosin),phagocytosis of apoptotic cells,fibroblast migration,insulin signaling,and epithelial clonal expansion in the pathogenesis of diabetic nephropathy.Linkage analyses of diabetic retinopathy overlapped only in 1q36 region and current results from GWAS for diabetic retinopathy are inconsistent.Conclusive results from genetic studies for diabetic neuropathy are lacking.For now,small sample sizes,confounding by population stratification,different phenotype definitions between studies,ethnic-specific associations,the influence of environmental factors,and the possible contribution of rare variants may explain the inconsistencies between studies.展开更多
AIM: To investigate the relationship of iron indices with diabetes mellitus(DM) in those without hemochromatosis.METHODS: This cross-sectional study examined data collected during the Third National Health and Nutriti...AIM: To investigate the relationship of iron indices with diabetes mellitus(DM) in those without hemochromatosis.METHODS: This cross-sectional study examined data collected during the Third National Health and Nutrition Examination Survey(NHANES III). Only those who fasted properly and were not anemic with transferrin saturation < 45% were included(n = 6849). Insulin sensitivity and beta cell function were calculated from fasting glucose and insulin concentrations. Indices of iron metabolism were examined in the presence or absence of DM. We examined the relationship of insulin sensitivity and beta cell function with serum ferritin concentration. The influence of C-reactive protein and liver enzymes was also investigated.RESULTS: Serum ferritin concentration was significantly higher in diabetic subjects(P = 0.0001 to< 0.000001). The difference remained significant after adjustment for age, body mass index, alcohol consumption, and mineral/iron supplement(P = 0.03 to< 0.000001). In those who did not take insulin, serum ferritin concentration was negatively associated with insulin sensitivity(P = 0.05 to 0.00001), but not with beta cell function. The alanine aminotransferase was correlated with serum ferritin concentration(P = 0.02 to< 0.000001) but not with insulin sensitivity, suggesting the role of the liver in iron-associated insulin resistance.CONCLUSION: As most of diabetes is type 2 diabetes and insulin resistance is a cardinal feature of type 2diabetes, disordered iron metabolism could play a role in the pathogenesis of insulin resistance and type 2diabetes through its effect on liver function.展开更多
BACKGROUND Although much information is available regarding hepatitis C virus infection and diabetes,less is known about the relationship between hepatitis A virus(HAV)infection and diabetes.AIM To examine the roles o...BACKGROUND Although much information is available regarding hepatitis C virus infection and diabetes,less is known about the relationship between hepatitis A virus(HAV)infection and diabetes.AIM To examine the roles of HAV in diabetes risk.METHODS This cross-sectional study population included data from the National Health and Nutrition Examination Survey collected between 2005-2012.Adult subjects(≥20 years old)with available body mass index measurements,defined diabetes status,history of HAV vaccination,and HAV serology were included.HAV vaccination was based on self-reported history.Successful HAV immunization was defined as the presence of both vaccination and anti-HAV antibody.HAV infection was defined by the absence of vaccination but presence of anti-hepatitis A antibody.The odds ratio(OR)for diabetes with 95%confidence intervals(95%CI)was calculated for each HAV status and then adjusted for covariates.Sensitivity tests,based on different definitions of diabetes,were performed to verify the results.RESULTS Among 19942 subjects,4229 subjects(21.21%)received HAV vaccination and HAV antibody was present in 9224 subjects(46.25%).Although HAV infection was associated with an increased risk of diabetes(OR:1.13;95%CI:1.08-1.18),HAV vaccination was not associated with diabetes(OR:1.06;95%CI:0.95-1.18),and successful HAV immunization had no impact on the risk of diabetes(OR:1.11;95%CI:0.97-1.27).Thus,HAV infection was an unlikely cause of diabetes.Alternatively,in non-vaccinated subjects,diabetes increased the risk of HAV infection by 40%(OR:1.40,95%CI:1.27-1.54).CONCLUSION An association between HAV infection and diabetes is observed which is best explained by an increased risk of HAV infection in diabetic patients.Diabetic subjects are more susceptible to HAV.Thus,HAV vaccination is highly recommended in diabetic patients.展开更多
文摘Diabetic kidney disease(DKD) is one of the most common diabetic complications, as well as the leading cause of chronic kidney disease and end-stage renal disease around the world. To prevent the dreadful consequence, development of new assays for diagnostic of DKD has always been the priority in the research field of diabetic complications. At present, urinary albumin-to-creatinine ratio and estimated glomerular filtration rate(eG FR) are the standard methods for assessing glomerular damage and renal function changes in clinical practice. However, due to diverse tissue involvement in different individuals, the so-called "non-albuminuric renal impairment" is not uncommon, especially in patients with type 2 diabetes. On the other hand, the precision of creatinine-based GFR estimates is limited in hyperfiltration status. These facts make albuminuria and eG FR less reliable indicators for early-stage DKD. In recent years, considerable progress has been made in the understanding of the pathogenesis of DKD, along with the elucidation of its genetic profiles and phenotypic expression of different molecules. With the help of ever-evolving technologies, it has gradually become plausible to apply the thriving information in clinical practice. The strength and weakness of several novel biomarkers, genomic, proteomic and metabolomic signatures in assisting the early diagnosis of DKD will be discussed in this article.
文摘Diabetic complications including diabetic nephropathy,retinopathy,and neuropathy are as major causes of morbidity and mortality in diabetes individuals worldwide and current therapies are still unsatisfactory.One of the reasons for failure to develop effective treatment is the lack of fundamental understanding for underlying mechanisms.Genetic studies are powerful tools to dissect disease mechanism.The heritability(h2) was estimated to be 0.3-0.44 for diabetic nephropathy and 0.25-0.50 for diabetic retinopathy respectively.Previous linkage studies for diabetic nephropathy have identified overlapped linkage regions in 1q43-44,3q21-23,3q26,10p12-15,18q22-23,19q13,22q11-12.3 in multiple ethnic groups.Genome-wide association studies(GWAS) of diabetic nephropathy have been conducted in several populations.However,most of the identified risk loci could not be replicated by independent studies with a few exceptions including those in ELMO1,FRMD3,CARS,MYO16/IRS2,and APOL3-MYH9 genes.Functional studies of these genes revealed the involvement of cytoskeleton reorganization(especially non-muscle type myosin),phagocytosis of apoptotic cells,fibroblast migration,insulin signaling,and epithelial clonal expansion in the pathogenesis of diabetic nephropathy.Linkage analyses of diabetic retinopathy overlapped only in 1q36 region and current results from GWAS for diabetic retinopathy are inconsistent.Conclusive results from genetic studies for diabetic neuropathy are lacking.For now,small sample sizes,confounding by population stratification,different phenotype definitions between studies,ethnic-specific associations,the influence of environmental factors,and the possible contribution of rare variants may explain the inconsistencies between studies.
文摘AIM: To investigate the relationship of iron indices with diabetes mellitus(DM) in those without hemochromatosis.METHODS: This cross-sectional study examined data collected during the Third National Health and Nutrition Examination Survey(NHANES III). Only those who fasted properly and were not anemic with transferrin saturation < 45% were included(n = 6849). Insulin sensitivity and beta cell function were calculated from fasting glucose and insulin concentrations. Indices of iron metabolism were examined in the presence or absence of DM. We examined the relationship of insulin sensitivity and beta cell function with serum ferritin concentration. The influence of C-reactive protein and liver enzymes was also investigated.RESULTS: Serum ferritin concentration was significantly higher in diabetic subjects(P = 0.0001 to< 0.000001). The difference remained significant after adjustment for age, body mass index, alcohol consumption, and mineral/iron supplement(P = 0.03 to< 0.000001). In those who did not take insulin, serum ferritin concentration was negatively associated with insulin sensitivity(P = 0.05 to 0.00001), but not with beta cell function. The alanine aminotransferase was correlated with serum ferritin concentration(P = 0.02 to< 0.000001) but not with insulin sensitivity, suggesting the role of the liver in iron-associated insulin resistance.CONCLUSION: As most of diabetes is type 2 diabetes and insulin resistance is a cardinal feature of type 2diabetes, disordered iron metabolism could play a role in the pathogenesis of insulin resistance and type 2diabetes through its effect on liver function.
文摘BACKGROUND Although much information is available regarding hepatitis C virus infection and diabetes,less is known about the relationship between hepatitis A virus(HAV)infection and diabetes.AIM To examine the roles of HAV in diabetes risk.METHODS This cross-sectional study population included data from the National Health and Nutrition Examination Survey collected between 2005-2012.Adult subjects(≥20 years old)with available body mass index measurements,defined diabetes status,history of HAV vaccination,and HAV serology were included.HAV vaccination was based on self-reported history.Successful HAV immunization was defined as the presence of both vaccination and anti-HAV antibody.HAV infection was defined by the absence of vaccination but presence of anti-hepatitis A antibody.The odds ratio(OR)for diabetes with 95%confidence intervals(95%CI)was calculated for each HAV status and then adjusted for covariates.Sensitivity tests,based on different definitions of diabetes,were performed to verify the results.RESULTS Among 19942 subjects,4229 subjects(21.21%)received HAV vaccination and HAV antibody was present in 9224 subjects(46.25%).Although HAV infection was associated with an increased risk of diabetes(OR:1.13;95%CI:1.08-1.18),HAV vaccination was not associated with diabetes(OR:1.06;95%CI:0.95-1.18),and successful HAV immunization had no impact on the risk of diabetes(OR:1.11;95%CI:0.97-1.27).Thus,HAV infection was an unlikely cause of diabetes.Alternatively,in non-vaccinated subjects,diabetes increased the risk of HAV infection by 40%(OR:1.40,95%CI:1.27-1.54).CONCLUSION An association between HAV infection and diabetes is observed which is best explained by an increased risk of HAV infection in diabetic patients.Diabetic subjects are more susceptible to HAV.Thus,HAV vaccination is highly recommended in diabetic patients.
