The Standards of Medical Care in Diabetes released by the American Diabetes Association (ADA) is one of the most important guidelines for clinicians. Based on the latest evidence of clinical studies, the Standards of Medical Care in Diabetes is annually updated by ADA. The statements of ADA on diagnosis, assessment, and management in diabetes are recommended for clinicians, patients, and researchers. The latest edition of Standards of Medical Care in Diabetes was published in a supplementary issue of Diabetes Care in January 2018. This interpretation will focus on the updated contents and their best evidence and clinical importance in this guideline.
Gitelman syndrome (GS) is an autosomal recessive kidney disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. The disorder is named for Gitelman, an American nephrologist. He first described it in 1966, after observing a pair of sisters with the disorder. The disorder is caused by inactivating mutations in the SLC12A3 gene, resulting in improper function of the thiazide-sensitive sodium-chloride co-transporter located in the distal convoluted tubule of the kidney. GS was formerly considered a subset of Bartter syndrome until the distinct genetic and molecular bases of these disorders were identified. GS is usually managed by a liberal salt intake together with oral magnesium and potassium supplements. This review aims to establish an initial framework to enable clinical auditing and thus improve quality control of care.
Polycystic ovary syndrome (PCOS) affects many women of reproductive age, including ovarian and metabolic dysfunction. Major therapeutic goals include weight loss and improved insulin resistance. The effects of weight loss and increased insulin sensitivity of glucagon-like peptide-1 (GLP-1) receptor agonists provide another opportunity and pathway for the treatment of PCOS patients, especially those with metabolic abnormalities. This paper reviews the metabolism and reproductive outcomes about GLP-1 receptor agonists for PCOS by searching for literatures of clinical trials from PubMed in the past 10 years, in oder to provide new ideas and clinical evidence for clinical treatment of PCOS.
Diabetes is characterised by hyperglycaemia resulted as the relative or absolute insulin deficiency which is closely related to islet beta cell failure. Apoptosis is the core mechanism of beta cell failure according to the studies on human islet. However, apoptosis can’t fully explain the loss of beta cell mass in the process of type 2 diabetes or the protective effect of early intervention. Recently, some other possible mechanisms of beta cell dysfunction have been proposed and dedifferentiation of beta cell draws extensive attention. Evidences of beta cell dedifferentiation in type 2 diabetes patients and animal models outlined and the transcription factors which determine beta cells of identity during this procedure are discussed in this review.
The islet transplantation site can be divided into two categories: orthotopic islet transplantation and ectopic islet transplantation. Orthotopic islet transplantation refers to that the insulin secreted and released from the transplanted islet will be metabolized into the liver through the hepatic portal vein system, which does not change the original insulin metabolic pathway, including the portal vein of the liver, the greater omentum. The insulin secreted by the ectopic islet transplantation changes the original metabolic pathway of insulin. The ideal islet transplantation site generally has the following characteristics: high success rate transplantation, high long-term survival rate of graft, simple operation, less trauma, less complications, low risk, easy to repeat detection and so on. This article provides a review of the current research status of each islet transplantation site, in order to provide reference for future related research.
Hypertension is a strong risk factor for atherosclerotic cardiovascular disease (ASCVD), heart failure, and microvascular complications. Hypertension is common among patients with diabetes. Recently, the American Diabetes Association (ADA) published a new position statement which updated the assessment and treatment for hypertensive patients with diabetes. This interpretation is intended to help Chinese clinicians to understand the new ADA position statement.
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
Objective To investigate the long-term dynamic changes of liver function and glucose-lipid metabolism in human immunodeficiency virus (HIV)-infected patients with metabolic dysfunction-associated fatty liver disease (MAFLD) after antiretroviral therapy (ART). Methods HIV-infected patients who visited Public Health Clinical Center of Chengdu between October 1st, 2012 and June 30th, 2013 were recruited and divided into two groups according to whether they had MAFLD or not. All of them were treated with the first-line regimen of tenofovir + lamivudine + efavirenz for 156 weeks, and the anthropometric indices, liver function, and levels of glucose, lipids and uric acid were measured at baseline and at each follow-up time point. In addition, the long-term dynamic characteristics of liver function and glucose and lipid metabolism parameters of the two groups were compared during the 156 weeks of ART treatment. Results A total of 61 male HIV-infected patients were enrolled. The prevalence of MAFLD in them was 31.1% (19/61) at baseline and increased by 4.9 percentage points per year after ART. Before the start of follow-up (week 0), the levels of alanine aminotransferase (ALT) [(46.23±27.09) vs. (28.00±17.43) U/L, P=0.002] and γ-glutamyl transpeptidase (GGT) [(41.46±9.89) vs. (24.02±10.72) U/L, P<0.001] were higher in the MAFLD group than those in the non-MAFLD group, while the between-group differences in the levels of aspartate aminotransferase (AST) [(33.33±15.61) vs. (28.98±12.43) U/L, P=0.248] and alkaline phosphatase [(85.30±21.27) vs. (83.41±24.47) U/L, P=0.773] were not statistically significant. During the 156-week follow-up period, the 4 items of liver function gradually increased in the MAFLD group, especially from week 120 onwards, 3 of which (ALT, AST and GGT) were significantly higher than those in the non-MAFLD group (P<0.05). In addition, the levels of fasting blood glucose, triglyceride, total cholesterol, and low-density lipoprotein were also significantly higher in the MAFLD group than those in the non-MAFLD group at some time points during the 156-week follow-up period (P<0.05). Conclusions Compared with HIV-infected patients without MAFLD, HIV-infected patients with MAFLD are more likely to develop impaired liver function and disorders of glucose and lipid metabolism during long-term tenofovir + lamivudine + efavirenz regimen ART treatment. Therefore, close clinical monitoring of liver function and glucose and lipid metabolism related parameters is required for such patients.