World Journal of Diabetes最新文献

Background: Adult-onset diabetes is most often considered to be type 2 diabetes. However, other types of diabetes can develop in adults, including exocrine pancreas disease-associated diabetes, also called type 3c diabetes. Differential diagnosis between these types of diabetes still remains a diagnostic challenge.

Aim: To define anthropometric and laboratory markers that will allow for early diagnosis of pancreatic disease-associated diabetes.

Methods: The study group included 44 patients with pancreatogenic diabetes (26 with pancreatic cancer and 18 with chronic pancreatitis), while the control group consisted of 35 patients with type 2 diabetes. We analyzed several parameters, including sex, age, body mass index (BMI), fasting plasma glucose, fasting C-peptide and insulin with homeostasis model assessment of insulin resistance (HOMA-IR) index calculation, adrenomedullin, adiponectin and creatinine levels with epidermal growth factor receptor (eGFR) calculation. We also developed an equation, termed type 3c diabetes index, which utilized BMI, fasting insulin and adrenomedullin levels, and eGFR to better identify patients with type 3c diabetes.

Results: Compared to patients with type 2 diabetes, patients with pancreatogenic diabetes had significantly lower BMI (25.11 ± 4.87 kg/m² vs 30.83 ± 5.21 kg/m²), fasting C-peptide (0.81 ± 0.42 nmol/L vs 1.71 ± 0.80 nmol/L), insulin (76.81 ± 63.34 pmol/L vs 233.19 ± 164.51 pmol/L) and HOMA-IR index, despite similar fasting plasma glucose levels. Patients with pancreatogenic diabetes also had lower adrenomedullin levels (0.41 ± 0.25 ng/mL vs 0.63 ± 0.38 ng/mL) but higher adiponectin levels (13.08 ± 7.20 μg/mL vs 8.28 ± 4.01 μg/mL) and eGFR levels (100.53 ± 21.60 mL/min/1.73 m² vs 85.14 ± 19.24 mL/min/1.73 m²). Finally, patients with pancreatogenic diabetes had significantly lower Type 3c diabetes index values.

Conclusion: Patients with pancreatogenic diabetes differ from patients with type 2 diabetes in anthropometric and laboratory parameters. The type 3c diabetes index had the highest discriminating value, above any single parameter.

Background: The increasing number of type 2 diabetes mellitus (T2DM) patients leads to higher rates of morbidity and mortality related to lung cancer.

Aim: To investigate the utility of the proliferating cell nuclear antigen Ki-67 in patients with lung adenocarcinoma in situ (AIS) complicated by T2DM.

Methods: One hundred patients with AIS and T2DM (group A), 100 patients with AIS alone (group B), and 60 patients with benign lung lesions (group C) admitted to the Department of Thoracic Surgery and Endocrinology of the First Affiliated Hospital of Soochow University from November 2021 to December 2022 were enrolled. Ki-67 expression was compared among the groups.

Results: Group A had significantly higher levels of fasting plasma glucose (FPG), total cholesterol (TC), total triglyceride, low-density lipoprotein cholesterol, glycosylated hemoglobin (HbA1c), and insulin than groups B and C (P < 0.01). Meanwhile, group B had higher insulin levels than group C (P < 0.01). Group A exhibited a significantly higher average Ki-67 positivity rate than group B (P < 0.01). The Ki-67 positivity rate in group A was 86.87%, while the positivity rate in group B was 77%. Ki-67 was positively correlated with FPG (P < 0.01) and HbA1c levels (P < 0.01). Ki-67, FBG, insulin, HbA1c, high-density lipoprotein cholesterol and TC were independent factors for patients with AIS complicated by T2DM.

Conclusion: Ki-67 expression was higher in patients with AIS complicated by T2DM than in patients with AIS alone. Therefore, detecting the Ki-67 level might assist in the diagnosis of AIS in patients with T2DM.

Background: Tacrolimus (FK506) is a key calcineurin inhibitor used to prevent organ transplant rejection and is effective in improving graft survival. However, it is linked to hyperglycemia and insulin resistance, contributing to new-onset diabetes after transplantation and negatively affecting islet function.

Aim: To study the effects of tacrolimus on the insulin signaling pathway of hepatocytes.

Methods: HL7702 cells were treated with different concentrations of tacrolimus (0.1 mg/L, 1 mg/L, 5 mg/L) for 24 hours. The proteins involved in insulin signaling were detected by Western blotting.

Results: Compared with the control group, phosphorylation of insulin receptor substrate (IRS) 1 at Ser 307 and Ser 323 were increased significantly when the tacrolimus concentration reached 1 and 5 mg/L. Phosphorylation of IRS1 at Ser 1101 was also increased, although not significantly. However, phosphorylation of Ribosomal protein S6 kinase beta-1 at Thr 389 was decreased significantly. The levels of phosphorylated glycogen synthase kinase 3α Ser 21 and Ser 9 were increased. Surprisingly, phosphorylation of glycogen synthase at Ser 641 was increased. There was no significant change in the activity of glycogen phosphorylase.

Conclusion: Tacrolimus has no direct effect on hepatic glucose metabolism, but inhibits IRS1-mediated insulin signaling. This may be one of the underlying mechanisms by which tacrolimus induces insulin resistance.

Background: The prevalence of diabetes and its association with microcirculatory dysfunction presents a significant challenge in contemporary global health. Addressing this nexus is crucial for developing targeted therapeutic interventions.

Aim: To trace the progression and delineate the current state of interdisciplinary research concerning diabetes and microcirculation.

Methods: Employing a bibliometric approach, this study scrutinizes 12886 peer-reviewed publications retrieved from the PubMed and Web of Science databases. The focus is on elucidating the research trajectory and thematic concentrations at the confluence of diabetes and microcirculation.

Results: Research outputs have surged since 2011, with the United States, China, and the United Kingdom leading in the quantity and quality of publications. This analysis revealed that journals such as Diabetes Care and The New England Journal of Medicine, along with top research institutions, have significantly contributed to advancing the understanding of microvascular processes affected by diabetes. The central themes identified include inflammation, oxidative stress, and endothelial dysfunction, which are critical in mediating the microvascular complications of diabetes.

Conclusion: This bibliometric evaluation reveals an evolving landscape focusing on diabetes and microcirculatory dysfunction. The complexity of diabetic microvascular issues encouraged multidisciplinary research strategies that are imperative for global health outcomes.

Background: Gestational diabetes mellitus (GDM) is a growing public health concern, particularly in regions with diverse ethnic populations. Understanding the incidence and risk factors of GDM is crucial for early prevention and management, especially in underrepresented areas like Guizhou Province, China, where geographic and ethnic diversity may influence the disease's prevalence and risk profiles.

Aim: To investigate the incidence of GDM and identify its associated risk and protective factors among different ethnic groups in Guizhou Province, providing essential data for early prevention strategies.

Methods: A multi-center retrospective study was conducted, dividing participants into GDM and non-GDM groups according to standardized diagnostic criteria. Data were collected from 103629 deliveries across 40 hospitals in Guizhou. Various demographic, clinical, and laboratory parameters were analyzed using logistic regression to identify risk and protective factors for GDM.

Results: Among the 103629 deliveries, 18957 cases of GDM were identified, with an incidence of approximately 18.3%. The risk of GDM was higher in the Han ethnic group compared to minority ethnic groups. The Dong ethnic group had the lowest incidence among the minorities. Key risk factors identified included older age (especially > 35 years), higher pre-pregnancy body mass index (BMI), light physical activity, gravidity, family history of diabetes, hemoglobin, aspartate aminotransferase, alanine aminotransferase, and direct bilirubin. Protective factors included higher education level, total protein, and albumin. There were also differences based on blood type, with type A associated with higher risk.

Conclusion: The incidence rate in Guizhou is 18.3%. Older age (especially > 35 years), Han ethnicity, lower education level, higher pre-pregnancy BMI, light physical activity, and higher gravidity are the main risk factors for GDM. Laboratory findings indicate that higher hemoglobin, higher liver function parameters (alanine aminotransferase, aspartate aminotransferase, and direct bilirubin), and lower total protein and albumin are associated with a higher risk of GDM. Blood type A has a higher risk of GDM compared to blood types AB and O.

Background: The preservation of islet β-cell function in elderly patients with type 2 diabetes mellitus (T2DM) is a top priority for diabetic control.

Aim: To assess the preservation of islet β-cell function among elderly Chinese patients with T2DM after different anti-diabetic treatments.

Methods: In this longitudinal observational study, elderly patients with T2DM treated with insulin, oral antidiabetic drugs or a combination of both were enrolled to disclose their islet β-cell function between baseline and follow-up. Islet β-cell function was determined by the plasma Homeostasis Model for β-cell function (HOMA-β), C-peptide and area under the curve (AUC) based on oral glucose tolerance test. Changes in β-cell function (decrement or increment from baseline) between different therapy groups were the outcomes.

Results: In total, 745 elderly patients (≥ 60 years) with T2DM [insulin monotherapy, n = 105; oral anti-diabetic drugs (OAD) monotherapy, n = 321; insulin plus OAD, n = 319] had their baseline and follow-up β-cell function assessed during a median observation period of 4.5 years (range, 3.0-7.2 years). Overall, islet β-cell function (HOMA-β, fasting C-peptide, fasting insulin, AUC_c-pep, AUC_ins, AUC_c-pep/AUC_glu, AUC_ins/AUC_glu) consistently deteriorated over time regardless of the three different antidiabetic treatments. No statistical differences in decrement were observed among the three groups regarding the islet β-cell function indices. All three groups showed an increased ratio of delayed insulin secretion response after 4.5 years of observation.

Conclusion: In Chinese elderly patients with T2DM, islet β-cell function progressively declines regardless of insulin supplement or insulin plus OAD treatments.

Background: Numerous epidemiological studies have found that pesticide exposure is associated with the incidence of type 2 diabetes (T2D); however, the underlying mechanisms remain unknown. DNA methylation may play a role in this process.

Aim: To identify the genes associated with pesticide exposure and T2D by reviewing the current literature.

Methods: We systematically searched PubMed and Embase for relevant studies that examined the association between pesticide exposure and DNA methylation, and studies on DNA methylation and T2D through January 15, 2024.

Results: We identified six genes (Alu, CABLES1, CDH1, PDX1, PTEN, PTPRN2) related to pesticide exposure and T2D. We also suggested future research directions to better define the role of DNA methylation in the association between pesticide exposure and T2D.

Conclusion: DNA methylation of specific genes may play a vital role in the association between pesticide exposure and T2D.

Background: Type 2 diabetes mellitus (T2DM) often leads to vascular complications, such as albuminuria. The role of insulin autoantibodies (IAA) and their interaction with D-dimer in this context remains unclear.

Aim: To investigate the characteristics of IAA and its effect on albuminuria in T2DM patients.

Methods: We retrospectively analyzed clinical data from 115 T2DM patients with positive IAA induced by exogenous insulin, and 115 age- and sex-matched IAA-negative T2DM patients as controls. Propensity scores were calculated using multivariate logistic regression. Key variables were selected using the least absolute shrinkage and selection operator (LASSO) algorithm. We constructed a prediction model and analyzed the association between IAA and albuminuria based on demographic and laboratory parameters.

Results: The IAA-positive group had significantly higher D-dimer levels [0.30 (0.19-0.55) mg/L vs 0.21 (0.19-0.33) mg/L, P = 0.008] and plasma insulin levels [39.1 (12.0-102.7) μU/mL vs 9.8 (5.5-17.6) μU/mL, P < 0.001] compared to the IAA-negative group. Increases in the insulin dose per weight ratio, diabetes duration, and urinary albumin-to-creatinine ratio (UACR) were observed but did not reach statistical significance. The LASSO model identified plasma insulin and D-dimer as key factors with larger coefficients. D-dimer was significantly associated with UACR in the total and IAA-positive groups but not in the IAA-negative group. The odds ratio for D-dimer elevation (> 0.5 g/L) was 2.88 (95% confidence interval: 1.17-7.07) in the IAA-positive group (P interaction < 0.05).

Conclusion: D-dimer elevation is an independent risk factor for abnormal albuminuria and interacts with IAA in the development of abnormal albuminuria in T2DM patients.

Background: Food insecurity (FI) during pregnancy negatively impacts maternal health and raises the risk of gestational diabetes mellitus (GDM) and pregnancy-induced hypertension (PIH), resulting in adverse outcomes for both mother and baby.

Aim: To investigate the relationships between FI and pregnancy outcomes, particularly GDM and PIH, while also examining the mediating role of the dietary diversity score (DDS).

Methods: A cross-sectional study was undertaken to examine this relationship, involving 600 pregnant women. Participants were women aged 18 years or older who provided complete data on FI and pregnancy outcomes. The FI was measured via the Household Food Security Survey Module, with GDM defined as fasting plasma glucose levels of ≥ 5.1 mmol/L or a 2-hour oral glucose tolerance test value of ≥ 8.5 mmol/L. The DDS is determined by evaluating one's food consumption based on nine distinct food groups. A logistic regression model was used to explore the relationship between FI and PIH, and GDM.

Results: Seventeen percent of participants reported experiencing FI during pregnancy. The study found a significant association between FI and an elevated risk of GDM [odds ratio (OR) = 3.32, 95%CI: 1.2-5.4]. Once more, food-insecure pregnant women had higher rates of PIH (OR = 0.10, 95%CI: 0.02-0.45) and they also faced a higher likelihood of neonatal complications, such as neonatal intensive care unit's admissions and the birth of infants with extremely low birth weight. The FI was further linked to metabolic disruptions, such as elevated fasting blood sugar (FBS), low-density lipoprotein cholesterol, and triglyceride levels. Our results indicate that the DDS acts as a significant mediator in the relationship between FI and the incidence of GDM. In particular, the mediation analysis showed that approximately 65% of the effect was mediated through DDS (P = 0.002).

Conclusion: These findings underscore the serious challenges that FI presents during pregnancy and its effects on maternal and infant health. Additionally, the study explored how DDS mediates the relationship between FI and the incidence of GDM.

Background: Plantamajoside (PMS) has shown potential in mitigating cell damage caused by high glucose (HG) levels. Despite this, the precise therapeutic effects of PMS on type 2 diabetes mellitus (T2DM) and the underlying regulatory mechanisms require further exploration.

Aim: To investigate PMS therapeutic effects on T2DM in mice and elucidate its mechanisms of action through in vivo and in vitro experiments.

Methods: An in vitro damage model of MIN6 cells was established using HG and palmitic acid (PA). PMS's protective effect on cell damage was assessed. Next, transcriptomics was employed to examine how PMS treatment affects gene expression of MIN6 cells. Furthermore, the effect of PMS on protein processing in endoplasmic reticulum and apoptosis pathways was validated. A T2DM mouse model was used to validate the therapeutic effects and mechanisms of PMS in vivo.

Results: PMS intervention ameliorated cell injury in HG + PA-induced MIN6 cell damage. Transcriptomic analysis revealed that protein processing in the endoplasmic reticulum and apoptosis pathways were enriched in cells treated with PMS, with significant downregulation of the gene Dnajc1. Further validation indicated that PMS significantly inhibited the expression of apoptosis-related factors (Bax, CytC) and endoplasmic reticulum stress (ERS)-related factors [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting the expression of Bcl-2 and Dnajc1. Additionally, the inhibitory effects of PMS on ERS and apoptosis were abolished upon Dnajc1 silencing. Furthermore, in vivo experiments demonstrated that PMS intervention effectively improved pancreatic damage, suppressed the expression of apoptosis-related factors (Bax, CytC), and ERS-related factors [ATF6, XBP1, Ddit3 (CHOP), GRP78], while promoting the expression of Bcl-2 and Dnajc1 in a T2DM model mice.

Conclusion: PMS intervention could alleviate pancreatic tissue damage effectively. The mechanism of action involves Dnajc1 activation, which subsequently inhibits apoptosis and ERS, ameliorating damage to pancreatic β-cells.