Possible mechanisms of Alzheimer's disease-related cognitive impairment in patients with diabetes mellitus are shown in this figure. DPP-4i may modulate Aβ accumulation in the process of AD-related cognitive impairment.
Possible mechanisms of Alzheimer's disease-related cognitive impairment in patients with diabetes mellitus are shown in this figure. DPP-4i may modulate Aβ accumulation in the process of AD-related cognitive impairment.
Weight variability is associated with cardiovascular outcomes in diabetic patients. However, whether the guideline-recommended intensive lifestyle intervention (ILI) will affect this association in overweight or obese adults with diabetes is not well established.
In 3,859 participants from the Action for Health in Diabetes (Look AHEAD) trial, the associations of 4 year weight variability measured by variability independent of the mean (VIM) with major adverse cardiovascular event (MACE) and secondary outcomes in ILI and diabetes support & education (DSE) arm were evaluated.
During a median follow-up of 9.6 years, 255 (12.9%) participants in the ILI arm and 247 (13.2%) participants in the DSE arm developed MACE. Participants with the highest quartile of weight variability (VIM Q4) experienced a 2.23-fold higher risk of MACE compared with the lowest quartile (VIM Q1) in the DSE arm (hazard ratio [HR] 2.23; 95% CI 1.51–3.30). Compared with the lowest weight variability (VIM Q1), participants with the highest weight variability (VIM Q4) were associated with higher risks of secondary cardiovascular composite outcome (HR 1.88; 95% CI 1.20–2.95), all-cause mortality (HR 3.19; 95% CI 1.75–5.82), and myocardial infarction (HR 1.95; 95% CI 1.12–3.37) in the DSE arm.
Among the overweight or obese individuals with type 2 diabetes mellitus, rising weight variability was independently associated with increased MACE risks in the DSE arm. Therefore, a guideline-recommended ILI strategy for weight loss should be adopted to improve cardiovascular outcomes without worrying about the effect of weight fluctuations.
Long non-coding RNAs (lncRNAs) exert essential functions in the pathogenesis of diabetic nephropathy (DN). LncRNA T-cell factor 7 (TCF7) and semaphorin-3A (SEMA3A) have been found to be involved in the progression of diabetic nephropathy. However, whether the effect of TCF7 on the pathogenesis of diabetic nephropathy is mediated by SEMA3A remains unclear.
TCF7, miR-16-5p, and SEMA3A were quantified by a qRT-PCR or immunoblotting method. A CCK-8 assay gauged the cell viability. Measurement of cell apoptosis was done using flow cytometry. RNA immunoprecipitation (RIP), dual-luciferase reporter, and RNA pull-down assays were utilized to assay the targeted interactions among the variables.
The TCF7 and SEMA3A levels were elevated in serum from patients with diabetic nephropathy. TCF7 silencing or SEMA3A depletion ameliorated high glucose (HG)-induced podocyte injury. Moreover, TCF7 silencing protected against HG-induced podocyte injury by down-regulating SEMA3A. TCF7 targeted miR-16-5p, and miR-16-5p targeted SEMA3A. Furthermore, TCF7 affected the expression of SEMA3A by competing specifically for shared miR-16-5p.
These findings suggested that TCF7 silencing attenuated high glucose-induced podocyte damage partially through the miR-16-5p/SEMA3A regulation cascade.
This commentary is on a recent report on the regulation mechanism of beta cell proliferation.
Diet therapy is a vital approach to manage type 2 diabetes and prediabetes. However, the comparative efficacy of different eating patterns is not clear enough. We aimed to compare the efficacy of various eating patterns for glycemic control, anthropometrics, and serum lipid profiles in the management of type 2 diabetes and prediabetes.
We conducted a network meta-analysis using arm-based Bayesian methods and random effect models, and drew the conclusions using the partially contextualized framework. We searched twelve databases and yielded 9,534 related references, where 107 studies were eligible, comprising 8,909 participants.
Eleven diets were evaluated for 14 outcomes. Caloric restriction was ranked as the best pattern for weight loss (SUCRA 86.8%) and waist circumference (82.2%), low-carbohydrate diets for body mass index (81.6%), and high-density lipoprotein (84.0%), and low-glycemic-index diets for total cholesterol (87.5%) and low-density lipoprotein (86.6%). Other interventions showed some superiorities, but were imprecise due to insufficient participants and needed further investigation. The attrition rates of interventions were similar. Meta-regression suggested that macronutrients, energy intake, and weight may modify outcomes differently. The evidence was of moderate-to-low quality, and 38.2% of the evidence items met the minimal clinically important differences.
The selection and development of dietary strategies for diabetic/prediabetic patients should depend on their holistic conditions, i.e., serum lipid profiles, glucometabolic patterns, weight, and blood pressure. It is recommended to identify the most critical and urgent metabolic indicator to control for one specific patient, and then choose the most appropriate eating pattern accordingly.
Diabetes and hepatitis B are both global problems. The influence of diabetes on complications and prognosis of hepatitis B has been widely studied. However, the association between hepatitis B virus (HBV) infection and the prevalence of diabetes-related complications is less documented and is uncertain.
This was a retrospective study. We collected information from a large clinical database. A total of 1,090 Chinese inpatients with type 2 diabetes were included.
The participants were divided into two groups, including 135 patients with HBV infection and 955 patients without HBV infection. Patients with HBV infection were younger and had worse control of blood glucose than those without HBV infection. No significant difference was found in the prevalence of diabetic retinopathy, neuropathy, nephropathy, diabetic ketosis or diabetic ketoacidosis between the patients with HBV infection and the patients without HBV infection. The prevalence of macrovascular complications was 54.1% and 64.4% in diabetes patients complicated with HBV infection and without HBV infection, respectively. The P-value was <0.05. However, through the logistic regression analysis, we found HBV infection was not an independent risk factor for macrovascular complications of diabetes.
There was no significant correlation between the prevalence of macrovascular complications, microvascular complications of diabetes, diabetic ketosis or diabetic ketoacidosis and HBV infection status.
The publication of invaluable papers in the Journal of Diabetes Investigation depends on the prompt, careful review of submitted manuscripts. We would like to thank the Editorial Board members, the International Editorial Board members, the Assistant Editorial Board members and the following experts for reviewing manuscripts from September 1, 2021 to August 31, 2022.
Vasudha Ahuja
Jun Aida
Toru Aizawa
Satoru Akazawa
Sadanori Akita
Yutaro Akiyama
Gulali Aktas
Hitoshi Ando
Keiko Arai
Shin-Ichi Araki
Osamu Arisaka
Shunichiro Asahara
Yoshimasa Aso
Masayuki Baba
Tetsuya Babazono
Jae Hyun Bae
J Baelde
Yuqian Bao
Neal Barshes
Ryotaro Bouchi
Xiaoling Cai
Soner Cander
Ali J. Chakera
Subrata Chakrabarti
Yi-Cheng Chang
Harn-Shen Chen
Yang Ching Chen
Kenneth Cheng
Ken Chiu
Nf Chu
Ohad Cohen
Qinghua Cui
Hiroyuki Daida
Makoto Daimon
Taura Daisuke
Undurti Das
Takahisa Deguchi
Kentaro Doi
Ken Ebihara
Jun Eguchi
Amany El-Sikaily
Masanori Emoto
Joel Francis
Rumi Fujikawa
Junji Fujikura
Kei Fujimoto
Shimpei Fujimoto
Tomomi Fujisawa
Yoshihito Fujita
Yukihiro Fujita
Yoshio Fujitani
Kei Fukami
Atsushi Fukao
Astunori Fukuhara
Michiaki Fukui
Kenji Furukawa
Shinya Furukawa
Hiroto Furuta
Nazim Ghouri
Charlie Gilbride
Atsushi Goto
Yashdeep Gupta
Kyoung Hwa Ha
Masahide Hamaguchi
Akihiro Hamasaki
Hidetaka Hamasaki
Liyuan Han
Xiaoling Han
Toshiaki Hanafusa
Rikinari Hanayama
Masumi Hara
Goji Hasegawa
Koshi Hashimoto
Yoshitaka Hashimoto
Yuji Hataya
Akinori Hayashi
Yoshitaka Hayashi
Yasuaki Hayashino
Tatsuhito Himeno
Takumi Hirata
Takahisa Hirose
Yushi Hirota
Low-Tone Ho
Chang Won Hong
Ruby Hoo
Mika Hori
Ichiro Horie
Yukio Horikawa
Ryota Hosomi
Tetsuya Hosooka
Cheng Hu
Chia-Luen Huang
Chuiguo Huang
Chun-Jui Huang
Cn Huang
Yu Huang
Chii-Min Hwu
J Hyett
Yasuo Ido
Noriko Ihana-Sugiyama
Katsumi Iizuka
Kaori Ikeda
Junta Imai
Kenjiro Imai
Minako Imamura
Daisuke Inoue
Tatsuhide Inoue
Junichiro Irie
Yasushi Ishigaki
Hisamitsu Ishihara
Tetsuya Ishikawa
Mohammad Safiqul Islam
Arata Itoh
Katsuomi Iwakura
Naoko Iwasaki
Yusaku Iwasaki
Masanori Iwase
Minoru Iwata
N Jahan
Zahra Jamali
T.-S. Jap
Troels Staehelin Jensen
Jae-Han Jeon
Xiaofan Jia
Guozhi Jiang
Sang-Man Jin
Rozmin Jiwani
Ji Eun Jun
Elnaggar Nabil K.
Keizo Ka
We herein describe a case of type 1 diabetes that presented with a pontine lesion during two hyperglycemic crises accompanied by marked fluctuations in serum osmotic pressure and blood pressure. Magnetic resonance imaging showed swollen pons with osmotic demyelination syndrome characteristics accompanying cytotoxic edema at the first crisis. The involvement of vasogenic edema was also assumed in the second crisis. Neurological symptoms were milder than magnetic resonance imaging findings. The patient recovered after 7 days without sequelae in both crises. Based on these findings, a pontine lesion needs to be considered in patients with poorly controlled diabetes showing rapid metabolic and blood pressure changes, as observed in hyperglycemic crises. Cytotoxic edema leading to osmotic demyelination syndrome and vasogenic edema caused by vascular endothelial cell damage might both be involved in the pathogenesis of a pontine lesion.
Recent preclinical studies have provided insight on imeglimin's action on pancreatic β-cells and the mechanisms underlying its clinical benefits. Imeglimin may enhance glucose-induced insulin secretion (GIIS) and inhibit apoptosis of pancreatic ß-cells leading to preserved β-cell mass by maintaining or restoring the functional and structural integrity of the mitochondria and the endoplasmic reticulum homeostasis in pancreatic β-cells.
Youth-onset diabetes (YOD) is a variant of type 2 diabetes with heterogeneous pathophysiology that occurs in adolescents. It is different from young-onset diabetes, which denotes diabetes diagnosed before the age of 40 years. Genetic and ethnic background might play an important role in the pathogenesis of YOD, in that it is associated with a strong family history of diabetes and a particular ethnic group, such as Hispanic people1. The incidence of YOD is currently rising in accordance with the increasing prevalence of obesity in adolescents.
Compared with adult-onset type 2 diabetes, YOD shows a more severe impairment in pancreatic β-cell function, which is further complicated by increasing insulin resistance associated with obesity and puberty. Furthermore, YOD is frequently associated with higher rates of microvascular and macrovascular complications, despite a shorter disease duration than other types of diabetes. The development of these complications at an earlier age leads to increased mortality of patients with YOD. The mortality rate of YOD is even higher than that of type 1 diabetes1. To make matters worse, there are very limited antidiabetic drugs approved for the treatment of YOD. To date, no medication has proven to be effective in preventing the rapid and relentless deterioration of β-cell function in YOD. Even the therapeutic failure rate of metformin, which is used as the first-line drug for type 2 diabetes, is higher2.
Glucagon-like peptide-1 receptor agonists, liraglutide and exenatide, have been approved for the treatment of YOD. Recently, the results of a new clinical trial titled the Assessment of Weekly Administration of LY2189265 in Diabetes–Pediatric Study (AWARD-PEDS) to examine whether once-weekly dulaglutide is effective and safe for youth (age 10 to <18 years) with type 2 diabetes has been published3. This study was a double-blind, placebo-controlled, 26-week phase III trial that included patients treated with lifestyle modifications, metformin, basal insulin or metformin plus basal insulin. The primary end-point was the change in glycated hemoglobin (HbA1c) after 26 weeks from baseline. After the double-blind treatment period, an open-label extension period of another 26 weeks was followed, where all participants received dulaglutide treatment.
The mean age of the study participants was 14.5 ± 2.0 years (the proportion of Tanner stage 5 was 70% in females and 59% in males), and the mean body mass index was 34.1 ± 8.8 kg/m2. Their mean HbA1c at baseline was 8.1 ± 1.3%, and the duration of diabetes was 2.0 ± 1.7 years. At the time of enrollment, the study participants were treated with diet and exercise only (9%), metformin only (63%), basal insulin only (3%) and metformin plus basal insulin (25%). The completion rate of this study was as high as 95% for the first 26 weeks, and 90% for the a
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