diabetic complication
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Author(s):  
Mikołaj Kamiński ◽  
Michał Kulecki ◽  
Paweł Lachowski ◽  
Dominika Kasprzak ◽  
Ania Kulczycka ◽  
...  

Abstract Background Erectile dysfunction (ED) affects approximately 38% of individuals with type 1 diabetes (T1DM). Skin autofluorescence (AF) reflects skin advanced glycation end product (AGE) deposits and is a marker of long-term glycemia control. Objective The study investigates the relationship between ED and diabetes control in patients with T1DM. Methods Adult patients with T1DM visiting the Diabetology Department were cross-sectionally investigated. Medical history, anthropometric features, and laboratory findings were collected. All individuals filled the International Index of Erectile Function (IIEF-5). IIEF-5 total score < 22 represented the presence of ED. AF was measured on the volar aspect of the forearm using AGE Reader. Insulin resistance (IR) was assessed by the estimated glucose disposal rate. Descriptive statistics and multivariate logistic regression analyses were performed. The adjusted covariates were general risk factors of ED. Results Of a total of n = 70 patients, n = 30 (42.9%) suffered from ED. The presence of ED was associated with higher glycated hemoglobin level (OR, 95% CI; 1.62, 1.02–2.60; p = 0.043), presence of at least one diabetic complication (3.49, 1.10–11.03; p = 0.03), and skin AF (9.20, 1.60–52.94; p = 0.01), but not with IR (0.78, 0.57–2.60; p = 0.12). Skin AF values ≥ 2.2 indicates presence of ED with a sensitivity of 70.0% and a specificity of 77.5%. Area under the curve was equal to 0.72 (95% CI: 0.60–0.85). Conclusions The presence of ED in individuals with T1DM is associated with HbA1c, the presence of at least one diabetic complication, and skin AF.


2022 ◽  
Vol 13 ◽  
pp. 215013192110666
Author(s):  
Young-Rock Hong ◽  
Ara Jo ◽  
Jinhai Huo ◽  
Michelle I. Cardel ◽  
Arch G. Mainous

Teach-back method can help promote interactive communication between patients and providers. However, the mechanism of how teach-back operates in routine care is uninvestigated. Using pathway analysis, we explored the potential pathways of patient teach-back to health outcomes among individuals with diabetes. Study sample included 2901 US adults with diabetes ascertained from the 2011 to 2016 Longitudinal Medical Expenditure Panel Survey. Our pathway model analysis showed that patient teach-back was associated with better interaction with providers, shared decision-making, and receiving lifestyle advice. Teach-back had a direct negative effect on condition-specific hospitalization and indirect negative effects through lifestyle advice and diabetic complication. Teach-back method may promote active interactions between patients and providers by creating an opportunity to be more engaged in shared decision-making and receive additional health advice from providers. These improvements seem to be associated with a reduction in risks for complications and related hospitalization.


2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Ping Na Zhang ◽  
Meng Qi Zhou ◽  
Jing Guo ◽  
Hui Juan Zheng ◽  
Jingyi Tang ◽  
...  

Diabetic nephropathy (DN) is a progressive microvascular diabetic complication. Growing evidence shows that persistent mitochondrial dysfunction contributes to the progression of renal diseases, including DN, as it alters mitochondrial homeostasis and, in turn, affects normal kidney function. Pharmacological regulation of mitochondrial networking is a promising therapeutic strategy for preventing and restoring renal function in DN. In this review, we have surveyed recent advances in elucidating the mitochondrial networking and signaling pathways in physiological and pathological contexts. Additionally, we have considered the contributions of nontraditional therapy that ameliorate mitochondrial dysfunction and discussed their molecular mechanism, highlighting the potential value of nontraditional therapies, such as herbal medicine and lifestyle interventions, in therapeutic interventions for DN. The generation of new insights using mitochondrial networking will facilitate further investigations on nontraditional therapies for DN.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing Xiao ◽  
Yinu Zhao ◽  
Hongjing Sun ◽  
Jia Xu ◽  
Wenjie Li ◽  
...  

Abstract Background Diabetic retinopathy (DR) is a diabetic complication and the primary cause of blindness in the world. However, the treatments of DR are challenging given its complicated pathogenesis. Here, we investigated the molecular mechanisms of DR by focusing on the function of E2F1/miR-423-5p/HIPK2/HIF1α/VEGF axis. Methods Cultured retinal endothelial cells (hRMECs, hRECs) were treated with 25 mM glucose to mimic the high glucose-induced DR in vitro. Streptozotocin (STZ) was injected into mice to induce DR in mice. qRT-PCR, western blotting, immunohistochemistry, and ELISA were employed to measure levels of E2F1, miR-423-5p, HIPK2, HIF1α, and VEGF. H&E staining was utilized to examine retinal neovascularization. CCK-8 assay, transwell assay, and vascular tube formation assay were used to assess the cell viability, migration, and angiogenesis. Dual luciferase assay was performed to validate interactions between E2F1 and miR-423-5p, miR-423-5p and HIPK2. Results HG treatment increased the cell viability, migration, and angiogenesis accompanied by upregulation of E2F1, miR-423-5p, HIF1α, and VEGF levels, but reduction in HIPK2 expression. Knockdown of E2F1 or miR-423-5p suppressed the HG-induced increases in cell viability, migration, and angiogenesis. E2F1 transcriptionally activated miR-423-5p expression and miR-423-5p mimics blocked the effects of E2F1 knockdown on angiogenesis. Moreover, miR-423-5p directly targeted HIPK2 to disinhibit HIF1α/VEGF signaling. Knockdown of HIPK2 reversed the effects of miR-423-5p inhibitor on cell viability, migration, and angiogenesis. Knockdown of E2F1 suppressed neovascularization during DR in vivo. Conclusions E2F1 activates miR-423-5p transcription during DR to promote angiogenesis via suppressing HIPK2 expression to disinhibit HIF1α/VEGF signaling. Strategies targeting E2F1/miR-423-5p/HIPK2 axis could be potentially used for DR treatment.


2021 ◽  
Vol 10 (23) ◽  
pp. 5637
Author(s):  
Evanthia Gouveri ◽  
Nikolaos Papanas

The present narrative review presents emerging data regarding the association between diabetes mellitus and olfactory dysfunction and discusses the role of olfactory dysfunction in glucose metabolism. We searched relevant published articles in PubMed and Google Scholar until October 2021. Main key words included “olfactory dysfunction”, “diabetes mellitus”, and “glucose metabolism”. Olfactory dysfunction has been associated with diabetes mellitus. Furthermore, it has been proposed to be a diabetic complication, given that it has been linked with microvascular complications, such as diabetic peripheral neuropathy. Interestingly, it has been suggested that olfactory dysfunction is a manifestation of central neuropathy in diabetes, a hypothesis based on the observation that diabetes, olfactory dysfunction, and cognitive decline often coexist. However, evidence is limited and inconsistent. More importantly, olfactory and endocrine systems are closely linked, and olfactory dysfunction plays a significant role in glucose metabolism and obesity. Indeed, food behaviour and energy balance are influenced by olfaction status.


2021 ◽  
pp. 113-128
Author(s):  
Duck-Jong Han ◽  
Izumi Hiratsuka ◽  
Yi-Ming Shyr ◽  
Shin-E Wang ◽  
Takashi Kenmochi

2021 ◽  
Vol 12 ◽  
Author(s):  
Xingyu Chang ◽  
Guomao Zhu ◽  
Zongyan Cai ◽  
Yaqi Wang ◽  
Rongna Lian ◽  
...  

Diabetic retinopathy (DR) is a common diabetic complication and the main cause of blindness worldwide, which seriously affects the quality of life of patients. Studies have shown that noncoding RNA (ncRNA) has distinct differentiated expression in DR and plays an important role in the occurrence and development of DR. ncRNAs represented by microRNAs (miRNAs), lncRNAs (lncRNAs), and circRNAs (circRNAs) have been shown to be widely involved in the regulation of gene expression and affect multiple biological processes of retinopathy. This article will review three RNAs related to the occurrence and development of DR on the basis of previous studies (especially their effects on retinal microangiopathy, retinal pigment epithelial cells, and retinal nerve cells) and discuss their underlying mechanisms and connections. Overall, this review will help us better understand the role of ncRNAs in the occurrence and development of DR and provide ideas for exploring potential therapeutic directions and targets.


Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1360
Author(s):  
Natalie Youssef ◽  
Mohamed Noureldein ◽  
Rachel Njeim ◽  
Hilda E. Ghadieh ◽  
Frederic Harb ◽  
...  

Diabetic kidney disease (DKD), a serious diabetic complication, results in podocyte loss and proteinuria through NADPH oxidases (NOX)-mediated ROS production. DUOX1 and 2 are NOX enzymes that require calcium for their activation which enters renal cells through the pivotal TRPC channels. Hypoglycemic drugs such as liraglutide can interfere with this deleterious mechanism imparting reno-protection. Herein, we aim to investigate the reno-protective effect of GLP1 receptor agonist (GLP1-RA), via its effect on TRPC6 and NADPH oxidases. To achieve our aim, control or STZ-induced T1DM Sprague–Dawley rats were used. Rats were treated with liraglutide, metformin, or their combination. Functional, histological, and molecular parameters of the kidneys were assessed. Our results show that treatment with liraglutide, metformin or their combination ameliorates DKD by rectifying renal function tests and protecting against fibrosis paralleled by restored mRNA levels of nephrin, DUOX1 and 2, and reduced ROS production. Treatment with liraglutide reduces TRPC6 expression, while metformin treatment shows no effect. Furthermore, TRPC6 was found to be directly interacting with nephrin, and indirectly interacting with DUOX1, DUOX2 and GLP1-R. Our findings suggest that treatment with liraglutide may prevent the progression of diabetic nephropathy by modulating the crosstalk between TRPC6 and NADPH oxidases.


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