Vascular damage in obesity and diabetes: Highlighting links between endothelial dysfunction and metabolic disease in zebrafish and man.
Vascular damage in obesity and diabetes: Highlighting links between endothelial dysfunction and metabolic disease in zebrafish and man. Curr Vasc Pharmacol. 2018 Oct 30;: Authors: Wiggenhauser LM, Kroll J Abstract Endothelial dysfunction is an initial pathophysiological mechanism of vascular damage and is further recognized as an independent predictor of a negative prognosis in diabetes-induced micro- and macrovascular complications. Insight into the capability of zebrafish to model metabolic disease like obesity and type II diabetes has increased and new evidence on the induction of vascular pathologies in zebrafish through metabolic disease is available. Here, we raise the question, if zebrafish can be utilized to study the initial impairments of vascular complications in metabolic disorders. In this review, we focus on the advances made to develop models of obesity and type II diabetes in zebrafish, discuss the key points and characteristics of these models, while highlighting the available information linked to the development of endothelial dysfunction in zebrafish and man. We show that larval and adult zebrafish develop metabolic dysregulation in settings of obesity and diabetes, exhibiting pathophysiological mechanisms, which mimic the human condition. The most important genes related to endothelial dysfunction are present in zebrafish and further display similar functions as in mammals. Several suggested contributors to endothelial dysfunction fo...
This study included 250 subjects with NAFLD and 500 non-NAFLD controls. Clinical, anthropological and biochemical data were collected. Subjects with body mass index (BMI)>= 25 kg/m2 were taken as obese and subjects with BMI
In this study, we showed that hyper-O-GlcNAcylation reduced the expression of myogenin, a transcription factor critical for terminal muscle development, in C2C12 myoblasts differentiation by O-GlcNAcylation on Thr9 of myocyte-specific enhancer factor 2c. Furthermore, we showed that O-GlcNAcylation on Mef2c inhibited its DNA binding affinity to myogenin promoter. Taken together, we demonstrated that hyper-O-GlcNAcylation attenuates skeletal muscle differentiation by increased O-GlcNAcylation on Mef2c, which downregulates its DNA binding affinity. PMID: 32736694 [PubMed - as supplied by publisher]
In this study, we observed that (EX-4)2-Fc also has anti-inflammatory functions in adipose tissue. After the treatment of diet-induced obesity (DIO) mice with (EX-4)2-Fc, we found that the inflammatory response in adipose tissue was significantly attenuated. (Ex-4)2-Fc can reduce obesity-associated proinflammatory cytokine levels and macrophage numbers in DIO mice. In addition, (EX-4)2-Fc treatment resulted in proinflammatory M1-type macrophages beginning to transform into anti-inflammatory M2-type macrophages. The inflammatory mitogen-activated protein kinase (MAPK) signalling pathway and nuclear factor kappa B (NF-&kappa...
ConclusionsThe overlap of people with IFG, IGT and elevated HbA1c is small, and some factors are associated with only one criterion. Knowledge on sociodemographic and socioeconomic risk factors can be used to effectively target interventions to people at high risk for type 2 diabetes.
ConclusionIn severely obese women, muscle mass and function were inversely associated with age, smoking status, endocrine parameters, hypercholesterolemia, and comorbidities such as diabetes. Thus, the results of this investigation are relevant in supporting the development of clinical interventions to aid in the prevention of sarcopenia in adult women with severe obesity.
In this study, we examined the effects of oxytocin on the Aβ-induced impairment of synaptic plasticity in mice. To investigate the effect of oxytocin on synaptic plasticity, we prepared acute hippocampal slices for extracellular recording and assessed long-term potentiation (LTP) with perfusion of the Aβ active fragment (Aβ25-35) in the absence and presence of oxytocin. We found that oxytocin reversed the impairment of LTP induced by Aβ25-35 perfusion in the mouse hippocampus. These effects were blocked by pretreatment with the selective oxytocin receptor antagonist L-368,899. Furthermore, the tr...
Publication date: Available online 31 July 2020Source: Journal of Herbal MedicineAuthor(s): Salimeh Hajiahmadi, Azadeh Nadjarzadeh, Mojgan Gharipour, Mahdieh Hosseinzadeh, Hossein Fallahzadeh, Mohammad Ali Mohsenpour
ConclusionThis paper presents a comprehensive synthesis of estimates of chronically ill patients ’ WTP for medical treatment and identifies the key factors determining WTP through a meta-regression analysis. The main finding is that economic and political institutions, cultural traits, the types of disease, socio-economic characteristics, and valuation methods all influence WTP estimates.