scholarly journals The localization of HPV and CMV in the adipose tissues of female diabetic type 1 rats and the possibility of having a role of reactivity of COVID-19 in diabetic subjects as a new medical hypothesis

2020 ◽  
Vol 10 (3) ◽  
pp. 71-73
Author(s):  
Ahed J Alkhatib

Introduction: Diabetes has various impacts on human body. It is thought that diabetes is predisposed by obesity. Obesity may due to several factors including genetically-environmental factors. The recent views that viruses may act as etiology for obesity. Study objectives: The main objectives of the present study were to investigate the possibility that CMV and HPV of having a role in initiating episodes of obesity and diabetes, and to test the hypothesis that co-existence of multi-viruses including corona virus may work synergistically to increase the impact of COVID-19 on diabetic patients. Methodology: In this study, a diabetic model was induced, the localization of HPV and CMV was determined using immunohistochemistry. Results: Study findings showed that both viruses HPV and CMV exist in the adipose tissue of diabetic rats. Both viruses were brown in color. Conclusions: Taken together, both CMV and HPV exist in the adipose tissue of diabetic rats, and this may explain the phenomenon of autoimmunity in diabetes from one side and from another side, we may explain the occurrence of synergistic effects of COVID-19 virus and the other viruses mentioned in this study.

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Ilja L Kruglikov ◽  
Manasi Shah ◽  
Philipp E Scherer

Obesity and diabetes are established comorbidities for COVID-19. Adipose tissue demonstrates high expression of ACE2 which SARS- CoV-2 exploits to enter host cells. This makes adipose tissue a reservoir for SARS-CoV-2 viruses and thus increases the integral viral load. Acute viral infection results in ACE2 downregulation. This relative deficiency can lead to disturbances in other systems controlled by ACE2, including the renin-angiotensin system. This will be further increased in the case of pre-conditions with already compromised functioning of these systems, such as in patients with obesity and diabetes. Here, we propose that interactions of virally-induced ACE2 deficiency with obesity and/or diabetes leads to a synergistic further impairment of endothelial and gut barrier function. The appearance of bacteria and/or their products in the lungs of obese and diabetic patients promotes interactions between viral and bacterial pathogens, resulting in a more severe lung injury in COVID-19.


Metabolites ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 179 ◽  
Author(s):  
Mercedes Clemente-Postigo ◽  
Alberto Tinahones ◽  
Rajaa El Bekay ◽  
María M. Malagón ◽  
Francisco J. Tinahones

White adipose tissue (WAT) is a highly adaptive endocrine organ that continuously remodels in response to nutritional cues. WAT expands to store excess energy by increasing adipocyte number and/or size. Failure in WAT expansion has serious consequences on metabolic health resulting in altered lipid, glucose, and inflammatory profiles. Besides an impaired adipogenesis, fibrosis and low-grade inflammation also characterize dysfunctional WAT. Nevertheless, the precise mechanisms leading to impaired WAT expansibility are yet unresolved. Autophagy is a conserved and essential process for cellular homeostasis, which constitutively allows the recycling of damaged or long-lived proteins and organelles, but is also highly induced under stress conditions to provide nutrients and remove pathogens. By modulating protein and organelle content, autophagy is also essential for cell remodeling, maintenance, and survival. In this line, autophagy has been involved in many processes affected during WAT maladaptation, including adipogenesis, adipocyte, and macrophage function, inflammatory response, and fibrosis. WAT autophagy dysregulation is related to obesity and diabetes. However, it remains unclear whether WAT autophagy alteration in obese and diabetic patients are the cause or the consequence of WAT malfunction. In this review, current data regarding these issues are discussed, focusing on evidence from human studies.


2019 ◽  
Vol 22 (09) ◽  
pp. 154-160
Author(s):  
Hasanain Khaleel Shareef ◽  
Ahmed Adil Ali ◽  
Rafah F. Al-Jebori

2021 ◽  
Vol 22 (11) ◽  
pp. 5843
Author(s):  
Chloé Turpin ◽  
Aurélie Catan ◽  
Olivier Meilhac ◽  
Emmanuel Bourdon ◽  
François Canonne-Hergaux ◽  
...  

The development and progression of atherosclerosis (ATH) involves lipid accumulation, oxidative stress and both vascular and blood cell dysfunction. Erythrocytes, the main circulating cells in the body, exert determinant roles in the gas transport between tissues. Erythrocytes have long been considered as simple bystanders in cardiovascular diseases, including ATH. This review highlights recent knowledge concerning the role of erythrocytes being more than just passive gas carriers, as potent contributors to atherosclerotic plaque progression. Erythrocyte physiology and ATH pathology is first described. Then, a specific chapter delineates the numerous links between erythrocytes and atherogenesis. In particular, we discuss the impact of extravasated erythrocytes in plaque iron homeostasis with potential pathological consequences. Hyperglycaemia is recognised as a significant aggravating contributor to the development of ATH. Then, a special focus is made on glycoxidative modifications of erythrocytes and their role in ATH. This chapter includes recent data proposing glycoxidised erythrocytes as putative contributors to enhanced atherothrombosis in diabetic patients.


Author(s):  
Abbas Alimoradian ◽  
Fatemeh Samimi ◽  
Hadise Aslfalah ◽  
Seied Amirhossein Latifi ◽  
Mehdi Salehi ◽  
...  

Abstract Objectives Pain associated with various underlying pathologies is a major cause of morbidity and diminished life quality in diabetic patients. Effective control of pain requires the use of analgesics with the best efficacy and with minimal side effects. Therefore, our aim in this study was to investigate the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on pain in diabetic rats. Methods In this study, we investigated the analgesic effects of drugs belonging to three different classes of NSAIDs in a rat model of diabetes. Four diabetic groups received normal saline, diclofenac, piroxicam and ketorolac, respectively, and four non-diabetic groups received normal saline, diclofenac, piroxicam and ketorolac. Type 1 diabetes was induced in rats by a single injection of streptozotocin (60 mg/kg bw). Formalin (50 µL of 2.5%) nociception assay was used to examine the effect of treatment with diclofenac, piroxicam and ketorolac on acute and chronic pain in healthy and diabetic rats. Results Piroxicam showed significant analgesic effects both in the acute phase of pain (5–10 min after injection of formalin into the left hind paw), and in the chronic phase (20–60 min after formalin injection) in healthy as well as diabetic rats. Diclofenac and ketorolac also reduced pain scores in healthy rats. However, these two drugs failed to diminish pain in diabetic rats. Conclusion Our data point for better efficacy of piroxicam in controlling pain in diabetes.


2013 ◽  
Vol 126 (7) ◽  
pp. 471-482 ◽  
Author(s):  
Vaibhav B. Patel ◽  
Nirmal Parajuli ◽  
Gavin Y. Oudit

Diabetes mellitus results in severe cardiovascular complications, and heart disease and failure remain the major causes of death in patients with diabetes. Given the increasing global tide of obesity and diabetes, the clinical burden of diabetes-induced cardiovascular disease is reaching epidemic proportions. Therefore urgent actions are needed to stem the tide of diabetes which entails new prevention and treatment tools. Clinical and pharmacological studies have demonstrated that AngII (angiotensin II), the major effector peptide of the RAS (renin–angiotensin system), is a critical promoter of insulin resistance and diabetes mellitus. The role of RAS and AngII has been implicated in the progression of diabetic cardiovascular complications and AT1R (AngII type 1 receptor) blockers and ACE (angiotensin-converting enzyme) inhibitors have shown clinical benefits. ACE2, the recently discovered homologue of ACE, is a monocarboxypeptidase which converts AngII into Ang-(1–7) [angiotensin-(1–7)] which, by virtue of its actions on the MasR (Mas receptor), opposes the effects of AngII. In animal models of diabetes, an early increase in ACE2 expression and activity occurs, whereas ACE2 mRNA and protein levels have been found to decrease in older STZ (streptozotocin)-induced diabetic rats. Using the Akita mouse model of Type 1 diabetes, we have recently shown that loss of ACE2 disrupts the balance of the RAS in a diabetic state and leads to AngII/AT1R-dependent systolic dysfunction and impaired vascular function. In the present review, we will discuss the role of the RAS in the pathophysiology and treatment of diabetes and its complications with particular emphasis on potential benefits of the ACE2/Ang-(1–7)/MasR axis activation.


2017 ◽  
Vol 16 (3) ◽  
pp. 3648-3656 ◽  
Author(s):  
Bin Zhou ◽  
Yan Leng ◽  
Shao-Qing Lei ◽  
Zhong-Yuan Xia

2010 ◽  
Vol 7 (4) ◽  
pp. 8-11 ◽  
Author(s):  
N A Petunina ◽  
N E Al'tshuler ◽  
N G Rakova ◽  
L V Trukhina

The review presents a recent data from the literature on the physiologic and pathophysiologic role of adipose tissue hormones (adiponectin, resistin, leptin). The article details the role of adipocytokines in atherogenesis. It also presents the results of studies depicting the relationship between subclinical hypothyroidism, lipid metabolism and insulin resistance as well as the impact of thyroid dysfunction upon the secretion of adipocytokines.


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