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1.
The Multifunctionality of CD36 in Diabetes Mellitus and Its Complications-Update in Pathogenesis, Treatment and Monitoring.
Puchałowicz, K, Rać, ME
Cells. 2020;(8)
Abstract
CD36 is a multiligand receptor contributing to glucose and lipid metabolism, immune response, inflammation, thrombosis, and fibrosis. A wide range of tissue expression includes cells sensitive to metabolic abnormalities associated with metabolic syndrome and diabetes mellitus (DM), such as monocytes and macrophages, epithelial cells, adipocytes, hepatocytes, skeletal and cardiac myocytes, pancreatic β-cells, kidney glomeruli and tubules cells, pericytes and pigment epithelium cells of the retina, and Schwann cells. These features make CD36 an important component of the pathogenesis of DM and its complications, but also a promising target in the treatment of these disorders. The detrimental effects of CD36 signaling are mediated by the uptake of fatty acids and modified lipoproteins, deposition of lipids and their lipotoxicity, alterations in insulin response and the utilization of energy substrates, oxidative stress, inflammation, apoptosis, and fibrosis leading to the progressive, often irreversible organ dysfunction. This review summarizes the extensive knowledge of the contribution of CD36 to DM and its complications, including nephropathy, retinopathy, peripheral neuropathy, and cardiomyopathy.
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2.
Diabetes and COVID-19: evidence, current status and unanswered research questions.
Gupta, R, Hussain, A, Misra, A
European journal of clinical nutrition. 2020;(6):864-870
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Abstract
Patients with diabetes who get coronavirus disease 2019 (COVID-19) are at risk of a severe disease course and mortality. Several factors especially the impaired immune response, heightened inflammatory response and hypercoagulable state contribute to the increased disease severity. However, there are many contentious issues about which the evidence is rather limited. There are some theoretical concerns about the effects of different anti-hyperglycaemic drugs. Similarly, despite the recognition of angiotensin converting enzyme 2 (ACE2) as the receptor for severe acute respiratory syndrome coronavirus 2 (SARS CoV-2), and the role of ACE2 in lung injury; there are conflicting results with the use of angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) in these patients. Management of patients with diabetes in times of restrictions on mobility poses some challenges and novel approaches like telemedicine can be useful. There is a need to further study the natural course of COVID-19 in patients with diabetes and to understand the individual, regional and ethnic variations in disease prevalence and course.
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Obesity, Diabetes and COVID-19: An Infectious Disease Spreading From the East Collides With the Consequences of an Unhealthy Western Lifestyle.
Holly, JMP, Biernacka, K, Maskell, N, Perks, CM
Frontiers in endocrinology. 2020;:582870
Abstract
The pandemic of COVID-19, caused by the coronavirus, SARS-CoV-2, has had a global impact not seen for an infectious disease for over a century. This acute pandemic has spread from the East and has been overlaid onto a slow pandemic of metabolic diseases of obesity and diabetes consequent from the increasing adoption of a Western-lifestyle characterized by excess calorie consumption with limited physical activity. It has become clear that these conditions predispose individuals to a more severe COVID-19 with increased morbidity and mortality. There are many features of diabetes and obesity that may accentuate the clinical response to SARS-CoV-2 infection: including an impaired immune response, an atherothrombotic state, accumulation of advanced glycation end products and a chronic inflammatory state. These could prime an exaggerated cytokine response to viral infection, predisposing to the cytokine storm that triggers progression to septic shock, acute respiratory distress syndrome, and multi-organ failure. Infection leads to an inflammatory response and tissue damage resulting in increased metabolic activity and an associated increase in the mechanisms by which cells ingest and degrade tissue debris and foreign materials. It is becoming clear that viruses have acquired an ability to exploit these mechanisms to invade cells and facilitate their own life-cycle. In obesity and diabetes these mechanisms are chronically activated due to the deteriorating metabolic state and this may provide an increased opportunity for a more profound and sustained viral infection.
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Microbiota and Diabetes Mellitus: Role of Lipid Mediators.
Salazar, J, Angarita, L, Morillo, V, Navarro, C, Martínez, MS, Chacín, M, Torres, W, Rajotia, A, Rojas, M, Cano, C, et al
Nutrients. 2020;(10)
Abstract
Diabetes Mellitus (DM) is an inflammatory clinical entity with different mechanisms involved in its physiopathology. Among these, the dysfunction of the gut microbiota stands out. Currently, it is understood that lipid products derived from the gut microbiota are capable of interacting with cells from the immune system and have an immunomodulatory effect. In the presence of dysbiosis, the concentration of lipopolysaccharides (LPS) increases, favoring damage to the intestinal barrier. Furthermore, a pro-inflammatory environment prevails, and a state of insulin resistance and hyperglycemia is present. Conversely, during eubiosis, the production of short-chain fatty acids (SCFA) is fundamental for the maintenance of the integrity of the intestinal barrier as well as for immunogenic tolerance and appetite/satiety perception, leading to a protective effect. Additionally, it has been demonstrated that alterations or dysregulation of the gut microbiota can be reversed by modifying the eating habits of the patients or with the administration of prebiotics, probiotics, and symbiotics. Similarly, different studies have demonstrated that drugs like Metformin are capable of modifying the composition of the gut microbiota, promoting changes in the biosynthesis of LPS, and the metabolism of SCFA.
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5.
Preconditioning of Human Decidua Basalis Mesenchymal Stem/Stromal Cells with Glucose Increased Their Engraftment and Anti-diabetic Properties.
Basmaeil, Y, Rashid, MA, Khatlani, T, AlShabibi, M, Bahattab, E, Abdullah, ML, Abomaray, F, Kalionis, B, Massoudi, S, Abumaree, M
Tissue engineering and regenerative medicine. 2020;(2):209-222
Abstract
BACKGROUND Mesenchymal stem/stromal cells (MSCs) from the decidua basalis (DBMSCs) of the human placenta have important functions that make them potential candidates for cellular therapy. Previously, we showed that DBMSC functions do not change significantly in a high oxidative stress environment, which was induced by hydrogen peroxide (H2O2) and immune cells. Here, we studied the consequences of glucose, another oxidative stress inducer, on the phenotypic and functional changes in DBMSCs. METHODS DBMSCs were exposed to a high level of glucose, and its effect on DBMSC phenotypic and functional properties was determined. DBMSC expression of oxidative stress and immune molecules after exposure to glucose were also identified. RESULTS Conditioning of DBMSCs with glucose improved their adhesion and invasion. Glucose also increased DBMSC expression of genes with survival, proliferation, migration, invasion, anti-inflammatory, anti-chemoattractant and antimicrobial properties. In addition, DBMSC expression of B7H4, an inhibitor of T cell proliferation was also enhanced by glucose. Interestingly, glucose modulated DBMSC expression of genes involved in insulin secretion and prevention of diabetes. CONCLUSION These data show the potentially beneficial effects of glucose on DBMSC functions. Preconditioning of DBMSCs with glucose may therefore be a rational strategy for increasing their therapeutic potential by enhancing their engraftment efficiency. In addition, glucose may program DBMSCs into insulin producing cells with ability to counteract inflammation and infection associated with diabetes. However, future in vitro and in vivo studies are essential to investigate the findings of this study further.
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Development of a subset of ICNP Nursing Diagnoses for the promotion of self-care in people with diabetes mellitus: a multi-center observational study.
Bezze, S, Ausili, D, Erba, I, Redini, S, Re, S, Di Mauro, S
Annali di igiene : medicina preventiva e di comunita. 2020;(1):38-49
Abstract
INTRODUCTION Self-care is a key for people with diabetes mellitus (DM) to avoid severe complications and to maintain quality of life. Person-centered and accurate nursing care plans can help nurses to deliver effective self-care promotion interventions. Few studies focused on nursing diagnoses that are specific for diabetes self-care education, and none of them used the International Classification for Nursing Practice (ICNP). International Catalogues of ICNP nursing diagnoses are missing in this field. AIMS To identify the ICNP nursing diagnoses that are useful to promote self-care in people with DM; to describe the prevalence of ICNP nursing diagnoses in self-care of people with DM. METHODS A subset of 55 ICNP nursing diagnoses was developed based on the Middle Range Theory of Self-care of Chronic Illness, and most recent diabetes clinical guidelines. Then, the subset was tested through a multicenter cross-sectional design involving a consecutive sample of 170 adults with confirmed diagnosis of Type 1 or Type 2 DM. Data were collected by medical records, physical examinations and semi-structured interviews. RESULTS 1343 nursing diagnoses were identified, with an average of 8 nursing diagnoses per patient. The 100% of the nursing diagnoses were described using the pre-developed subset. Overall, the five prevalent nursing diagnoses were: Body weight problem (56.4%), Non adherence to immunization regime (53.5%), Conflicting attitude toward dietary regime (41.7%), Impaired weight monitoring (39.4%), and Lack of knowledge about blood glucose diagnostic test result (32.3%). Nursing diagnoses by self-care maintenance, monitoring and management were also described. CONCLUSIONS A huge amount of nursing diagnoses was identified suggesting the need of intensive education. Clinicians and administrators can use this subset to improve the accuracy of the documentation of diabetes care. In Public Health, the subset can be used to assess the cost-effectiveness of diabetes healthcare services. Future research is needed to assess the effectiveness of this subset in settings that are different from the one where it was developed. Finally, this subset could be a starting point to develop and International ICNP Catalogue for diabetes care.
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Neutrophil extracellular traps: The core player in vascular complications of diabetes mellitus.
Berezin, A
Diabetes & metabolic syndrome. 2019;(5):3017-3023
Abstract
Diabetes mellitus (DM) is the most important metabolic disease with major threat for public health and increased risk of premature death. The prevalence of DM steadily rises in developing and developed countries achieving the epidemic level. Manifestation and progression of DM corresponds to developing vasculopathies, such as retinopathy, micro- and macro angiopathies, which negatively influence on clinical outcomes and quality-of-life. Although there are remarkable differences in the prevalence of vasculopathy in various types of DM, hyperglycemia and lipotoxicity are discussed as a major factors contributing to vascular complications partly through inducing neutrophil extracellular trap (NET). The NET or NETosis is unique form of cell death, which is an important core component of innate immune system. The review is dedicated the role of NET as a link between endothelium, inflammation and thrombosis that is crucial for development of DM-induced vasculopathy. It has suggested that NET formation could be not just a target for the DM care, but also a biomarker for stratification of DM patients at higher risk of vascular complications.
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Environmental Signals Influencing Myeloid Cell Metabolism and Function in Diabetes.
Ratter, JM, Tack, CJ, Netea, MG, Stienstra, R
Trends in endocrinology and metabolism: TEM. 2018;(7):468-480
Abstract
The environment induces metabolic reprogramming of immune cells via specific signaling pathways. Recent studies have revealed that changes in cell metabolism affect key immune cell functions including cytokine production and migration. In diabetes, these functions are either insufficiently or excessively activated, translating into diabetes-associated complications, including increased susceptibility to infection and accelerated cardiovascular disease. Diabetes alters the abundance of environmental signals, including glucose, insulin, and lipids. Subsequently, changes in environmental signals drive metabolic reprogramming, impair immune cell function, and ultimately contribute to diabetes-associated complications. We review here recent studies on changes in innate immune cell metabolism, especially in myeloid cells, that are driven by environmental signals relevant to diabetes, and discuss therapeutic perspectives of targeting metabolism of immune cells in diabetes.
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9.
Extra-Skeletal Effects of Vitamin D.
Bouillon, R
Frontiers of hormone research. 2018;:72-88
Abstract
There are very solid data to confirm that the vitamin D endocrine system is important not only for calcium transport or bone homeostasis but also for operational functions in most cells of the body. Preclinical studies convincingly demonstrated coherent actions of the vitamin D endocrine system on the proliferation/differentiation of most cells (and thus possibly on the evolution of cancer). The most plausible target tissues include skeletal and cardiac muscle, all immune cells, many cells involved in cardiovascular homeostasis, brain cells, and reproductive tissues. These data have been generated in models of (near) total absence of vitamin D action or when exposed to very high concentrations of the active hormone, 1,25-dihydroxyvitamin D or its analogs. In humans, observational data frequently demonstrate a link between poor vitamin D status and a large number of major human diseases such as cancer, muscle weakness and falls, infections or autoimmune diseases, hypertension and cardiovascular risks and events, obesity, diabetes and all aspects of the metabolic syndrome, and other health problems. Intervention studies so far have not convincingly demonstrated a positive effect on such extra-skeletal health outcomes. A very large number of ongoing studies (about 3,000), however, should help to clarify the role of vitamin D on the musculoskeletal system and on global health.
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10.
TLR4 is a link between diabetes and Alzheimer's disease.
Huang, NQ, Jin, H, Zhou, SY, Shi, JS, Jin, F
Behavioural brain research. 2017;:234-244
Abstract
Recently, more and more studies have shown that there is an essential link between diabetes mellitus (DM) and Alzheimer's disease (AD). In addition, innate immunity plays an important role in the occurrence and development of DM and AD, which increase the risk of developing type 2 diabetes (T2D) and AD. Although the pathogenesis of those diseases is still a matter of debate, the important role of Toll-like receptor 4 (TLR4) in the two diseases has been receiving much attention at present. TLR4 and insulin resistance do have close ties, and chronic TLR4 activation may contribute to the insulin resistance. Aside from this, TLR4-mediated chronic inflammation also causes many DM complications such as diabetic nephropathy, diabetic retinopathy and diabetic neuropathy and has a profound impact on the internal environment of the body and brain's microenvironment. In parallel, TLR4 is widely distributed in the brain and also has an important role in the central nervous system (CNS) via regulation of neuroinflammation. The cerebrum under the circumstances of insulin resistance may lead to mitochondrial dysfunction in neurons. Interestingly, in the initial stage, the activation of TLR4 has a useful scavenging effect on amyloid beta (Aβ), but chronic long-term activation leads to Aβ deposition in the brain. Therefore we speculate that the TLR4 signaling pathway may be a potential link between DM and AD.