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1.
Sci Rep ; 12(1): 188, 2022 01 07.
Article in English | MEDLINE | ID: covidwho-1612207

ABSTRACT

Patients with diabetes are more likely to be infected with Coronavirus disease 2019 (COVID-19), and the risk of death is significantly higher than ordinary patients. Dipeptidyl peptidase-4 (DPP4) is one of the functional receptor of human coronavirus. Exploring the relationship between diabetes mellitus targets and DPP4 is particularly important for the management of patients with diabetes and COVID-19. We intend to study the protein interaction through the protein interaction network in order to find a new clue for the management of patients with diabetes with COVID-19. Diabetes mellitus targets were obtained from GeneCards database. Targets with a relevance score exceeding 20 were included, and DPP4 protein was added manually. The initial protein interaction network was obtained through String. The targets directly related to DPP4 were selected as the final analysis targets. Importing them into String again to obtain the protein interaction network. Module identification, gene ontology (GO) analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis were carried out respectively. The impact of DPP4 on the whole network was analyzed by scoring the module where it located. 43 DPP4-related proteins were finally selected from the diabetes mellitus targets and three functional modules were found by the cluster analysis. Module 1 was involved in insulin secretion and glucagon signaling pathway, module 2 and module 3 were involved in signaling receptor binding. The scoring results showed that LEP and apoB in module 1 were the highest, and the scores of INS, IL6 and ALB of cross module associated proteins of module 1 were the highest. DPP4 is widely associated with key proteins in diabetes mellitus. COVID-19 may affect DPP4 in patients with diabetes mellitus, leading to high mortality of diabetes mellitus combined with COVID-19. DPP4 inhibitors and IL-6 antagonists can be considered to reduce the effect of COVID-19 infection on patients with diabetes.


Subject(s)
COVID-19/metabolism , Diabetes Mellitus, Type 2/metabolism , Dipeptidyl Peptidase 4/metabolism , Protein Interaction Maps , SARS-CoV-2/physiology , COVID-19/complications , COVID-19/drug therapy , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Dipeptidyl-Peptidase IV Inhibitors/therapeutic use , Drug Discovery , Humans , Protein Interaction Maps/drug effects
2.
Bull Exp Biol Med ; 172(3): 283-287, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1611428

ABSTRACT

We studied laboratory parameters of patients with COVID-19 against the background of chronic pathologies (cardiovascular pathologies, obesity, type 2 diabetes melitus, and cardiovascular pathologies with allergy to statins). A decrease in pH and a shift in the electrolyte balance of blood plasma were revealed in all studied groups and were most pronounced in patients with cardiovascular pathologies with allergy to statin. It was found that low pH promotes destruction of lipid components of the erythrocyte membranes in patients with chronic pathologies, which was seen from a decrease in Na+/K+-ATPase activity and significant hyponatrenemia. In patients with cardiovascular pathologies and allergy to statins, erythrocyte membranes were most sensitive to a decrease in pH, while erythrocyte membranes of obese patients showed the greatest resistance to low pH and oxidative stress.


Subject(s)
COVID-19/complications , Hyponatremia/etiology , Hypoxia/complications , Sodium-Potassium-Exchanging ATPase/physiology , Aged , COVID-19/metabolism , Cardiovascular Diseases/complications , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/virology , Case-Control Studies , Chronic Disease , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/virology , Drug Hypersensitivity/complications , Drug Hypersensitivity/metabolism , Drug Hypersensitivity/virology , Erythrocyte Membrane/metabolism , Erythrocytes/metabolism , Female , Fluid Shifts/physiology , Humans , Hydrogen-Ion Concentration , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Hyponatremia/metabolism , Hyponatremia/virology , Hypoxia/metabolism , Lipid Peroxidation/physiology , Male , Middle Aged , Obesity/complications , Obesity/metabolism , Obesity/virology , Oxidative Stress/physiology , SARS-CoV-2/physiology , Sodium/metabolism , Stress, Physiological/physiology
3.
Front Endocrinol (Lausanne) ; 12: 731974, 2021.
Article in English | MEDLINE | ID: covidwho-1485049

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing a worldwide epidemic. It spreads very fast and hits people of all ages, especially patients with underlying diseases such as diabetes. In this review, we focus on the influences of diabetes on the outcome of SARS-CoV-2 infection and the involved mechanisms including lung dysfunction, immune disorder, abnormal expression of angiotensin-converting enzyme 2 (ACE2), overactivation of mechanistic target of rapamycin (mTOR) signaling pathway, and increased furin level. On the other hand, SARS-CoV-2 may trigger the development of diabetes. It causes the damage of pancreatic ß cells, which is probably mediated by ACE2 protein in the islets. Furthermore, SARS-CoV-2 may aggravate insulin resistance through attacking other metabolic organs. Of note, certain anti-diabetic drugs (OADs), such as peroxisome proliferator-activated receptor γ (PPARγ) activator and glucagon-like peptide 1 receptor (GLP-1R) agonist, have been shown to upregulate ACE2 in animal models, which may increase the risk of SARS-CoV-2 infection. However, Metformin, as a first-line medicine for the treatment of type 2 diabetes mellitus (T2DM), may be a potential drug benefiting diabetic patients with SARS-CoV-2 infection, probably via a suppression of mTOR signaling together with its anti-inflammatory and anti-fibrosis function in lung. Remarkably, another kind of OADs, dipeptidyl Peptidase 4 (DPP4) inhibitor, may also exert beneficial effects in this respect, probably via a prevention of SARS-CoV-2 binding to cells. Thus, it is of significant to identify appropriate OADs for the treatment of diabetes in the context of SARS-CoV-2 infections.


Subject(s)
COVID-19/epidemiology , COVID-19/metabolism , Diabetes Mellitus, Type 2/epidemiology , Diabetes Mellitus, Type 2/metabolism , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , Angiotensin-Converting Enzyme 2/metabolism , Animals , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , COVID-19/drug therapy , Diabetes Mellitus, Type 2/drug therapy , Dipeptidyl-Peptidase IV Inhibitors/pharmacology , Dipeptidyl-Peptidase IV Inhibitors/therapeutic use , Humans , Hypoglycemic Agents/pharmacology , Hypoglycemic Agents/therapeutic use , Lung/drug effects , Lung/metabolism , T-Lymphocytes/drug effects , T-Lymphocytes/metabolism , TOR Serine-Threonine Kinases/antagonists & inhibitors , TOR Serine-Threonine Kinases/metabolism
4.
Int J Mol Sci ; 22(18)2021 Sep 17.
Article in English | MEDLINE | ID: covidwho-1448875

ABSTRACT

The metabolic syndrome (MetS) consists of a cluster of metabolic abnormalities including central obesity, insulin resistance, glucose intolerance, hypertension, and atherogenic dyslipidemia [...].


Subject(s)
Metabolic Syndrome/metabolism , Obesity/metabolism , Animals , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/physiopathology , Humans , Insulin Resistance/physiology , Metabolic Syndrome/physiopathology , Obesity/physiopathology
5.
Proc Natl Acad Sci U S A ; 118(38)2021 09 21.
Article in English | MEDLINE | ID: covidwho-1392993

ABSTRACT

COVID-19 induces a robust, extended inflammatory "cytokine storm" that contributes to an increased morbidity and mortality, particularly in patients with type 2 diabetes (T2D). Macrophages are a key innate immune cell population responsible for the cytokine storm that has been shown, in T2D, to promote excess inflammation in response to infection. Using peripheral monocytes and sera from human patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and a murine hepatitis coronavirus (MHV-A59) (an established murine model of SARS), we identified that coronavirus induces an increased Mφ-mediated inflammatory response due to a coronavirus-induced decrease in the histone methyltransferase, SETDB2. This decrease in SETDB2 upon coronavirus infection results in a decrease of the repressive trimethylation of histone 3 lysine 9 (H3K9me3) at NFkB binding sites on inflammatory gene promoters, effectively increasing inflammation. Mφs isolated from mice with a myeloid-specific deletion of SETDB2 displayed increased pathologic inflammation following coronavirus infection. Further, IFNß directly regulates SETDB2 in Mφs via JaK1/STAT3 signaling, as blockade of this pathway altered SETDB2 and the inflammatory response to coronavirus infection. Importantly, we also found that loss of SETDB2 mediates an increased inflammatory response in diabetic Mϕs in response to coronavirus infection. Treatment of coronavirus-infected diabetic Mφs with IFNß reversed the inflammatory cytokine production via up-regulation of SETDB2/H3K9me3 on inflammatory gene promoters. Together, these results describe a potential mechanism for the increased Mφ-mediated cytokine storm in patients with T2D in response to COVID-19 and suggest that therapeutic targeting of the IFNß/SETDB2 axis in T2D patients may decrease pathologic inflammation associated with COVID-19.


Subject(s)
Coronavirus/metabolism , Diabetes Mellitus, Type 2/metabolism , Histone-Lysine N-Methyltransferase/metabolism , Inflammation Mediators/metabolism , Inflammation/virology , Macrophages/metabolism , Animals , COVID-19/immunology , Coronavirus Infections/genetics , Coronavirus Infections/immunology , Cytokine Release Syndrome , Cytokines/metabolism , Diabetes Mellitus, Type 2/genetics , Female , Histone-Lysine N-Methyltransferase/genetics , Humans , Inflammation/metabolism , Inflammation/physiopathology , Male , Mice , Mice, Inbred C57BL , NF-kappa B/metabolism , SARS-CoV-2/metabolism , Signal Transduction
6.
J Immunotoxicol ; 18(1): 93-104, 2021 07 24.
Article in English | MEDLINE | ID: covidwho-1373514

ABSTRACT

The aging immune system is characterized by a low-grade chronic systemic inflammatory state ("inflammaging") marked by elevated serum levels of inflammatory molecules such as interleukin (IL)-6 and C-reactive protein (CRP). These inflammatory markers were also reported to be strong predictors for the development/severity of Type 2 diabetes, obesity, and COVID-19. The levels of these markers have been positively associated with those of advanced glycation end-products (AGEs) generated via non-enzymatic glycation and oxidation of proteins and lipids during normal aging and metabolism. Based on the above observations, it is clinically important to elucidate how dietary AGEs modulate inflammation and might thus increase the risk for aging-exacerbated diseases. The present narrative review discusses the potential pro-inflammatory properties of dietary AGEs with a focus on the inflammatory mediators CRP, IL-6 and ferritin, and their relations to aging in general and Type 2 diabetes in particular. In addition, underlying mechanisms - including those related to gut microbiota and the receptors for AGEs, and the roles AGEs might play in affecting physiologies of the healthy elderly, obese individuals, and diabetics are discussed in regard to any greater susceptibility to COVID-19.


Subject(s)
COVID-19/metabolism , Diabetes Mellitus, Type 2/metabolism , Glycation End Products, Advanced/metabolism , Inflammation Mediators/metabolism , SARS-CoV-2/physiology , Aging , Animals , Diet , Dysbiosis , Gastrointestinal Microbiome , Glycation End Products, Advanced/immunology , Homeostasis , Humans , Immunity , Lipid Metabolism
7.
Expert Opin Drug Saf ; 20(11): 1309-1315, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1366929

ABSTRACT

INTRODUCTION: A number of anti-diabetic treatments have been favored during the continuing spread of the current SARS-CoV-2 pandemic. Glucagon like peptide-1 receptor agonists (GLP1-RAs) are a group of antidiabetic drugs, the glucose reducing effect of which is founded on augmenting glucose-dependent insulin secretion with concomitant reduction of glucagon secretion and delayed gastric emptying. Apart from their glucose lowering effects, GLP1-RAs also exert a plethora of pleiotropic activities in the form of anti-inflammatory, anti-thrombotic and anti-obesogenic properties, with beneficial cardiovascular and renal impact. All these make this class of drugs a preferred option for managing patients with type 2 diabetes (T2D), and potentially helpful in those with SARS-CoV2 infection. AREAS COVERED: In the present article we propose a hypothetical molecular mechanism by which GLP1-RAs may interact with SARS-CoV-2 activity. EXPERT OPINION: The beneficial properties of GLP1-RAs may be of specific importance during COVID-19 infection for the most fragile patients with chronic comorbid conditions such as T2D, and those at higher cardiovascular and renal disease risk. Yet, further studies are needed to confirm our hypothesis and preliminary findings available in the literature.


Subject(s)
COVID-19/drug therapy , Diabetes Mellitus, Type 2/drug therapy , Glucagon-Like Peptide-1 Receptor/agonists , Hypoglycemic Agents/therapeutic use , Incretins/therapeutic use , Animals , COVID-19/epidemiology , COVID-19/metabolism , COVID-19/virology , Diabetes Mellitus, Type 2/epidemiology , Diabetes Mellitus, Type 2/metabolism , Glucagon-Like Peptide-1 Receptor/metabolism , Humans , Hypoglycemic Agents/adverse effects , Incretins/adverse effects , Signal Transduction , Treatment Outcome
8.
Front Endocrinol (Lausanne) ; 12: 665134, 2021.
Article in English | MEDLINE | ID: covidwho-1305637

ABSTRACT

Introduction: Neuropilin-1(NRP1) is a cofactor that enhances SARS-CoV-2 coronavirus cell infectivity when co-expressed with angiotensin-converting enzyme 2(ACE2). The Renin-Angiotensin System (RAS) is activated in type 2 diabetes (T2D); therefore, the aim of this study was to determine if hypoglycaemia-induced stress in T2D would potentiate serum NRP1(sNRP1) levels, reflecting an increased risk for SARS-CoV-2 infection. Methods: A case-control study of aged-matched T2D (n = 23) and control (n = 23) subjects who underwent a hyperinsulinemic clamp over 1-hour to hypoglycemia(<40mg/dl) with subsequent timecourse of 4-hours and 24-hours. Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement determined RAS-related proteins: renin (REN), angiotensinogen (AGT), ACE2, soluble NRP1(sNRP1), NRP1 ligands (Vascular endothelial growth factor, VEGF and Class 3 Semaphorins, SEM3A) and NRP1 proteolytic enzyme (A Disintegrin and Metalloproteinase 9, ADAM9). Results: Baseline RAS overactivity was present with REN elevated and AGT decreased in T2D (p<0.05); ACE2 was unchanged. Baseline sNRP1, VEGF and ADAM9 did not differ between T2D and controls and remained unchanged in response to hypoglycaemia. However, 4-hours post-hypoglycemia, sNRP1, VEGF and ADAM9 were elevated in T2D(p<0.05). SEMA3A was not different at baseline; at hypoglycemia, SEMA3A decreased in controls only. Post-hypoglycemia, SEMA3A levels were higher in T2D versus controls. sNRP1 did not correlate with ACE2, REN or AGT. T2D subjects stratified according to ACE inhibitor (ACEi) therapies showed no difference in sNRP1 levels at either glucose normalization or hypoglycaemia. Conclusion: Hypoglycemia potentiated both plasma sNRP1 level elevation and its ligands VEGF and SEMA3A, likely through an ADAM9-mediated mechanism that was not associated with RAS overactivity or ACEi therapy; however, whether this is protective or promotes increased risk for SARS-CoV-2 infection in T2D is unclear. Clinical Trial Registration: https://clinicaltrials.gov, identifier NCT03102801.


Subject(s)
ADAM Proteins/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Diabetes Mellitus, Type 2/metabolism , Hypoglycemia/metabolism , Membrane Proteins/metabolism , Neuropilin-1/metabolism , Semaphorin-3A/metabolism , Vascular Endothelial Growth Factor A/metabolism , Aged , Angiotensins/metabolism , COVID-19 , Female , Glucose Clamp Technique , Humans , Male , Middle Aged , Protective Factors , Renin/metabolism , Risk Factors , SARS-CoV-2
9.
Front Endocrinol (Lausanne) ; 12: 658304, 2021.
Article in English | MEDLINE | ID: covidwho-1305636

ABSTRACT

Objective: Detailed proteomic analysis in a cohort of patients with differing severity of COVID-19 disease identified biomarkers within the complement and coagulation cascades as biomarkers for disease severity has been reported; however, it is unclear if these proteins differ sufficiently from other conditions to be considered as biomarkers. Methods: A prospective, parallel study in T2D (n = 23) and controls (n = 23). A hyperinsulinemic clamp was performed and normoglycemia induced in T2D [4.5 ± 0.07 mmol/L (81 ± 1.2 mg/dl)] for 1-h, following which blood glucose was decreased to ≤2.0 mmol/L (36 mg/dl). Proteomic analysis for the complement and coagulation cascades were measured using Slow Off-rate Modified Aptamer (SOMA)-scan. Results: Thirty-four proteins were measured. At baseline, 4 of 18 were found to differ in T2D versus controls for platelet degranulation [Neutrophil-activating peptide-2 (p = 0.014), Thrombospondin-1 (p = 0.012), Platelet factor-4 (p = 0.007), and Kininogen-1 (p = 0.05)], whilst 3 of 16 proteins differed for complement and coagulation cascades [Coagulation factor IX (p < 0.05), Kininogen-1 (p = 0.05), and Heparin cofactor-2 (p = 0.007)]; STRING analysis demonstrated the close relationship of these proteins to one another. Induced euglycemia in T2D showed no protein changes versus baseline. At hypoglycemia, however, four proteins changed in controls from baseline [Thrombospondin-1 (p < 0.014), platelet factor-4 (p < 0.01), Platelet basic protein (p < 0.008), and Vitamin K-dependent protein-C (p < 0.00003)], and one protein changed in T2D [Vitamin K-dependent protein-C, (p < 0.0002)]. Conclusion: Seven of 34 proteins suggested to be biomarkers of COVID-19 severity within the platelet degranulation and complement and coagulation cascades differed in T2D versus controls, with further changes occurring at hypoglycemia, suggesting that validation of these biomarkers is critical. It is unclear if these protein changes in T2D may predict worse COVID-19 disease for these patients. Clinical Trial Registration: https://clinicaltrials.gov/, identifier NCT03102801.


Subject(s)
Blood Coagulation Factors/metabolism , COVID-19/metabolism , Diabetes Mellitus, Type 2/metabolism , Hypoglycemia/metabolism , Aged , Biomarkers/metabolism , Blood Coagulation , Case-Control Studies , Complement Activation , Factor IX/metabolism , Female , Glucose Clamp Technique , Heparin Cofactor II/metabolism , Humans , Kininogens/metabolism , Male , Middle Aged , Peptides/metabolism , Platelet Activation , Platelet Factor 4/metabolism , Prospective Studies , Protein C/metabolism , Proteomics , SARS-CoV-2 , Severity of Illness Index , Thrombospondin 1/metabolism , beta-Thromboglobulin/metabolism
11.
Adv Food Nutr Res ; 96: 251-310, 2021.
Article in English | MEDLINE | ID: covidwho-1240122

ABSTRACT

Since the discovery of manifest Zn deficiency in 1961, the increasing number of studies demonstrated the association between altered Zn status and multiple diseases. In this chapter, we provide a review of the most recent advances on the role of Zn in health and disease (2010-20), with a special focus on the role of Zn in neurodegenerative and neurodevelopmental disorders, diabetes and obesity, male and female reproduction, as well as COVID-19. In parallel with the revealed tight association between ASD risk and severity and Zn status, the particular mechanisms linking Zn2+ and ASD pathogenesis like modulation of synaptic plasticity through ProSAP/Shank scaffold, neurotransmitter metabolism, and gut microbiota, have been elucidated. The increasing body of data indicate the potential involvement of Zn2+ metabolism in neurodegeneration. Systemic Zn levels in Alzheimer's and Parkinson's disease were found to be reduced, whereas its sequestration in brain may result in modulation of amyloid ß and α-synuclein processing with subsequent toxic effects. Zn2+ was shown to possess adipotropic effects through the role of zinc transporters, zinc finger proteins, and Zn-α2-glycoprotein in adipose tissue physiology, underlying its particular role in pathogenesis of obesity and diabetes mellitus type 2. Recent findings also contribute to further understanding of the role of Zn2+ in spermatogenesis and sperm functioning, as well as oocyte development and fertilization. Finally, Zn2+ was shown to be the potential adjuvant therapy in management of novel coronavirus infection (COVID-19), underlining the perspectives of zinc in management of old and new threats.


Subject(s)
Autism Spectrum Disorder/metabolism , COVID-19/metabolism , Diabetes Mellitus, Type 2/metabolism , Neurodegenerative Diseases/metabolism , Obesity/metabolism , Reproduction , Zinc/metabolism , Alzheimer Disease/metabolism , Animals , COVID-19/drug therapy , Female , Humans , Male , Neurodevelopmental Disorders/metabolism , Nutritional Status , Parkinson Disease/metabolism , Zinc/deficiency , Zinc/therapeutic use
12.
Biochem Soc Trans ; 49(2): 987-995, 2021 04 30.
Article in English | MEDLINE | ID: covidwho-1118826

ABSTRACT

Type-2 Diabetes is associated with one of the co-morbidities due to SARS-Coronavirus 2 (SARS-Cov2) infection. Clinical studies show out of control glucose levels in SARS-Cov2 infected patients with type-2 diabetes. There is no experimental evidence suggesting aberrant molecular pathway(s) that explains why SARS-Cov2 infected patients with type-2 diabetes have uncontrolled glucose homeostasis and are co-morbid. In this article, we have highlighted major proteins involved in SARS-Cov2 infection, like, ACE 2, proteases like, TMPRSS2, Furin and their connectivity to insulin signaling molecules like, PI3K, Akt, AMPK, MAPK, mTOR, those regulate glucose homeostasis and the possible outcome of that cross-talk. We also raised concerns about the effect of anti-SARS-Cov2 drugs on patients with type-2 diabetes with reference to insulin signaling and the outcome of their possible cross-talk. There are no studies to decipher the possibilities of these obvious cross-talks. The major objective of this article is to urge the scientific community to explore the possibility of determining whether derangement of insulin signaling could be one of the possible causes of the patients with type-2 diabetes being co-morbid due to SARS-Cov2 infection.


Subject(s)
COVID-19/metabolism , Diabetes Mellitus, Type 2/metabolism , Insulin/metabolism , Signal Transduction , Angiotensin-Converting Enzyme 2/metabolism , Antiviral Agents/therapeutic use , COVID-19/epidemiology , COVID-19/virology , Comorbidity , Diabetes Mellitus, Type 2/blood , Diabetes Mellitus, Type 2/epidemiology , Humans , SARS-CoV-2/drug effects , SARS-CoV-2/physiology , Serine Endopeptidases/metabolism
13.
Cell ; 184(6): 1530-1544, 2021 03 18.
Article in English | MEDLINE | ID: covidwho-1118348

ABSTRACT

The prevalence of type 2 diabetes and obesity has risen dramatically for decades and is expected to rise further, secondary to the growing aging, sedentary population. The strain on global health care is projected to be colossal. This review explores the latest work and emerging ideas related to genetic and environmental factors influencing metabolism. Translational research and clinical applications, including the impact of the COVID-19 pandemic, are highlighted. Looking forward, strategies to personalize all aspects of prevention, management and care are necessary to improve health outcomes and reduce the impact of these metabolic diseases.


Subject(s)
COVID-19/epidemiology , Diabetes Mellitus, Type 2/epidemiology , Diabetes Mellitus, Type 2/therapy , Obesity/epidemiology , Obesity/therapy , Pandemics , Precision Medicine/methods , SARS-CoV-2 , COVID-19/virology , Circadian Rhythm , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/metabolism , Epigenesis, Genetic , Genetic Predisposition to Disease , Humans , Inflammation/immunology , Inflammation/metabolism , Obesity/genetics , Obesity/metabolism , Prevalence , Risk Factors , Thermotolerance
14.
Diabetes Metab Syndr ; 15(2): 569-571, 2021.
Article in English | MEDLINE | ID: covidwho-1116549

ABSTRACT

BACKGROUND AND AIMS: We aimed to study newly diagnosed diabetes in patients with mild to moderate COVID-19. METHODS: This was a retrospective cohort study of COVID-19 patients who were admitted to a tertiary care hospital in India from May to October 2020. RESULTS: Of 102 patients, 21 (20.6%) had newly diagnosed diabetes on admission. Of which, four (19.0%) had marked hyperglycemia with no ketosis or ketoacidosis. CONCLUSION: In this study of patients with mild to moderate COVID-19, newly diagnosed diabetes and marked hyperglycemia in those with newly diagnosed diabetes were common.


Subject(s)
Blood Glucose/metabolism , COVID-19/physiopathology , Diabetes Mellitus, Type 2/diagnosis , Glycated Hemoglobin A/metabolism , Adult , Anticoagulants/therapeutic use , COVID-19/complications , COVID-19/therapy , Cohort Studies , Dexamethasone/therapeutic use , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Female , Glucocorticoids/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Humans , India , Male , Middle Aged , Oxygen Inhalation Therapy , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index
15.
J Endocrinol ; 249(1): R25-R41, 2021 04.
Article in English | MEDLINE | ID: covidwho-1112513

ABSTRACT

In this narrative review, we provide an overview of the role of physical activity as part of differing exposomes (our combined non-genetic exposures from conception onwards) and environmental influences on metabolic health. We discuss 'beneficial' exposomes (green/natural outdoor spaces, sun exposure, healthy diets and features of built environments) that could synergise with physical activity to prevent metabolic dysfunction, particularly that related to lifestyle diseases of obesity, type 2 diabetes and metabolic syndrome. Physical activity may also reduce the capacity of some adverse exposomes, specifically those with significant levels of air pollution, to contribute towards metabolic dysfunction. Other exposomes, such as those experienced during pandemics (including COVID-19), potentially limit opportunities for physical activity, and there may be unexpected combined effects of physical activity with other infections (e.g. adenovirus-36) on metabolic health. Finally, we discuss how environments could be better optimised to create exposomes that promote the health benefits of physical activity and likely future directions of this research field.


Subject(s)
COVID-19/physiopathology , Diabetes Mellitus, Type 2/physiopathology , Exposome , Life Style , Obesity/physiopathology , COVID-19/prevention & control , COVID-19/virology , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/prevention & control , Exercise/physiology , Health Promotion/methods , Humans , Obesity/metabolism , Obesity/prevention & control , Risk Factors , SARS-CoV-2/physiology
16.
Endocr J ; 68(2): 201-210, 2021 Feb 28.
Article in English | MEDLINE | ID: covidwho-1110113

ABSTRACT

To investigate the acute effects of the coronavirus disease 2019 (COVID-19) on the lifestyle and metabolic parameters in patients with type 2 diabetes mellites. This cross-sectional and retrospective cohort study induced 203 patients who completed a questionnaire regarding stress levels and lifestyles. Data regarding stress levels, sleep time, exercise, and total diet, snack, and prepared food intake were obtained from the questionnaires. The changes in the body weight or HbA1c levels were determined by comparing the values at the time the questionnaire was administered to those noted 3 months ago. Increased levels of stress and decreased exercise levels were reported in approximately 40% and >50%. During the COVID-19 pandemic. There was a negative correlation between stress and exercise (r = -0.285, p < 0.001) and a positive correlation between stress and prepared food intake (r = 0.193, p = 0.009). Decreased exercise levels (r = -0.33, p < 0.001) and increased snack consumption (r = 0.24, p = 0.002) were associated with increased body weight. Furthermore, increased total diet intake (r = 0.16, p = 0.031) was associated with increased HbA1c levels. These relationships remained significant for patients aged <65 years and patients who did not engage in regular exercise. Many patients experienced stress and lifestyle changes due to the COVID-19 pandemic, and these changes were associated with increased body weight and HbA1c levels.


Subject(s)
Body Weight , COVID-19 , Diabetes Mellitus, Type 2/metabolism , Diet , Exercise , Glycated Hemoglobin A/metabolism , Sleep , Stress, Psychological , Aged , Blood Glucose/metabolism , Cross-Sectional Studies , Diabetes Mellitus, Type 2/drug therapy , Fast Foods , Female , Glycemic Control , Humans , Hypoglycemic Agents/therapeutic use , Life Style , Male , Middle Aged , Retrospective Studies , SARS-CoV-2 , Snacks
17.
Endocr Rev ; 41(3)2020 06 01.
Article in English | MEDLINE | ID: covidwho-1110054

ABSTRACT

Individuals with diabetes are at increased risk for bacterial, mycotic, parasitic, and viral infections. The severe acute respiratory syndrome (SARS)-CoV-2 (also referred to as COVID-19) coronavirus pandemic highlights the importance of understanding shared disease pathophysiology potentially informing therapeutic choices in individuals with type 2 diabetes (T2D). Two coronavirus receptor proteins, angiotensin-converting enzyme 2 (ACE2) and dipeptidyl peptidase-4 (DPP4) are also established transducers of metabolic signals and pathways regulating inflammation, renal and cardiovascular physiology, and glucose homeostasis. Moreover, glucose-lowering agents such as the DPP4 inhibitors, widely used in subjects with T2D, are known to modify the biological activities of multiple immunomodulatory substrates. Here, we review the basic and clinical science spanning the intersections of diabetes, coronavirus infections, ACE2, and DPP4 biology, highlighting clinical relevance and evolving areas of uncertainty underlying the pathophysiology and treatment of T2D in the context of coronavirus infection.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Pneumonia, Viral/complications , Angiotensin-Converting Enzyme 2 , Animals , COVID-19 , Coronavirus Infections/metabolism , Diabetes Mellitus, Type 1/complications , Diabetes Mellitus, Type 1/metabolism , Diabetes Mellitus, Type 2/metabolism , Dipeptidyl Peptidase 4/metabolism , Dipeptidyl-Peptidase IV Inhibitors/pharmacology , Dipeptidyl-Peptidase IV Inhibitors/therapeutic use , Gastrointestinal Tract/metabolism , Humans , Insulin/therapeutic use , Lung/metabolism , Obesity/complications , Obesity/metabolism , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/metabolism , Receptors, Coronavirus , Receptors, Virus/metabolism , Risk Factors , SARS-CoV-2 , Serine Endopeptidases/metabolism
18.
Biochim Biophys Acta Mol Basis Dis ; 1867(4): 166044, 2021 04 01.
Article in English | MEDLINE | ID: covidwho-1103717

ABSTRACT

Diabetes-associated morbidity and mortality is predominantly due to complications of the disease that may cause debilitating conditions, such as heart and renal failure, hepatic insufficiency, retinopathy or peripheral neuropathy. Fibrosis, the excessive and inappropriate deposition of extracellular matrix in various tissues, is commonly found in patients with advanced type 1 or type 2 diabetes, and may contribute to organ dysfunction. Hyperglycemia, lipotoxic injury and insulin resistance activate a fibrotic response, not only through direct stimulation of matrix synthesis by fibroblasts, but also by promoting a fibrogenic phenotype in immune and vascular cells, and possibly also by triggering epithelial and endothelial cell conversion to a fibroblast-like phenotype. High glucose stimulates several fibrogenic pathways, triggering reactive oxygen species generation, stimulating neurohumoral responses, activating growth factor cascades (such as TGF-ß/Smad3 and PDGFs), inducing pro-inflammatory cytokines and chemokines, generating advanced glycation end-products (AGEs) and stimulating the AGE-RAGE axis, and upregulating fibrogenic matricellular proteins. Although diabetes-activated fibrogenic signaling has common characteristics in various tissues, some organs, such as the heart, kidney and liver develop more pronounced and clinically significant fibrosis. This review manuscript summarizes current knowledge on the cellular and molecular pathways involved in diabetic fibrosis, discussing the fundamental links between metabolic perturbations and fibrogenic activation, the basis for organ-specific differences, and the promises and challenges of anti-fibrotic therapies for diabetic patients.


Subject(s)
Diabetes Mellitus, Type 1/pathology , Diabetes Mellitus, Type 2/pathology , Animals , Diabetes Mellitus, Type 1/genetics , Diabetes Mellitus, Type 1/metabolism , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/metabolism , Disease Progression , Epigenesis, Genetic , Fibroblasts/metabolism , Fibroblasts/pathology , Fibrosis , Glucose/genetics , Glucose/metabolism , Humans , Inflammation/genetics , Inflammation/metabolism , Inflammation/pathology , Signal Transduction
19.
Drug Saf ; 43(12): 1211-1221, 2020 12.
Article in English | MEDLINE | ID: covidwho-1092871

ABSTRACT

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a major advance in the fields of diabetology, nephrology, and cardiology. The cardiovascular and renal benefits of SGLT2 inhibitors are likely largely independent of their glycaemic effects, and this understanding is central to the use of these agents in the high-risk population of people with type 2 diabetes and chronic kidney disease. There are a number of potential safety issues associated with the use of SGLT2 inhibitors. These include the rare but serious risks of diabetic ketoacidosis and necrotising fasciitis of the perineum. The data regarding a possibly increased risk of lower limb amputation and fracture with SGLT2 inhibitor therapy are conflicting. This article aims to explore the potential safety issues associated with the use of SGLT2 inhibitors, with a particular focus on the safety of these drugs in people with type 2 diabetes and chronic kidney disease. We discuss strategies that clinicians can implement to minimise the risk of adverse effects including diabetic ketoacidosis and volume depletion. Risk mitigation strategies with respect to SGLT2 inhibitor-associated diabetic ketoacidosis are of particular importance during the current coronavirus disease 2019 (COVID-19) pandemic.


Subject(s)
Diabetes Mellitus, Type 2/drug therapy , Diabetic Ketoacidosis/chemically induced , Fasciitis, Necrotizing/chemically induced , Hypovolemia/chemically induced , Renal Insufficiency, Chronic/complications , Sodium-Glucose Transporter 2 Inhibitors/adverse effects , Acute Kidney Injury/chemically induced , Amputation/statistics & numerical data , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Fournier Gangrene/chemically induced , Fractures, Bone/chemically induced , Humans , Hypoglycemia/chemically induced , Patient Education as Topic , Perineum , Reproductive Tract Infections/chemically induced , Risk Factors , Urinary Tract Infections/chemically induced
20.
Eur J Clin Invest ; 50(7): e13262, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-1081113

ABSTRACT

The Covid-19 pandemic confronted us with unknown clinical pictures, also in diabetology and endocrinology. Sharing clinical experiences is therefore of enormous importance. Actually, information about the care given in the Covid-19 ward (in contrast to that provided in the Emergency Room/ICU) is still sparse. The last weeks we built experience and gathered knowledge while giving hospital care to patients who had a pre-existent endocrine disease (and diabetes; most patients suffered from a type two diabetes). In our contribution we presented our insights obtained from this intensive period obtained in the Covid-19 ward.


Subject(s)
Coronavirus Infections/therapy , Diabetes Mellitus, Type 2/drug therapy , Hyperglycemia/drug therapy , Hypoglycemic Agents/therapeutic use , Insulin/therapeutic use , Pneumonia, Viral/therapy , Adrenal Insufficiency/complications , Adrenal Insufficiency/drug therapy , Belgium , Betacoronavirus , Blood Glucose/metabolism , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/metabolism , Diabetes Complications , Diabetes Insipidus/complications , Diabetes Insipidus/therapy , Diabetes Mellitus/drug therapy , Diabetes Mellitus/metabolism , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Disease Management , Glycated Hemoglobin A/metabolism , Hospital Units , Hospitalization , Humans , Hyperglycemia/etiology , Hyperglycemia/metabolism , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/metabolism , SARS-CoV-2
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