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1.
Int J Mol Sci ; 23(19)2022 Oct 01.
Article in English | MEDLINE | ID: covidwho-2066134

ABSTRACT

Skeletal muscle serves as the optimal effective organ to balance glucose homeostasis, but insulin resistance (IR) in skeletal muscle breaks this balance by impeding glucose uptake and causes metabolic disorders. IR in skeletal muscle is caused by multiple factors, and it has been reported that systemic low-grade inflammation is related to skeletal muscle IR, though its molecular mechanisms need to be ulteriorly studied. Pyroptosis is a novel inflammatory-mediated type of cell death. It has recently been reported that pyroptosis is associated with a decline in insulin sensitivity in skeletal muscle. The appropriate occurrence of pyroptosis positively eliminates pathogenic factors, whereas its excessive activation may aggravate inflammatory responses and expedite disease progression. The relationship between pyroptosis and IR in skeletal muscle and its underlined mechanism need to be further illustrated. The role of pyroptosis during the process of IR alleviation induced by non-drug interventions, such as exercise, also needs to be clarified. In this paper, we review and describe the molecular mechanisms of pyroptosis and further comb the roles of its relevant key factors in skeletal muscle IR, aiming to propose a novel theoretical basis for the relationship between pyroptosis and muscle IR and provide new research targets for the improvement of IR-related diseases.


Subject(s)
Insulin Resistance , Glucose/metabolism , Humans , Inflammation/metabolism , Muscle, Skeletal/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Pyroptosis
2.
Diabetes Res Clin Pract ; 191: 110034, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-2035941

ABSTRACT

INTRODUCTION: The COVID-19 pandemic disproportionately affected patients who had comorbid diabetes mellitus. COVID-19 patients with diabetes experience significantly higher rates of complications and mortality. COVID-induced diabetes is a novel phenomenon observed in critically ill patients. The aims of this review were to explore the literature about COVID-induced diabetes and the pathophysiological mechanisms that could lead to this novel presentation. METHODS: A literature search was performed using PUBMED, Google Scholar, MEDLINE and Embase for original studies (meta-analyses, cross-sectional studies, case series, case reports) about new-onset diabetes following COVID infection, and the proposed biochemical pathways behind this presentation. It was assumed that the authors of the studies used the current diagnostic criteria for diagnosis of type 1 and type 2 diabetes. RESULTS: COVID-19 causes dysregulation of glucose homeostasis leading to new-onset diabetes and hyperglycaemia. This is also seen in patients with no previous risk factors for diabetes mellitus. The atypical glycaemic parameters and increased rates of DKA suggest that COVID-induced diabetes is a novel form of diabetes. A spectrum of COVID-induced diabetes has also been noted. COVID-induced diabetes is associated with remarkably higher mortality rates and worse outcomes compared to COVID-19 patients with pre-existing diabetes. The novel presentation of COVID-induced diabetes could be due to beta cell damage and insulin resistance caused by SARS-CoV-2. CONCLUSION: COVID-induced diabetes is essential to detect early, owing to its implications on prognosis. Further studies must include follow-up of these patients to better understand the trajectory of COVID-induced diabetes and the best management plan. It is also important to assess the beta cell function and insulin resistance of COVID-induced diabetes patients over time to better understand the underlying biochemical mechanisms.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Insulin Resistance , Blood Glucose , COVID-19/complications , Cross-Sectional Studies , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/epidemiology , Humans , Pandemics , SARS-CoV-2
3.
Nutr Metab Cardiovasc Dis ; 32(9): 2157-2167, 2022 09.
Article in English | MEDLINE | ID: covidwho-2008006

ABSTRACT

BACKGROUND AND AIMS: Menopause may reduce fat oxidation. We investigated whether sex hormone profile explains resting fat oxidation (RFO) or peak fat oxidation (PFO) during incremental cycling in middle-aged women. Secondarily, we studied associations of RFO and PFO with glucose regulation. METHOD AND RESULTS: We measured RFO and PFO of 42 women (age 52-58 years) with indirect calorimetry. Seven participants were pre- or perimenopausal, 26 were postmenopausal, and nine were postmenopausal hormone therapy users. Serum estradiol (E2), follicle-stimulating hormone, progesterone, and testosterone levels were quantified with immunoassays. Insulin sensitivity (Matsuda index) and glucose tolerance (area under the curve) were determined by glucose tolerance testing. Body composition was assessed with dual-energy X-ray absorptiometry; physical activity with self-report and accelerometry; and diet, with food diaries. Menopausal status or sex hormone levels were not associated with the fat oxidation outcomes. RFO determinants were fat mass (ß = 0.44, P = 0.006) and preceding energy intake (ß = -0.40, P = 0.019). Cardiorespiratory fitness (ß = 0.59, P = 0.002), lean mass (ß = 0.49, P = 0.002) and physical activity (self-reported ß = 0.37, P = 0.020; accelerometer-measured ß = 0.35, P = 0.024) explained PFO. RFO and PFO were not related to insulin sensitivity. Higher RFO was associated with poorer glucose tolerance (ß = 0.52, P = 0.002). CONCLUSION: Among studied middle-aged women, sex hormone profile did not explain RFO or PFO, and higher fat oxidation capacity did not indicate better glucose control.


Subject(s)
Glycemic Control , Insulin Resistance , Blood Glucose , Body Composition , Female , Glucose , Gonadal Steroid Hormones , Humans , Middle Aged
4.
Diabetes Care ; 45(10): 2406-2411, 2022 10 01.
Article in English | MEDLINE | ID: covidwho-1987390

ABSTRACT

OBJECTIVE: Although mortality from coronavirus disease 2019 (COVID-19) among youth with type 1 diabetes is rare, severe acute respiratory syndrome coronavirus 2 is associated with increased pediatric hospitalizations for diabetic ketoacidosis (DKA). To clarify whether the relationship between COVID-19 and DKA is coincidental or causal, we compared tissue glucose disposal (TGD) during standardized treatment for DKA between pediatric patients with COVID-19 and those without COVID-19. RESEARCH DESIGN AND METHODS: We retrospectively compared TGD during standardized therapy for DKA in all children with preexisting type 1 diabetes with or without COVID-19. Cases were assessed beginning with the first case of COVID-19-positive DKA on 19 June 2020 through 2 February 2022. RESULTS: We identified 93 COVID-19-negative patients and 15 COVID-19-positive patients who were treated for DKA, with similar baseline characteristics between groups. Median TGD was 46% lower among patients who had COVID-19 compared with those who did not (P = 0.013). CONCLUSIONS: These results suggest that COVID-19 provokes a metabolic derangement over and above factors that typically contribute to pediatric DKA. These findings underscore the significant and direct threat posed by COVID-19 in pediatric type 1 diabetes and emphasize the importance of mitigation and monitoring including through vaccination as a primary prevention.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 1 , Diabetic Ketoacidosis , Insulin Resistance , Adolescent , COVID-19/complications , Child , Diabetes Mellitus, Type 1/complications , Diabetic Ketoacidosis/etiology , Diabetic Ketoacidosis/therapy , Glucose , Humans , Retrospective Studies
5.
PLoS One ; 17(8): e0272000, 2022.
Article in English | MEDLINE | ID: covidwho-1968874

ABSTRACT

Lipid ratios and the triglyceride and glucose index (TyG) could be a simple biochemical marker of insulin resistance (IR). The current study was carried out to examine the correlation between triglyceride to high-density lipoprotein-cholesterol (TG/HDL-C), total cholesterol to HDL-C (TC/HDL-C), low-density lipoprotein-cholesterol to HDL-C ratio (LDL-C/HDL-C), as well as TyG index with the severity and mortality of severe coronavirus disease 2019 (COVID-19). A total of 1228 confirmed COVID-19 patients were included in the current research. Regression models were performed to evaluate the correlation between the lipid index and severity and mortality of COVID-19. The TyG index and TG/HDL-C levels were significantly higher in the severe patients (P<0.05). TG/HDL-C, LDL-C/HDL-C, TC/HDL-C ratios, and TyG index were significantly lower in survivor cases (P<0.05). Multivariate logistic regression analysis demonstrated that predictors of the severity adjusted for age, sex and BMI were TyG index, TG/HDL-C ratio (OR = 1.42 CI:1.10-1.82, OR = 1.06 CI: 1.02-1.11, respectively). This analysis showed that TG/HDL-C, TC/HDL-C, LDL-C/HDL-C ratios, and TyG index statistically are correlated with COVID-19 mortality (OR = 1.12 CI:1.06-1.18, OR = 1.24 CI:1.05-1.48, OR = 1.47 CI:1.19-1.80, OR = 1.52 CI:1.01-2.31, respectively). In summary, the TyG index and lipid ratios such as TC/HDL-C, TG/HDL-C, LDL-C/HDL-C could be used as an early indicator of COVID-19 mortality. Furthermore, the study revealed that TyG index and TG/HDL-C indices are biochemical markers of COVID-19 severe prognosis.


Subject(s)
COVID-19 , Insulin Resistance , Biomarkers , Blood Glucose/analysis , COVID-19/therapy , Cholesterol, HDL , Cholesterol, LDL , Critical Care Outcomes , Glucose , Humans , Triglycerides
6.
Biomed Pharmacother ; 153: 113456, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1966381

ABSTRACT

Dexamethasone acts as an immunosuppressive drug and has been used recently in the management of specific coronavirus disease 2019 (COVID-19) cases; however, various adverse effects could limit its use. In this work, we studied the mitigation effects of black pepper oil (BP oil) on glycemic parameters, dyslipidemia, oxidative and nitrosative stress and pancreatic fibrosis in dexamethasone-treated rats. Animals were divided into five groups that were treated with vehicle, dexamethasone (10 mg/kg, SC) or black pepper oil (BP oil, 0.5 mL, or 1 mL/kg) or metformin (50 mg/kg) plus dexamethasone for 4 consecutive days. Serum insulin, blood glucose, total cholesterol, triglycerides, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) were higher in the dexamethasone group vs the control group and decreased in BP oil and metformin groups relative to the dexamethasone group. Pancreatic nitric oxide, inducible nitric oxide synthase and malondialdehyde levels were increased in the dexamethasone group vs the control group and decreased in BP oil and metformin groups relative to the dexamethasone group. Pancreatic endothelial nitric oxide synthase and reduced glutathione were declined in the dexamethasone group vs the control group. They were increased in BP oil and metformin groups relative to the dexamethasone group. Moreover, the pancreatic islets diameter and collagen deposition were assessed and found to be higher in the dexamethasone group vs the control group. BP oil and metformin groups showed to regress this effect. In conclusion, BP oil may alleviate hyperglycemia, hyperinsulinemia, insulin resistance, dyslipidemia and pancreatic structural derangements and fibrosis by suppressing oxidative stress, increasing endogenous antioxidant levels, modulating nitric oxide signaling, preventing pancreatic stellate cells transition and collagen deposition.


Subject(s)
Dexamethasone , Metformin , Pancreas , Piper nigrum , Plant Oils , Animals , Blood Glucose , COVID-19/drug therapy , Dexamethasone/adverse effects , Dexamethasone/pharmacology , Dyslipidemias/drug therapy , Fibrosis , Insulin Resistance , Metformin/pharmacology , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II/drug effects , Nitric Oxide Synthase Type II/metabolism , Oxidative Stress/drug effects , Pancreas/drug effects , Pancreas/pathology , Piper nigrum/chemistry , Plant Oils/pharmacology , Plant Oils/therapeutic use , Rats , Rats, Wistar
7.
Nutrients ; 14(14)2022 Jul 07.
Article in English | MEDLINE | ID: covidwho-1928617

ABSTRACT

BACKGROUND: Non-alcoholic fatty liver disease is a chronic disease caused by the accumulation of fat in the liver related to overweight and obesity, insulin resistance, hyperglycemia, and high levels of triglycerides and leads to an increased cardiovascular risk. It is considered a global pandemic, coinciding with the pandemic in 2020 caused by the "coronavirus disease 2019" (COVID-19). Due to COVID-19, the population was placed under lockdown. The aim of our study was to evaluate how these unhealthy lifestyle modifications influenced the appearance of metabolic alterations and the increase in non-alcoholic fatty liver disease. METHODS: A prospective study was carried out on 6236 workers in a Spanish population between March 2019 and March 2021. RESULTS: Differences in the mean values of anthropometric and clinical parameters before and after lockdown were revealed. There was a statistically significant worsening in non-alcoholic fatty liver disease (NAFLD) and in the insulin resistance scales, with increased body weight, BMI, cholesterol levels with higher LDL levels, and glucose and a reduction in HDL levels. CONCLUSIONS: Lockdown caused a worsening of cardiovascular risk factors due to an increase in liver fat estimation scales and an increased risk of presenting with NAFLD and changes in insulin resistance.


Subject(s)
COVID-19 , Insulin Resistance , Non-alcoholic Fatty Liver Disease , Adult , COVID-19/epidemiology , Communicable Disease Control , Humans , Liver/metabolism , Longitudinal Studies , Non-alcoholic Fatty Liver Disease/epidemiology , Non-alcoholic Fatty Liver Disease/metabolism , Pandemics , Prospective Studies , Risk Factors
9.
Int J Mol Sci ; 23(13)2022 Jun 29.
Article in English | MEDLINE | ID: covidwho-1917516

ABSTRACT

People with diabetes are more likely to have severe COVID-19 compared to the general population. Moreover, diabetes and COVID-19 demonstrate a certain parallelism in the mechanisms and organ damage. In this work, we applied bioinformatics analysis of associative molecular networks to identify key molecules and pathophysiological processes that determine SARS-CoV-2-induced disorders in patients with diabetes. Using text-mining-based approaches and ANDSystem as a bioinformatics tool, we reconstructed and matched networks related to hyperglycemia, diabetic complications, insulin resistance, and beta cell dysfunction with networks of SARS-CoV-2-targeted proteins. The latter included SARS-CoV-2 entry receptors (ACE2 and DPP4), SARS-CoV-2 entry associated proteases (TMPRSS2, CTSB, and CTSL), and 332 human intracellular proteins interacting with SARS-CoV-2. A number of genes/proteins targeted by SARS-CoV-2 (ACE2, BRD2, COMT, CTSB, CTSL, DNMT1, DPP4, ERP44, F2RL1, GDF15, GPX1, HDAC2, HMOX1, HYOU1, IDE, LOX, NUTF2, PCNT, PLAT, RAB10, RHOA, SCARB1, and SELENOS) were found in the networks of vascular diabetic complications and insulin resistance. According to the Gene Ontology enrichment analysis, the defined molecules are involved in the response to hypoxia, reactive oxygen species metabolism, immune and inflammatory response, regulation of angiogenesis, platelet degranulation, and other processes. The results expand the understanding of the molecular basis of diabetes and COVID-19 comorbidity.


Subject(s)
COVID-19 , Diabetes Complications , Diabetes Mellitus , Hyperglycemia , Insulin Resistance , Angiotensin-Converting Enzyme 2 , COVID-19/genetics , Comorbidity , Diabetes Complications/genetics , Diabetes Mellitus/epidemiology , Diabetes Mellitus/genetics , Dipeptidyl Peptidase 4/genetics , Gene Regulatory Networks , Humans , Hyperglycemia/complications , Hyperglycemia/genetics , SARS-CoV-2/genetics
10.
Lancet Diabetes Endocrinol ; 10(4): 284-296, 2022 04.
Article in English | MEDLINE | ID: covidwho-1915200

ABSTRACT

Non-alcoholic fatty liver disease (NAFLD) has become an epidemic, much like other non-communicable diseases (NCDs), such as cancer, obesity, diabetes, and cardiovascular disease. The pathophysiology of NAFLD, particularly involving insulin resistance and subclinical inflammation, is not only closely linked to that of those NCDs but also to a severe course of the communicable disease COVID-19. Genetics alone cannot explain the large increase in the prevalence of NAFLD during the past 2 decades and the increase that is projected for the next decades. Impairment of glucose and lipid metabolic pathways, which has been propelled by the worldwide increase in the prevalence of obesity and type 2 diabetes, is most likely behind the increase in people with NAFLD. As the prevalence of NAFLD varies among subgroups of patients with diabetes and prediabetes identified by cluster analyses, stratification of people with diabetes and prediabetes by major pathological mechanistic pathways might improve the diagnosis of NAFLD and prediction of its progression. In this Review, we aim to understand how diabetes can affect the development of hepatic steatosis and its progression to advanced liver damage. First, we emphasise the extent to which NAFLD and diabetes jointly occur worldwide. Second, we address the major mechanisms that are involved in the pathogenesis of NAFLD and type 2 diabetes, and we discuss whether these mechanisms place NAFLD in an important position to better understand the pathogenesis of NCDs and communicable diseases, such as COVID-19. Third, we address whether this knowledge can be used for personalised treatment of NAFLD in the future. Finally, we discuss the current treatment strategies for people with type 2 diabetes and their effectiveness in treating the spectrum of hepatic diseases from simple steatosis to non-alcoholic steatohepatitis and hepatic fibrosis.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Insulin Resistance , Non-alcoholic Fatty Liver Disease , Prediabetic State , COVID-19/complications , COVID-19/epidemiology , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/epidemiology , Humans , Liver/metabolism , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/epidemiology , Prediabetic State/metabolism
11.
J Clin Lipidol ; 16(5): 643-648, 2022.
Article in English | MEDLINE | ID: covidwho-1907223

ABSTRACT

BACKGROUND: The COVID-19 pandemic has raised concerns for worsening cardiometabolic health in children. OBJECTIVE: This study evaluates the impact of the COVID-19 pandemic and subsequent social restrictions on pediatric cardiometabolic health factors. METHODS: Retrospective review of patients in a pediatric lipid clinic in the year prior to (3/18/2019-3/17/2020) and during (3/18/2020-3/17/2021) the COVID-19 pandemic was performed. Physical findings (body mass index [BMI], waist circumference [WC], and blood pressure), laboratory markers of cardiometabolic health (lipid panel, insulin resistance, and liver transaminases), self-reported exercise time, and lipid-lowering medications (metformin, statin, omega-3 fatty acids, fenofibrate) were compared. RESULTS: 297 subjects met inclusion criteria. Among subjects prescribed no medications or on stable medication doses (n=241), there were few changes in lipid panels. Among subjects with new or increased medication doses between pre-pandemic and pandemic intervals (n=62), there were increases in triglycerides (p= 0.019) and HgbA1c (p=0.046). There was no change in z-scores for both BMI and WC for either group. CONCLUSION: We observed concerning trends in markers of cardiovascular disease health (dyslipidemia, insulin resistance, and diabetes), independent of changes in weight, in at-risk children during the recent COVID pandemic. Our findings suggest that this vulnerable population may benefit from more frequent monitoring and intense management during such events.


Subject(s)
COVID-19 , Cardiovascular Diseases , Dyslipidemias , Insulin Resistance , Humans , Child , Pandemics , COVID-19/epidemiology , Waist Circumference , Body Mass Index , Triglycerides , Cardiovascular Diseases/complications , Cardiovascular Diseases/epidemiology , Dyslipidemias/epidemiology , Risk Factors
12.
BMJ Open ; 12(4): e060520, 2022 04 26.
Article in English | MEDLINE | ID: covidwho-1886766

ABSTRACT

INTRODUCTION: Shift workers are at an increased risk of developing obesity and type 2 diabetes. Eating and sleeping out of synchronisation with endogenous circadian rhythms causes weight gain, hyperglycaemia and insulin resistance. Interventions that promote weight loss and reduce the metabolic consequences of eating at night are needed for night shift workers. The aim of this study is to examine the effects of three weight loss strategies on weight loss and insulin resistance (HOMA-IR) in night shift workers. METHODS AND ANALYSIS: A multisite 18-month, three-arm randomised controlled trial comparing three weight loss strategies; continuous energy restriction; and two intermittent fasting strategies whereby participants will fast for 2 days per week (5:2); either during the day (5:2D) or during the night shift (5:2N). Participants will be randomised to a weight loss strategy for 24 weeks (weight loss phase) and followed up 12 months later (maintenance phase). The primary outcomes are weight loss and a change in HOMA-IR. Secondary outcomes include changes in glucose, insulin, blood lipids, body composition, waist circumference, physical activity and quality of life. Assessments will be conducted at baseline, 24 weeks (primary endpoint) and 18 months (12-month follow-up). The intervention will be delivered by research dietitians via a combination of face-to-face and telehealth consultations. Mixed-effect models will be used to identify changes in dependent outcomes (weight and HOMA-IR) with predictor variables of outcomes of group, time and group-time interaction, following an intention-to-treat approach. ETHICS AND DISSEMINATION: The study protocol was approved by Monash Health Human Research Ethics Committee (RES 19-0000-462A) and registered with Monash University Human Research Ethics Committee. Ethical approval has also been obtained from the University of South Australia (HREC ID: 202379) and Ambulance Victoria Research Committee (R19-037). Results from this trial will be disseminated via conference presentations, peer-reviewed journals and student theses. TRIAL REGISTRATION NUMBER: Australian New Zealand Clinical Trials Registry (ACTRN-12619001035112).


Subject(s)
Diabetes Mellitus, Type 2 , Insulin Resistance , Diabetes Mellitus, Type 2/prevention & control , Fasting , Humans , Obesity/therapy , Quality of Life , Randomized Controlled Trials as Topic , Victoria , Weight Loss
13.
Cells ; 11(12)2022 06 10.
Article in English | MEDLINE | ID: covidwho-1884017

ABSTRACT

Obesity is characterized by an increase in body weight associated with an exaggerated enlargement of the adipose tissue. Obesity has serious negative effects because it is associated with multiple pathological complications such as type 2 diabetes mellitus, cardiovascular diseases, cancer, and COVID-19. Nowadays, 39% of the world population is obese or overweight, making obesity the 21st century epidemic. Obesity is also characterized by a mild, chronic, systemic inflammation. Accumulation of fat in adipose tissue causes stress and malfunction of adipocytes, which then initiate inflammation. Next, adipose tissue is infiltrated by cells of the innate immune system. Recently, it has become evident that neutrophils, the most abundant leukocytes in blood, are the first immune cells infiltrating the adipose tissue. Neutrophils then get activated and release inflammatory factors that recruit macrophages and other immune cells. These immune cells, in turn, perpetuate the inflammation state by producing cytokines and chemokines that can reach other parts of the body, creating a systemic inflammatory condition. In this review, we described the recent findings on the role of neutrophils during obesity and the initiation of inflammation. In addition, we discuss the involvement of neutrophils in the generation of obesity-related complications using diabetes as a prime example.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Insulin Resistance , COVID-19/complications , Diabetes Mellitus, Type 2/pathology , Humans , Inflammation/pathology , Neutrophils/pathology , Obesity/pathology
14.
Horm Metab Res ; 54(8): 567-570, 2022 Aug.
Article in English | MEDLINE | ID: covidwho-1873583

ABSTRACT

The Covid-19 pandemic has provided new and strong evidence for poor outcomes of viral infection in patients with poor metabolic health. Insulin resistance is at the root of many metabolic conditions and a key driver of their progression as it promotes ineffectual inflammation whilst impairing immune functions. In a vicious circle, insulin resistance facilitates SARS-CoV-2 infection, whilst infection drives insulin resistance. We discuss the underlying mechanisms and explore ways to improve metabolic health and prevent insulin resistance through early detection and targeted nutritional interventions. With proven efficacy in prediabetes, type 2 diabetes, and their cardiovascular and organ complications, as much as non-alcoholic liver disease, we argue to extend such approaches to ensure resilience to the current pandemic and viral challenges beyond.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Insulin Resistance , COVID-19/complications , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/therapy , Humans , Immune System , Pandemics , Risk Reduction Behavior , SARS-CoV-2
15.
Signal Transduct Target Ther ; 6(1): 427, 2021 12 16.
Article in English | MEDLINE | ID: covidwho-1795805

ABSTRACT

Abnormal glucose and lipid metabolism in COVID-19 patients were recently reported with unclear mechanism. In this study, we retrospectively investigated a cohort of COVID-19 patients without pre-existing metabolic-related diseases, and found new-onset insulin resistance, hyperglycemia, and decreased HDL-C in these patients. Mechanistically, SARS-CoV-2 infection increased the expression of RE1-silencing transcription factor (REST), which modulated the expression of secreted metabolic factors including myeloperoxidase, apelin, and myostatin at the transcriptional level, resulting in the perturbation of glucose and lipid metabolism. Furthermore, several lipids, including (±)5-HETE, (±)12-HETE, propionic acid, and isobutyric acid were identified as the potential biomarkers of COVID-19-induced metabolic dysregulation, especially in insulin resistance. Taken together, our study revealed insulin resistance as the direct cause of hyperglycemia upon COVID-19, and further illustrated the underlying mechanisms, providing potential therapeutic targets for COVID-19-induced metabolic complications.


Subject(s)
COVID-19/blood , Hyperglycemia/blood , Insulin Resistance , Lipid Metabolism , Lipids/blood , SARS-CoV-2/metabolism , Adult , Aged , Biomarkers/blood , COVID-19/complications , Female , Humans , Hyperglycemia/etiology , Male , Middle Aged , Retrospective Studies
16.
Reprod Health ; 18(1): 156, 2021 Jul 26.
Article in English | MEDLINE | ID: covidwho-1779653

ABSTRACT

BACKGROUND: The most common endocrine and metabolic disorders in premenopausal women is polycystic ovary syndrome (PCOS), characterized by hyperandrogenism, chronic anovulation, and/or ultrasound evidence of small ovarian cysts. Obesity and insulin resistance are also the main factors influencing the clinical manifestations of this syndrome. Alzheimer's disease (AD) is the most typical progressive neurodegenerative disorder of the brain, and recent studies suggest a relationship between endocrinal dysregulation and neuronal loss during AD pathology. AIM: This study aimed to evaluate the common risk factors for Alzheimer's and PCOS based on previous studies. Knowing the common risk factors and eliminating them may prevent neurodegenerative Alzheimer's disease in the future. METHOD: In this narrative review, international databases, including Google Scholar, Scopus, PubMed, and the Web of Science, were searched to retrieve the relevant studies. The relevant studies' summaries were categorized to discuss the possible pathways that may explain the association between Alzheimer's and PCOS signs/symptoms and complications. RESULTS: According to our research, the factors involved in Alzheimer's and PCOS disorders may share some common risk factors. In patients with PCOS, increased LH to FSH ratio, decreased vitamin D, insulin resistance, and obesity are some of the most important factors that may increase the risk of Alzheimer's disease.


Polycystic ovary syndrome is a disorder of the female reproductive system that can be caused by hormonal disorders. The disease is detected by an ultrasound of the ovaries with small ovarian cysts. Obesity and insulin resistance are among the factors that can affect the clinical symptoms of this disease. Obesity due to high-fat consumption can affect cognitive functions with age. Alzheimer's is the most common disease associated with disorders in brain cells; a link between hormonal disorders and Alzheimer's has recently been reported. We conducted a review of reports and articles published in connection with polycystic ovary syndrome and neurodegenerative disorders in reputable scientific databases. Studies have shown that the factors involved in polycystic ovary syndrome and Alzheimer's disease may indicate that both diseases have common risk factors. It may be linked to the symptoms and/or complications of Alzheimer's disease and polycystic ovary syndrome. Future preclinical studies are needed to closely examine the mechanisms associated with polycystic ovary syndrome and the association with Alzheimer's. The novelty of our study is from the fact that the PCOS may be to some extent considered as a cause (exposure) among others of AD's (outcome) and the association might be confounded by some or all the risk factors assessed in this review. The nature of the method­the narrative review­is relatively subjective (in the determination of which studies to include, the way the studies are analyzed, and the conclusions drawn) and hence may not help mitigate bias.


Subject(s)
Alzheimer Disease , Anovulation , Hyperandrogenism , Insulin Resistance , Polycystic Ovary Syndrome , Alzheimer Disease/epidemiology , Alzheimer Disease/etiology , Female , Humans , Polycystic Ovary Syndrome/complications , Risk Factors
17.
Front Public Health ; 9: 727132, 2021.
Article in English | MEDLINE | ID: covidwho-1775851

ABSTRACT

BACKGROUND AND OBJECTIVES: Vitamin D status is closely related to blood glucose and bone metabolism in patients with type 2 diabetes (T2DM). Vitamin D affects bone density and bone metabolism, leading to osteopenia and osteoporosis. Insulin resistance increases the risk of osteoporosis in patients with T2DM. Our previous studies have shown a negative correlation between insulin resistance and 25-hydroxy vitamin D [25(OH)D] levels. The aim of the present study was to determine the association between vitamin D status and insulin resistance and bone metabolism in patients with T2DM. SUBJECTS AND METHODS: A retrospective cross-section research was carried out among 109 non-osteoporosis patients with T2DM. Their fasting blood glucose (FBG), 25(OH)D, fasting blood insulin (FINS), glycosylated hemoglobin (HbA1c), serum creatinine (SCr), calcium (Ca), phosphorus (P), insulin-like growth factor-1 (IGF-1), bone alkaline phosphatase (BALP), body mass index (BMI), glomerular filtration rate (eGFR), homeostatic model estimates of insulin resistance (HOMA-IR), and calcium-phosphorus product were measured routinely. RESULTS: Both in men and women, 25(OH)D was negatively correlated with BALP (ß = -0. 369, p ≤ 0.001)and HOMA-IR (ß = -0.349, p ≤ 0.001), and positively associated with IGF-1(ß = 0.672, p ≤ 0.05). There was a negative correlation between HOMA-IR and IGF-1 (ß = -0.464, p ≤ 0.001), and a positive correlation between HOMA-IR and BALP (ß = 0.344, p ≤ 0.05), adjusted by confounding factors. CONCLUSION: Our study demonstrates that 25(OH)D concentrations are negatively correlated with insulin resistance and bone turnover. Insulin resistance increases with the decrease of 25(OH)D concentration, which can enhance bone turnover, and increases the risk of osteoporosis in non-osteoporosis patients with T2DM. This is the first study to clarify the relationship between serum vitamin D status, insulin resistance, and bone metabolism in non-osteoporosis patients with T2DM in China.


Subject(s)
Diabetes Mellitus, Type 2 , Insulin Resistance , Osteoporosis , Bone Remodeling , Diabetes Mellitus, Type 2/complications , Female , Humans , Male , Osteoporosis/complications , Retrospective Studies , Vitamin D
18.
Iran J Med Sci ; 47(2): 114-122, 2022 03.
Article in English | MEDLINE | ID: covidwho-1761632

ABSTRACT

Background: Negative effects of statins on glucose metabolism have been reported. The present study aimed to investigate the effects of co-administration of vitamin E and atorvastatin on glycemic control in hyperlipidemic patients with type 2 diabetes mellitus (T2DM). Methods: A randomized double-blind clinical trial was conducted at Vali-e-Asr Teaching Hospital (Zanjan, Iran) from July 2017 to March 2018. A total of 30 T2DM female patients were allocated to two groups, namely atorvastatin with placebo (n=15) and atorvastatin with vitamin E (n=15). The patients received daily 20 mg atorvastatin and 400 IU vitamin E or placebo for 12 weeks. Anthropometric and biochemical measures were recorded pre- and post-intervention. Peroxisome proliferator-activated receptor-γ (PPAR-γ) expression was measured in peripheral blood mononuclear cells (PBMCs). Independent sample t test and paired t test were used to analyze between- and within-group variables, respectively. The analysis of covariance (ANCOVA) was used to adjust the effect of baseline variables on the outcomes. P<0.05 was considered statistically significant. Results: After baseline adjustment, there was a significant improvement in homeostatic model assessment for insulin resistance (HOMA-IR) (P=0.04) and serum insulin (P<0.001) in the atorvastatin with vitamin E group compared to the atorvastatin with the placebo group. In addition, co-administration of vitamin E with atorvastatin significantly upregulated PPAR-γ expression (OR=5.4, P=0.04) in the PBMCs of T2DM patients. Conclusion: Co-administration of vitamin E and atorvastatin reduced insulin resistance and improved PPAR-γ mRNA expression. Further studies are required to substantiate our findings. Trial registration number: IRCT 20170918036256N.


Subject(s)
Diabetes Mellitus, Type 2 , Insulin Resistance , Atorvastatin/metabolism , Atorvastatin/pharmacology , Atorvastatin/therapeutic use , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Double-Blind Method , Female , Humans , Leukocytes, Mononuclear/metabolism , PPAR gamma/genetics , PPAR gamma/metabolism , Vitamin E/metabolism , Vitamin E/pharmacology , Vitamin E/therapeutic use
19.
Elife ; 112022 03 23.
Article in English | MEDLINE | ID: covidwho-1761118

ABSTRACT

The SARS-CoV-2 pandemic continues to rage around the world. At the same time, despite strong public health measures and high vaccination rates in some countries, a post-COVID-19 syndrome has emerged which lacks a clear definition, prevalence, or etiology. However, fatigue, dyspnea, brain fog, and lack of smell and/or taste are often characteristic of patients with this syndrome. These are evident more than a month after infection, and are labeled as Post-Acute Sequelae of CoV-2 (PASC) or commonly referred to as long-COVID. Metabolic dysfunction (i.e., obesity, insulin resistance, and diabetes mellitus) is a predisposing risk factor for severe acute COVID-19, and there is emerging evidence that this factor plus a chronic inflammatory state may predispose to PASC. In this article, we explore the potential pathogenic metabolic mechanisms that could underly both severe acute COVID-19 and PASC, and then consider how these might be targeted for future therapeutic approaches.


Subject(s)
COVID-19/complications , Disease Susceptibility , Energy Metabolism , COVID-19/epidemiology , COVID-19/etiology , COVID-19/metabolism , COVID-19/therapy , Diabetes Mellitus, Type 2 , Disease Management , Glucose/metabolism , Glucose Intolerance , Humans , Insulin Resistance , Islets of Langerhans/metabolism , Liver/metabolism , Metabolic Syndrome/epidemiology , Metabolic Syndrome/etiology , Metabolic Syndrome/metabolism , Metabolic Syndrome/therapy , Risk Assessment , Risk Factors , T-Lymphocytes/immunology , T-Lymphocytes/metabolism
20.
J Nutr ; 151(9): 2513-2521, 2021 09 04.
Article in English | MEDLINE | ID: covidwho-1758779

ABSTRACT

BACKGROUND: Although intake of Hass avocado has been cross-sectionally linked to lower abdominal obesity, knowledge of the effects of avocado consumption on abdominal adiposity and glycemic outcomes remains limited. OBJECTIVE: The effects of avocado consumption on abdominal adiposity, insulin resistance, oral-glucose-tolerance test (OGTT), and estimated ß-cell function were evaluated. METHODS: A total of 105 adults aged 25-45 y (61% female) with BMI ≥25 kg/m2 were randomly assigned to an intervention (N = 53) that received a daily meal with 1 fresh Hass avocado or a control (N = 52) that received an isocaloric meal with similar ingredients without avocado for 12 wk. DXA was used to assess the primary outcomes of abdominal adiposity [visceral adipose tissue (VAT), subcutaneous abdominal adipose tissue (SAAT), and the ratio of VAT to SAAT (VS Ratio)]. Fasted glucose and insulin were used to assess the primary outcomes of insulin resistance (HOMA-IR), and insulin sensitivity (Matsuda index) and ß-cell function (Insulinogenic index) were estimated using an OGTT. Changes between groups were compared using an ANCOVA. Secondary analyses were conducted based on sex. RESULTS: The control group exhibited a greater reduction in SAAT [-54.5 ± 155.8 g (control) compared with 17.4 ± 155.1 g (treatment), P = 0.017] and increase in VS Ratio [0.007 ± 0.047 (control) compared with -0.011 ± 0.044 (treatment), P = 0.024]. Among females, the treatment group exhibited a greater reduction in VAT [1.6 ± 89.8 g (control) compared with -32.9 ± 81.6 g (treatment), P = 0.021] and VS Ratio [0.01 ± 0.05 (control) compared with -0.01 ± 0.03 (treatment), P = 0.001]. Among males, there was no significant difference between groups in changes in abdominal adiposity or glycemic outcomes. CONCLUSIONS: Daily consumption of 1 fresh Hass avocado changed abdominal adiposity distribution among females but did not facilitate improvements in peripheral insulin sensitivity or ß-cell function among adults with overweight and obesity.This study was registered at clinicaltrials.gov as NCT02740439.


Subject(s)
Insulin Resistance , Persea , Adiposity , Body Mass Index , Female , Glucose Tolerance Test , Humans , Intra-Abdominal Fat , Male , Obesity , Obesity, Abdominal , Overweight
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