Metabolic Syndrome: A Comprehensive Update with New Insights

Metabolic syndrome (MetS) is generally defined as a cluster/complex of factors that are risk factors for cardiovascular disease (CVD) and type 2 diabetes (T2DM), including hyperglycemia, insulin resistance, hypertension, hypertriglyceridemia, decreased HDL-cholesterol concentration and central obesity. MetS is a health problem whose prevalence is increasing worldwide and negatively affects people's lives. Although MetS is essentially insulin resistance (IR), is not considered a disease, it consists of a combination of many risk factors that force the body metabolism to work abnormally. In addition to factors such as sedentary lifestyle and nutrition, hereditary factors are also important in the formation of MetS. The main components of MetS can be listed as hyperglycemia, hypertension, obesity and dyslipidemia. MetS has different definitions for different organizations. The basic components of these definitions are waist circumference, IR, high blood pressure and dyslipidemia (high triglyceride, low HDL cholesterol). The most recently agreed upon diagnostic criteria for MetS are increased waist circumference (society and country specific), high triglycerides, low HDL cholesterol, high blood pressure and high fasting blood glucose. For diagnosis, the presence of at least 3 of these parameters is required. When countries are examined in terms of the prevalence of MetS, different results are obtained from each country. The most important factor affecting the incidence of MetS in a country is the percentage of obesity and abdominal obesity in that country. Although obesity and physical activity factors have an impact on the incidence of MetS, it is an undeniable fact that genetic factors also have a significant impact. Lifestyle changes are at the core of MetS treatment. People with this syndrome need to change their diet, increase their physical activity and lose weight. Determining MetS risk levels and predisposing risk factors, determining whether they meet diagnostic criteria, and raising awareness through education and consultancy activities will be effective in combating the prevalence of MetS and cardiovascular risk factors. 

Metabolic Syndrome (MetS) is a condition characterized by the cooccurrence of several cardiovascular risk factors, including insulin resistance, obesity, dyslipidemia, and hypertension. The development of MetS is closely linked to visceral adiposity, which refers to fat accumulation around critical vital organs in the abdominal cavity. Visceral fat is metabolically active and produces adipokines, proteins that regulate energy balance and play a role in inflammation and atherosclerosis. Some adipokines, such as leptin and adiponectin, have beneficial effects on glucose homeostasis and are considered protective against MetS. However, other adipokines, such as visfatin and resistin, contribute to glucose intolerance and have pro-atherogenic properties. Visceral obesity also contributes to the development of MetS through its effects on blood pressure. It activates the sympathetic nervous system, the reninangiotensin-aldosterone system, and insulin resistance, leading to elevated blood pressure.

Another critical factor in the development of MetS is the activation of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1). LOX-1 is a protein that acts as a receptor for oxidized LDL on the cell surface. Its activation leads to the production of reactive oxygen species, a decrease in nitric oxide, and increased expression of molecules contributing to hypertension and vascular damage. LOX-1 is also involved in the development of other complications associated with MetS, such as nephropathy and left ventricular hypertrophy.

The renin-angiotensin-aldosterone system (RAAS) regulates blood volume, electrolyte balance, and vascular resistance. In patients with MetS, the activation of RAAS leads to increased levels of angiotensin II (Ang II) and aldosterone, which have various effects on blood pressure and sodium and water retention. Ang II also contributes to oxidative stress and inflammation in the vasculature. Insulin resistance, a key feature of MetS, disrupts the insulin signaling process in adipose tissue, leading to increased lipolysis and elevated levels of circulating free fatty acids. These fatty acids further worsen insulin resistance and contribute to impaired glucose metabolism.Oxidative stress, characterized by an imbalance between the production of reactive oxygen species and the body's antioxidant defenses, is closely associated with the development of MetS. Hyperlipidemia and hyperglycemia, standard features of MetS, are linked to increased oxidative stress and ROS production. Oxidative stress and the activation of RAAS and LOX-1 contribute to the progression of dyslipidemia, type 2 diabetes, hypertension, and cardiovascular diseases.

The oral-gut-liver axis is an emerging concept that suggests a relationship between oral infections, such as periodontitis, and metabolic dysfunction, including MetS and liver diseases. Periodontitis has been associated with chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD) and liver cirrhosis. The translocation of oral bacteria from the mouth to the gut may contribute to gut dysbiosis, increased intestinal permeability, and systemic inflammation, which can worsen liver functions.

Overall, the development of MetS involves the interplay of various factors, including visceral obesity, adipokines, LOX-1 activation, insulin resistance, oxidative stress, and the oral-gut-liver axis. Understanding these mechanisms is crucial for preventing and managing MetS and its associated complications. Further research is needed to fully elucidate the roles of individual factors and develop targeted interventions for MetS. 

Metabolic syndrome (MetS) is a disorder with central obesity, essential hypertension (HT), glucose tolerance disorder, diabetes mellitus (DM), dyslipidaemia, and an increased risk of cardiovascular disease (CVD), which occurs under the influence of genetic predisposition and is based on insulin resistance (IR). MetS is well defined in adults, although MetS is a complex multifactorial disease with a not entirely recognized definition in childhood. Nevertheless, MetS is described as the presence of obesity, IR, dyslipidaemia, and HT. The increase in the rate of MetS in children is at alarming levels. The first step in the prevention and treatment of MetS is to recommend and implement healthy lifestyle changes from an early age. Healthy lifestyle changes should include not only children but also all family members and should be targeted to be maintained throughout life. One method of preventing CVD in adulthood should be the care of children with MetS. It is necessary to carry out studies to prevent MetS and to measure the effect of these studies on the frequency of MetS. In terms of preventive medicine, children with a family history of T2DM and/or MetS burden, body obesity on physical examination, and IR findings such as acanthosis nigricans should be monitored more closely and early treatment should be initiated in cases with IR at-risk for T2DM. In line with the objectives, continuous training on the evaluation of childhood obesity is necessary for paediatricians and general practitioners.

Metabolic syndrome (MetS) is a collection of risk factors that should be evaluated for cardiovascular diseases, which are increasing in frequency worldwide. It is a prothrombotic and proinflammatory condition in which insulin resistance plays a central role and manifests itself with abdominal obesity, high triglyceride levels, atherogenic dyslipidemia, high blood pressure and high blood glucose. The intestinalblood barrier, also known as the intestinal barrier, plays an important role in maintaining the homeostasis of the organism. The intestinal barrier ensures nutrient uptake through the lumen and at the same time restricts the passage of harmful substances. Increasing evidence suggests a relationship between intestinal barrier function and other body systems. Many studies have identified insulin resistance and metabolic syndrome as risk factors for reflux oesophagitis. Insulin resistance is also associated with metabolic syndrome and is known as a fundamental factor in its development. Abdominal obesity in particular is an independent risk factor for erosive esophagitis and increases the symptoms of gastroesophageal reflux. Subcutaneous and visceral adipose tissues, the main feature of MetS, secrete a variety of bioactive substances known as adipocytokines. Activation of inflammatory signaling pathways in the metabolic syndrome results in altered circulating and tissue levels of proinflammatory and anti-inflammatory cytokines, leading to systemic inflammation and tissue damage. The process of microbial dysbiosis, in which the ratio of beneficial to harmful bacteria is disrupted, is associated with many diseases such as inflammatory bowel disease, cancer, obesity, diabetes and cardiovascular disease. There is a relationship between the human gut microbiome and obesity. 

Being overweight, hyperlipidemia, hypertension, type II diabetes mellitus(DM) or high blood sugar, and glucose intolerances are all clinical disorders collectively referred to as the metabolic syndrome (MetS). MetS affects multiple systems in the body, including cardiovascular, endocrine, urinary, nervous, and gastrointestinal systems. Atherosclerosis risk is increased by chronic inflammation and vascular endothelial dysfunction, which are both closely related to MetS. The risk of cardiovascular illnesses, the world's leading cause of mortality, is also increased by metabolic syndrome. Cancers such as the endometrium, breast, colon, liver, gallbladder, oesophageal, pancreas, kidney, and prostate, also chronic kidney disease, IBD (idiopathic inflammatory bowel disease), chronic gastritis, and dysplasia, are all caused by MetS enhanced by abdominal obesity, dyslipidemia, and poor glucose control. Besides, those with normal glucose metabolism are more likely to develop various peripheral nerve issues related to MetS. There is a connection between MetS and a number of cognitive deficiencies. Endocrine-disrupting substances (EDS) also have a detrimental effect on human health, which includes their influence on metabolic procedures. The gold standard for non-invasive pancreatic fat quantification is magnetic resonance spectroscopy (MRS). Anthropometry is quickly and accurately assessed on a wide scale by three-dimensional (3D) body surface scanners (BS). Indicators of waist circumference, sagittal diameter, and body weight are strongly correlated with areas of deep abdominal adipose tissue in both sexes. Each system listed above is examined in this chapter in relation to MetS, new diagnostic insights are presented, and pathogenesis and consequences that were not identified and treated as early on are summarized. 

MetS is a multifaceted disease that embraces multiple disorders such as obesity, hyperlipidemia, hyperglycemia, insulin resistance, and hypertension. These disorders are characterized by specific metabolic aberrations presenting at different stages, which can be detected and monitored through a wide panel of serum biomarkers. Providing a minimally invasive technique thus can help greatly in the prediction, early screening and management of metabolic syndrome in high-risk communities and minimize its complications.

However, no sole biomarker is sensitive nor distinct for the diagnosis of metabolic syndrome, arousing the necessity of performing a panel that includes related biomarkers.

Metabolic biomarkers associated with metabolic syndrome are released primarily due to lipid accumulation and the dysregulated production of adipokines (ex. leptin, adiponectin) or oxidative stress brought on by obesity (ex. malondialdehyde, F-2 isoprostanes, paraoxonase, and oxidized LDL) or the associated inflammatory reaction (ex.IL-6, IL-10, tumor necrosis factor (TNFα), uric acid as well as heparanase).

Since obesity and insulin resistance are the cornerstones in metabolic syndrome pathogenesis, Leptin, an adipokine whose function is to reduce appetite and increase energy expenditure, and adiponectin represent striking biomarkers for metabolic syndrome.

In addition, the importance of uric acid, the product of purine metabolism, as a prooxidant inflammatory marker that contributes to metabolic syndrome pathogenesis has also been elucidated in multiple studies.

Recently, a newly discovered metabolic syndrome biomarker, ‘’Heparanase (HPA)” is closely related to the degradation of heparan sulfate proteoglycan (HSPG) and is associated with inflammatory responses as it could be secreted by various immune cells including macrophages.

Since many studies have denoted the role of many biomarkers related to metabolic syndrome, this chapter will highlight the newly discovered ones that will help in the construction of a metabolic panel that could pave the way to precision medicine and help personalize the treatment given to metabolic syndrome patients.

 Metabolic syndrome (MetS) is an escalating epidemic that could influence more than one billion people worldwide. It is expressed as the presence of visceral obesity, hyperglycemia, dyslipidemia, and elevated blood pressure. MetS is a multifactorial disorder affecting all features of the community and extensively affects morbidity and mortality. Independently, the constituents of metabolic syndrome have the potential to influence the endothelium causing vascular dysfunction and interrupt vascular homeostasis. Since all components of MetS have unfavorable effects on the endothelium, endothelial dysfunction is more prevalent in MetS patients. Endothelial dysfunction could be a part of the pathogenesis of atherosclerosis in MetS. The nominated mechanisms of endothelial dysfunction linked with MetS are reduced NO production, upraised reactive oxygen species and high production of vasoconstrictors. All the elements of MetS especially the compromised endothelial function could participate in increasing the risks of cardiovascular disease, stroke, myocardial infarction and type 2 DM. Endothelial dysfunction, moreover, stimulates proinflammatory and oxidative stress pathways via endothelial mitochondrial reactive oxygen species (ROS) forcing vascular growth and remodeling. Because MetS is a multifactorial disorder, numerous signaling pathways manipulate the succeeding endothelial dysfunction. In the current review, we will discuss the incidence and pathogenesis of altered endothelial function in MetS. We will also discuss the impending effects of lifestyle measures and pharmacological interventions on endothelial function in patients with MetS .

Metabolic syndrome (MetS) has become a worldwide health problem, affecting children and adults globally. The prevalence of MetS is rising all over the world due to increasing obesity and sedentary lifestyles. MetS is caused by the interaction of both genetic and environmental factors.

MetS is characterized by complicated, multidimensional, and sophisticated molecular pathways that involve insulin resistance, inflammatory processes, and hereditary predispositions.

Here we are trying to focus on common molecular mechanisms that underlie MetS occurrence, aiming to offer a better understanding of their role in MetS and helping in developing prognostic/diagnostic tools and targeting novel therapeutic options.

This chapter provides background information on the genotype-phenotype associations of MetS by highlighting the importance of genetic concepts in modulating MetS. To date, many reports on genetic and epigenetic screening of MetS within a community have been published in the literature. We also mention several reports to perform community-based screening of MetS by identifying genetic and epigenetic variants. Later, these attempts will be discussed in detail in order to explain more about the modulation of MetS from the perspectives of phenotype-genotype associations. The relationship between MetS modulation and the personalized medicine approach is emphasized more by referring to the treatment and management strategies applied in a patient-specific manner. 

Metabolic syndrome (MetS) indicates a cluster of symptoms that include abdominal obesity, dyslipidemia, hypertension, and hyperglycemia. Even though the etiology of MetS is unknown, it is thought to be multifaceted, with a complicated interaction between genetic predisposition and significant changes in lifestyle behavior, such as physical inactivity, high carbohydrate diets, and alcohol and cigarette use. The circadian system regulates many physiological and behavioral rhythms, which operate on 24-hour cycles. Circadian rhythm disturbances are also seen in various clinical disorders linked to adipose tissue functioning. In addition, night-shift employees who have their rest-activity cycles reversed are more likely to acquire MetS. Individuals with MetS experienced more seasonal variations in mood and behavior, with obesity being a substantial risk factor for metabolic syndrome. MetS has been linked to psychiatric illnesses. In those diagnosed with major depressive disorder and bipolar disorder in adulthood, disruption to biological rhythms (sleep, social activities, and eating habits) has been linked to essential components of MetS. MetS and its components were found to be connected to a higher risk of suicide. It is apparent that the relationship between behavior and MetS is bidirectional, and each component can affect the other. Awareness of MetS-related factors can aid in identifying high-risk individuals and implementing disease prevention and control strategies, as well as lifestyle adjustments. Lifestyle modification can help to improve the MetS condition and behavior.

In the last 2 decades, the relation between nutrition and health has aroused great interest. In this chapter, the background information about the Complex geneenvironment interactions that contribute to MetS will be introduced by highlighting several Neutrogenomic strategies. The role of nutrition is a significant modifiable element modulating the expression of many genes involved in metabolism. This chapter will present the current state of neutrogenomic research discussing the different gene-nutrient interactions in the context of metabolic disease, the molecular mechanisms underlying many of these gene-nutrient interactions, and the shift toward personalized nutrition. Novel modern technologies in Neutrogenomics regarding transcriptomics and metabolomics will be explained.

One of the most common metabolic illnesses worldwide is the MetS. In the MetS and its related disorders, rationalized and evidence-based pharmacotherapeutic strategies are corner stones in the mitigation of polypharmacy. The pharmacology network approach and enhanced bioinformatics tools related to the epigenetic, genomic, transcriptomics, proteomic, and metabolomic levels are considered useful bench-side tools for the exploration of molecular preventive and therapeutic multitargets. Molecular multitarget therapy is regarded as a novel pharmacological strategy that forms the foundation of personalized and precision medicine. That will decrease the socioeconomic burden and will improve the health-related quality of life.

Metabolic syndrome (MetS) is a primary and increasing public health problem as a result of worldwide urbanization, excessive energy intake, and increasing sedentary lifestyles. MetS is a combination of the interrelated risk factors of cardiovascular disease, diabetes and obesity. These factors are dysglycemia, dyslipidemia, elevated blood pressure, insulin resistance or type 2 diabetes, and low HDL levels. Clinical and epidemiological studies show that these factors are strongly associated with cardiovascular risk factors. The worldwide incidence of MetS varies, depending on the region, urban or rural situation, as well as the gender, age, race, and ethnicity of the population studied. Effective preventive approaches include weight loss, dietary habits with high content of industrialized foods, the use of appropriate pharmacological agents, and exercise to reduce specific risk factors of MetS. Many physicians treat each of the components of MetS separately. But instead, a solution should be found to address all these factors together. As discussed in this chapter, exercise plays a very crucial role in controlling insulin activity, reducing the risk of cardiovascular disease, and maintaining weight control. Various studies have proven that effective exercise provides positive results in treating MetS components. The aim of this chapter is to explain the effects of physical activity on MetS in light of current information about MetS.

Chronic obstructive pulmonary disease (COPD) is a clinical condition characterized by progressive airflow limitation caused by an abnormal inflammatory response of the lungs to harmful particles or gases that is not fully reversible. Smoking is largely responsible for the development of the disease. Systemic inflammation induced by smoking contributes to the natural history and clinical manifestations of COPD by causing chronic heart failure, metabolic syndrome (MetS) and other chronic diseases. MetS is a collection of interrelated clinical and biochemical disorders. MetS includes abdominal obesity, elevated triglycerides and low high-density lipoprotein (HDL) (atherogenic dyslipidemia), elevated blood pressure, insulin resistance, prothrombotic and proinflammatory markers (elevated C-reactive protein (CRP), fibrinogen, and other coagulation factors) with or without glucose intolerance. In patients with COPD, one or more components of MetS may be present in comorbidities that develop as a result of systemic inflammation. The prevalence of metabolic syndrome in COPD patients was found to be 30% and the prevalence of type 2 diabetes (T2DM) was found to be between 10-23%. Especially oral steroids used in the treatment of COPD exacerbations increase the risk of T2DM. Treatment of MetS and T2DM in patients with COPD does not differ. 

 Metabolic syndrome (MetS) is a cluster of metabolic disturbances, including high body mass index (BMI), waist circumference, high blood pressure, rise in triglycerides, increased plasma glucose, and reduction in high-density lipoprotein (HDL) cholesterol, leading to increased cardiovascular morbidity and mortality along with an increased predisposition to other non-communicable diseases such as diabetes and certain cancers. Its incidence is on the rise in Western countries and is a risk factor for several common cancers. Although the individual components of metabolic syndrome are linked to cancer, studies showing a direct link between metabolic syndrome and cancer are limited. This review addresses the need to summarise the associated factors and mechanisms linking these two pathologies and to identify potential targets in therapy in patients with cancer and metabolic syndrome. Understanding this link would provide insight into the process of oncogenesis in patients with MetS. This chapter focuses on the biological and physiological alterations and specific factors associated with this process, including the insulin-like growth factor (IGF-1) pathway, estrogen signaling, visceral adiposity, hyperinsulinemia, hyperglycemia, aromatase activity, adipokinase production, angiogenesis, oxidative stress, DNA damage, and pro-inflammatory cytokines in these patients and their clinical implications in cancer therapy. New research is warranted in this area and should be systemically analyzed in all cancer types. A better understanding of this link will provide greater insight into the management of cancer patients by preventing metabolic syndrome and related alterations.

Metabolic syndrome (MS) is a diverse condition linked to an elevated risk of cardiovascular issues. Emerging evidence from various types of research, including experimental, translational, and clinical studies, has indicated that obstructive sleep apnoea (OSA) is connected to both existing and newly developing aspects of MS. The plausible biological explanation centers primarily around one of OSA's main features, intermittent hypoxia. This leads to heightened sympathetic activity with cardiovascular consequences, increased liver glucose production, insulin resistance due to inflammation in adipose tissue, dysfunction in pancreatic β-cells, elevated lipid levels through deteriorating fasting lipid profiles, and decreased removal of triglyceride-rich lipoproteins.

While several interconnected pathways exist, the clinical evidence primarily relies on observational data, making it difficult to establish causality. The co-occurrence of visceral obesity and potential confounding factors like medications complicates the assessment of OSA's independent impact on MS. In this chapter, we re-evaluate the evidence regarding how OSA and intermittent hypoxia may contribute to adverse effects on MS parameters independently of body fat. We place particular emphasis on recent findings from intervention studies. This chapter outlines the research gaps, the challenges faced in the field, potential directions for future exploration, and the necessity for more high-quality data from intervention studies that address the influence of both established and promising therapies for OSA and obesity. 

Composed of trillions of microorganisms, the human GutM plays a key role in maintaining general health and metabolic homeostasis. MetS is a complex and common health condition characterized by a number of metabolic abnormalities, including obesity, insulin resistance, hypertension, and dyslipidemia. Evidence emerging in recent years indicates that human GutM plays a crucial role in the pathophysiology of MetS. In this chapter, we will discuss the composition and functionality of GutM, as well as the dynamic and complex relationship between GutM's influence on metS development and progression. By reviewing relevant studies and literature, we will try to shed light on potential therapeutic strategies and innovative approaches targeting GutM, mitigating the negative effects of MetS.

Metabolic syndrome (MetS) is characterized by central obesity, glucose intolerance, dyslipidemia, and hypertension. This is attributed to an increased inflammatory state resulting from increased cytokine synthesis from adipose tissue. Almost all of the medical problems associated with metabolic syndrome can be more successfully remised in the long term by bariatric-metabolic surgery (BMS) compared to conservative methods. In past years, the benefits of BMS have been attributed to weight loss; however, currently, it has been well described that anti-inflammatory response and remission of T2DM and other comorbidities begin in the first weeks after procedures. Moreover, there is also sufficient evidence that BMS helps in the remission of integral components of MetS, such as hyperlipidemia, hypertension, and cardiovascular diseases, in the long term where many patients do not even require medical treatment. The International Diabetes Federation (IDF) and recent guidelines recommend that metabolic surgery may be considered if glycemic control is not achieved despite optimal treatment if the patient's body mass index (BMI) is 30kg/m2 and above. 

Metabolic syndrome is a condition characterized by a cluster of risk factors associated with cardiovascular disease. These metabolic factors include abdominal obesity, high blood pressure, impaired fasting glucose, high triglyceride levels, and low HDL cholesterol levels. Obstructive sleep apnea syndrome (OSAS) is a sleep disorder in which the air passages constrict during sleep, leading to repeated breathing interruptions. The prevalence of OSAS has increased over the years, particularly among aging individuals. Although the underlying reasons for airway obstruction involve various factors, such as overweight, anatomical abnormalities, shifts in airway dynamics, pharyngeal neuropathy, and fluid redistribution, these causes remain incompletely understood.

The primary characteristics of OSAS include repetitive interruptions in breathing, resulting in heightened susceptibility to a range of chronic ailments. These interruptions lead to intermittent episodes of low oxygen levels (hypoxia) and elevated carbon dioxide levels (hypercapnia), often accompanied by sleep disruptions due to arousal.

In this yet-to-be-published exploration, I navigate the intricate dynamics of human connection in the digital age, examining how technology both bridges and divides us. Through a blend of personal reflections and sociological analysis, I aim to shed light on the complexities of virtual relationships and their impact on our sense of belonging.

The prevalence of metabolic syndrome (MetS) is estimated to be about onefourth of the worldwide adult population, while Cushing's syndrome (CS) is significantly rarer (estimated incidence of 2 per million). However, linking the two has not only therapeutic but also potential public health implications. The worldwide increase of obesity and MetS poses the problem of correctly identifying patients potentially hiding CS without indiscriminately screening all patients presenting one or more symptoms consistent with cortisol excess, which showed to be not cost-effective. CS is associated with hyperglycemia, protein catabolism, immunosuppression, hypertension, weight gain, neurocognitive changes, and mood disorders. Obesity, insulin resistance, hypertension, functional hypercortisolism (Endogenous/Exogenous), and MetS are common features. Early diagnosis and treatment are important because untreated CS may result in mortality due to associated metabolic risks.

The prevalence of non-alcoholic fatty liver disease (NAFLD), one of the most common liver diseases, is rapidly increasing worldwide, parallel to the global obesity epidemic. NAFLD can progress to steatohepatitis, which is a more severe form of liver disease characterized by hepatocyte injury, inflammation, and fibrosis. NAFLD is closely related to metabolic syndrome (MetS)/insulin resistance, and these relationships are the subject of active research. Other than in MetS, visceral adiposity and pro-inflammatory state are also key in the development of NAFLD. In addition to human genetic variants linked to NAFLD risk to date are genes involved in the regulation of lipid metabolism, providing support for the hypothesis that NAFLD is fundamentally a metabolic disease.

Metabolic syndrome (MetS) is a condition of abdominal diseases characterised by insulin resistance, obesity, atherogenic dyslipidaemia, hypertension, and hypercoagulability and is a serious risk factor for the development of cardiovascular diseases (CVD) and type II diabetes mellitus (T2DM) [1]. The outbreak of SARS-CoV-2 infection has been named Coronavirus Disease 2019 (COVID-19) by the World Health Organisation (WHO). MetS is emerging as a significant risk factor for worse outcomes in people with COVID-19. Metabolic diseases, especially chronic diseases related to diabetes, lead to heart disease and some neurodegenerative diseases in old age. With SARS-CoV-2, researchers all over the world have investigated the relationship between metabolic diseases and the virus. In fact, COVID-19 management is not different from the management of patients with severe and serious diabetes and the management of other critical illnesses. In the mortality and morbidity of COVID19, the presence of comorbid diseases, especially diabetes (hypertension, obesity, diseases and drugs affecting the immune system, cardiovascular diseases, etc.) and advanced age are determinants. It has also been shown that patients with poor metabolic health are more susceptible to complications such as seizures, strokes, and encephalitis during COVID-19 due to factors accompanying previous illness. Chronic diseases are diseases that progress slowly, last three months or longer, are caused by more than one risk factor, usually show a complicated course, and affect the quality of life of the person. The end of COVID-19 as a global health emergency does not mean 'the end of COVID-19 as a global health threat'. The threat of different COVID-19 variants emerging that could cause new increases in morbidity and mortality remains. Monitoring and management of chronic diseases will not only positively change the course of COVID-19 but will also make it possible to use the limited resources in the health sector in the right way.

Thyroid diseases significantly influence metabolic parameters, including blood pressure regulation, glucose metabolism, obesity, hyperlipidemia, and nonalcoholic fatty liver disease (NAFLD). Hypothyroidism is often linked to hypertension, insulin resistance, and dyslipidemia, while hyperthyroidism may induce weight loss, insulin resistance, and dyslipidemia. Both hypo- and hyperthyroidism impact blood pressure regulation, glucose homeostasis, and adiposity. Dyslipidemia is frequently observed in thyroid disorders, with hypothyroidism associated with elevated cholesterol levels and hyperthyroidism with altered lipid profiles. Additionally, thyroid dysfunction contributes to the development of NAFLD. There is a close relationship between thyroid hormones and metabolic syndrome components, as well as the development of metabolic syndrome.

Metabolic syndrome occurs at an early age in women with polycystic ovary syndrome (PCOS), particularly among women with the highest insulin levels and body mass index. Obesity is a common characteristic of PCOS and is more common in women with PCOS. Excessive weight gain may reveal the latent PCOS condition. Most women with PCOS are hyperinsulinemic and insulin-resistant. Insulin resistance (IR) is a major cause of metabolic manifestations and is known to be a common finding in PCOS. PCOS is also associated with an increased risk of impaired glucose tolerance, type 2 gestational diabetes mellitus, lipid and lipoprotein abnormalities, and nonalcoholic fatty liver disease. The presence of obesity, IR, impaired glucose tolerance, diabetes mellitus type 2, and dyslipidemia may predispose to coronary heart disease in women with PCOS.