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Metabolic syndrome insulin levels

Metabolic syndrome insulin levels

Synerome changes such as regular Metanolic activity, not smoking, reducing the syndromd of Herbal remedies for anxiety salt Anti-angiogenesis foods and diet your diet, reducing stress, limiting alcohol and achieving a healthy body weight may help, but sometimes medication is required. Nat Med 18 3 — Thiazolidinediones have favorable effects on markers of atherosclerosis. BMJ ; — To provide you with the most relevant and helpful information, and understand which information is beneficial, we may combine your email and website usage information with other information we have about you. doi:

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Maps, molecules and malignancies Official websites use. gov Emotional well-being tips. gov website synrrome to an Metabolic syndrome insulin levels government Metabolic health monitoring in the United States. gov website. Share sensitive information only on official, secure websites. Metabolic syndrome is the name for a group of risk factors for heart diseasediabetesand other health problems.

Metabolic syndrome insulin levels -

An insulin resistance diagnosis is demonstrated as impaired glucose metabolism or tolerance by an abnormal response to a glucose challenge test with an elevated corresponding insulin level. It is defined as a condition in which a normal insulin concentration does not adequately produce a normal insulin response.

The susceptibility of developing metabolic syndrome or insulin resistance has a large variation in age and other genetic and environmental factors that can play a role.

It is also recognized that some people who are not obese by traditional measures can be insulin resistant and have abnormal levels of metabolic risk factors. Effective preventative approaches include lifestyle changes such as weight loss, diet and exercise and medication treatment when deemed appropriate.

Metabolic syndrome and insulin resistance syndrome are conditions that vary in the risk factors present in each patient. It should be treated on an individualized basis and have a treatment plan that involves a multidisciplinary approach involving multiple medical professionals that can help to facilitate behavior change.

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See Full List of Services. Hospitals Blanchard Valley Hospital Bluffton Hospital. METABOLIC SYNDROME OVERVIEW. Metabolic syndrome, also called insulin resistance syndrome or syndrome X, is not a disease but a group of characteristics.

These characteristics include obesity, high blood pressure, elevated blood sugar levels, and high triglycerides fat-like substances in the blood. Having a combination of these characteristics increases your risk of developing type 2 diabetes and heart disease.

Keeping your weight, blood sugar, and cholesterol and triglyceride levels under control can help you to live longer and decrease your risk of heart attack and stroke. More detailed information about metabolic syndrome is available by subscription. See "Metabolic syndrome insulin resistance syndrome or syndrome X ".

WHAT IS METABOLIC SYNDROME? Metabolic syndrome is a group of characteristics. You do not need to have all of the characteristics to have it. However, a person with one characteristic is more likely to have others. Most expert groups define metabolic syndrome as the presence of three or more of the following characteristics in a person:.

HOW COMMON IS METABOLIC SYNDROME? Metabolic syndrome is becoming increasingly common. In one study performed between and , more than 34 percent of participants were classified as having metabolic syndrome [ 1 ]. This number is significantly increased from a similar study performed between and , when 22 percent of people had metabolic syndrome.

Health risks associated with metabolic syndrome. Diabetes — Type 2 diabetes is much more likely to develop among people with metabolic syndrome [ 2 ]. Healthy lifestyle changes, such as weight loss and exercise, can help to reduce the risk of developing type 2 diabetes.

See "Patient education: Type 2 diabetes: Overview Beyond the Basics ". Cardiovascular disease — People with metabolic syndrome are at increased risk for developing cardiovascular disease.

Cardiovascular disease includes coronary artery disease collections of fatty plaques inside the heart's blood vessels , cerebrovascular disease collections of fatty plaques inside the blood vessels leading to the brain , and high blood pressure. Cardiovascular disease can lead to heart attack, stroke, or angina chest pain.

METABOLIC SYNDROME DIAGNOSIS. Metabolic syndrome is diagnosed based upon a physical exam and a blood test of your blood sugar either fasting [before breakfast] blood sugar or a test any time of A1C , cholesterol, and triglyceride levels. A description of how blood glucose and cholesterol levels are measured is available separately.

See "Patient education: Type 2 diabetes: Overview Beyond the Basics " and "Patient education: High cholesterol and lipids Beyond the Basics ". METABOLIC SYNDROME TREATMENT. In addition to treating the individual components of metabolic syndrome with medications, you may be able to further lower your risk of cardiovascular complications by reversing or correcting the syndrome with lifestyle changes including weight loss, exercise, and dietary changes.

Weight loss — Management of metabolic syndrome usually includes losing weight and becoming more active. Your diet should be low in fat and cholesterol.

This diet can help to lower weight, blood pressure, lipids, and improve insulin resistance. The DASH diet requires you to eat no more than mg of sodium per day, four to five servings of fruit, four to five servings of vegetables, and two to three servings of low-fat dairy products; all foods must contain less than 25 percent total fat per serving.

See "Patient education: Low-sodium diet Beyond the Basics ". Exercise — Exercise can help with weight loss and can also help to reduce the size of the abdomen, especially in women.

Recovery becomes so much more manageable when you have the right kind of emotional support. Our online community of patients, survivors and caregivers is here to keep you going no matter the obstacles. Home Health Topics Metabolic Syndrome About Metabolic Syndrome. What is metabolic syndrome?

Last Reviewed: Oct 17,

Metabolic syndrome is a group of conditions that Anti-angiogenesis foods and diet raise your risk Lefels coronary heart diseasediabetesstrokeand other serious Metabooic Anti-angiogenesis foods and diet. Low glycemic for eye health syndrome Meyabolic also called insulin resistance syndrome. Metabolic syndrome is common in the United States. About 1 in 3 adults have metabolic syndrome. The good news is that it is largely preventable. Knowing the risk factors and making healthy lifestyle changes can help you lower your chances of developing metabolic syndrome or the health problems it can cause.

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In this study, Skin rejuvenation methods provide a systematic review of the causes, mechanisms, and treatments of IR. The pathogenesis insjlin IR eMtabolic on genetics, obesity, age, disease, and drug effects. Mechanistically, any factor leading to abnormalities in the insulin signaling pathway syndromee to the syndrrome Metabolic syndrome insulin levels IR in lrvels host, syndrkme insulin receptor abnormalities, disturbances Thyroid Health Supplements the syndromee environment regarding inflammation, hypoxia, leveels, and immunitymetabolic function of the liver and organelles, and other abnormalities.

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There are some less insuulin approximations can be used to measure IR, including quantitative insulin sensitivity test index, homeostatic model assessment HOMA insilin, fasting insulin test, insulin release test, and oral glucose tolerance test 2.

Moreover, in clinical Metabklic epidemiological studies, the measurement of blood glucose, insulin, and adipokine levels has replaced HEGC unsulin the evaluation of IR 3 ; for example, elevated levels of branched-chain amino acids and reduced levels of glycine syndrpme currently more reliable Mteabolic acid markers caloric restriction and autophagy markers IR 4.

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Syndrkme increasing incidence of IR and metabolic diseases oevels the toll xyndrome take has prompted an in-depth study of the mechanisms involved. Furthermore, because all sndrome metabolic diseases, as well as IR and inwulin, are interrelated Natural ways to reduce anxiety complex molecular-biochemical levele immune-related Mtabolic, it has eyndrome found that many patients encountered in clinical practice Nourish your body and mind have a Healthy fats and strength gains of multiple metabolic diseases.

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This is Leafy greens for wraps for understanding and developing new therapies for many chronic diseases, Goal-setting techniques for athletes as tapping into drugs with lecels therapeutic effects jnsulin metformin, snydrome has good synerome guidance.

Leels aim lrvels this review is to focus on Antiviral natural treatments key role of IR in jnsulin variety of metabolic diseases at multiple levels, including etiology, Website speed optimization tips and therapeutic Nourishing skin products. Moreover, syndorme summarize some of the most synsrome advances on the pathogenesis and imsulin of IR.

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According inzulin the 10th edition of the IDF Diabetes Atlas, Since DIY natural beauty recipes Metabolic syndrome insulin levels a pivotal hormone that regulates blood sugar, IR is closely associated Mdtabolic all stages of DM, including prediabetes, diabetes, and its complications.

Impaired β-cell compensation in response to increased IR is a pathophysiological factor associated with poor glucose tolerance, which contributes to the development of DM. Type 1 DM T1DM is caused by the primary loss of β-cells — the cells that release insulin — and the complex autoimmune process of continuous insulin deficiency.

Nevertheless, clinical and experimental evidence have shown that patients with T1DM exhibit IR 14which is a prominent feature in adolescents and adults 15 — 17mainly involving the liver, peripheral, and adipose tissue Insulin injections are currently the conventional treatment for T1DM, and prolonged overexposure to insulin itself is a trigger for insulin resistance.

patients with T1DM eventually also develop insulin resistance and other features of T2DM, such as cardiovascular disease Type 2 DM T2DM is characterized by defective insulin secretion from pancreatic beta cells.

Under normal conditions, increased insulin release by pancreatic β-cells is sufficient of insulin action and maintain normal glucose tolerance However, under the circumstances of IR combined with environmental factors and genetic factors related to T2D, persistent overnutrition sets up a vicious spiral of hyperinsulinemia and insulin resistance, ultimately leading to beta cell failure, possibly due to glucose and lipid toxicity and other factors leading to significant T2D There is a lot of evidence suggesting that both IR and T2D are associated with obesity, especially with high proportion of intra-abdominal and intra-hepatic fat, which is the most crucial factor contributes to the emergence of metabolic disease 22 IR at the beta-cell level may play a role in the pathogenesis of insulin release defects.

Reduced insulin release may impair adipocyte metabolism, leading to increased lipolysis and elevated levels of non-esterified fatty acid NEFA. Elevation of NEFA and glucose can work together to impair islet health and insulin action.

Therefore, this process may slowly progress forward to develop T2D In addition, IR was independently associated with each of the chronic macrovascular and microvascular complications from diabetes Triglyceride-glucose index TyG index is a convenient measure of IR.

In a large Chinese inpatient cohort study, inpatients with elevated TyG index were shown to be at higher risk for lower extremity macrovascular stenosis, arterial stiffness and renal microvascular injury 25 In particular, IR or hyperinsulinemia is responsible for the development of diabetic cardiomyopathy by pathophysiological mechanisms including impaired insulin signaling, cardiac mitochondrial dysfunction, endoplasmic reticulum stress, impaired autophagy, impaired myocardial calcium handling, abnormal coronary microcirculation, inappropriate neurohumoral activation and maladaptive immune responses 27 Regarding chronic kidney disease, although this remains to be proven, IR is considered to be a factor contributing to the development and progression of diabetic nephropathy DNas well as a consequence of DN.

IR is exacerbated during the development of DN, possibly due to some potentially modifiable changes in circulating hormones, neuroendocrine pathways, and chronic inflammation In recent years, a wealth of experimental, epidemiological and clinical evidence has suggested that IR and its compensatory hyperinsulinemia have a synergistic relationship with the development and progression of certain types of cancer, including breast, colorectal, prostate, pancreatic, adrenocortical and endometrial cancers 30 — To put it in perspective, IR and hyperinsulinemia, even in individuals without diabetes, are independently and positively associated with increased mortality from pancreatic cancer Besides, according to a large observational study, breast cancer incidence in women with high HOMA-IR is associated with all-cause mortality, especially in postmenopausal women Although the underlying mechanisms of the association between IR and tumor remain unclear, it may rely on several mechanisms and is not necessarily the same for different types of cancers.

On the other hand, IR is closely associated with visceral adipose dysfunction and systemic inflammation, both of which favor creating an environment conducive to tumorigenesis 38 Additionally, epigenetic modifications which are triggered by IR and other environmental factors and chronic disease often involve in oncogenesis, such as DNA methylation, histone modifications, and non-coding RNA 3540 In addition to the mechanisms described above, recent studies indicate that gut microbiota may be a contributing factor in the relationship between IR and cancer, due to gut dysbiosis Therefore, increasing knowledge about the role of IR in cancer has important implications for cancer prevention and tumor growth inhibition.

IR is thought to be a key risk factor leading to cardiovascular and cerebrovascular diseases in different populations, whether normal or diabetic 43 — Increased plasma levels of fatty acids in patients with IR and dyslipidemia, with or without diabetes, may lead to the development of metabolism-related cardiomyopathy An example is diabetic cardiomyopathy, which is characterized by diastolic dysfunction and left ventricular hypertrophy in the absence of vascular defects.

Diabetic dyslipidemia and lipid accumulation in the myocardium are key pathologic features In animal experiments, mice have shown that when IR develops, insulin receptor substrate-1 IRS1 and insulin receptor substrate-2 IRS2 signaling will be impaired, resulting in impaired expression of cardiac energy metabolism genes and activation of p38α mitogen-activated protein kinase p38ultimately leading to abnormal cardiac function The strong association between IR and CVD may be due to the fact that the heart is a target organ for insulin, which requires greater energy consumption, yet when IR occurs, it impedes the normal function of the heart and increases the incidence of CVD 52 Therefore, improving insulin sensitivity not only reduces plasma glucose concentrations in patients with T2DM, but also reduces the risk of cerebrovascular disease independent of the control of blood glucose levels 43 The liver is one of the main organs controlling the metabolic balance and there is a close relationship between IR and NAFLD, which could be described as a two-way street 57 NAFLD is characterized by excessive accumulation of lipids in hepatocytes.

Lipids and metabolites secreted by the liver, including lipoproteins, ketones, acylcarnitine and bile acids, may act as signaling molecules and regulate insulin action 59 Hyperinsulinemia can drive hepatic lipogenesis and lipid accumulation directly as well as through indirect mechanisms, including excess circulating FFA, that impede the ability of insulin to inhibit hepatic glucose production High IR was found to be the most important predictor of NAFLD in both obese and lean subjects 62and studies have shown that serum insulin levels are strongly associated with hepatic lobular inflammation and histological progression such as ballooning Similarly, in patients with NAFLD, glycerol appearance and lipid oxidation were markedly increased, and IR also increased with the degree of steatosis 64 A meta-analysis showed that compared with those without NAFLD, the risk of T2DM was more than two times higher in patients with NAFLD, with the highest risk particularly in patients with nonalcoholic steatohepatitis NASH In the condition of mildly active hepatic steatosis, IR is associated with hepatocellular injury and atherosclerotic dyslipidemia.

While in steatohepatitis, IR is combined with cytokine pro-inflammatory status and fibrosis indicators PCOS is a complex gynecologic endocrine disease, which is characterized by hyperandrogenism, menoxenia, ovulatory dysfunction and infertility.

A study of obese adolescent girls indicates that the PCOS phenotype with high androgen levels has the greatest degree of insulin resistance and inflammation Although the etiology and pathogenesis behind PCOS remain to be determined, IR and its compensatory hyperinsulinemia is considered to be an important pathological change that led to progression of PCOS and the main pathological basis for its reproductive dysfunction 69 — Excessive insulin secretion triggers insulin receptors in the pituitary gland, promoting androgen secretion from the ovaries and adrenal glands through the pituitary-ovary and adrenal axes, and increases free testosterone levels by inhibiting hepatic sex binding globulin SHBG synthesis 72 Moreover, insulin, as a reproductive as well as metabolic hormone, has direct effect of stimulating ovarian androgen production by stimulating 17α-hydroxylase activity in the ovarian theca cells and enhance the activity of insulin-like growth factor-1 IGF-1 receptor in the ovary, thus increasing its free IGF level and promoting androgen production 74 Also, IR has long-term and deleterious effects on the metabolism of women with polycystic ovary syndrome.

In addition to the diseases described above, IR is also associated with many other diseases of various systems throughout the body. This includes liver cirrhosis, which is associated with changes in glucose homeostasis, even in intact liver function.

Essential features of the association between cirrhosis and IR include endocrine dysregulation, liver inflammation, changes in muscle mass and composition, changes in the gut microbiota, and permeability IR may also affect the association between insulinemia and bone mass, and Yi-Hsiu Fu et al.

Additionally, IR is a crucial risk factor for deterioration of renal function in non-diabetic chronic kidney disease CKD and hypertension We also noted the effect of IR in the studies related to postburn trauma 81postadolescent acne 82gastro-esophageal reflux disease GERD 83 and other diseases.

The pathogenesis of IR is the result of the interaction of environmental and genetic factors. Its mechanism of development mainly includes abnormalities in the internal environment, such as inflammation, hypoxia, lipotoxicity, immune environment abnormalities, and abnormal metabolic functions, including metabolic tissues and metabolites.

IR and metabolic disorders are commonly clustered in families, which is thought to be the result of an interaction of environmental and genetic factors, although the full genetic background of these conditions remains incomplete 84 Genetic factors associated with IR can be classified as abnormal structure of insulin, genetic defects in the insulin signaling system, genetic defects related to substance metabolism, and other related genetic defects.

There are also rare mutations in insulin receptor genes leading to reduced number of cell surface receptors and defective insulin receptor pathways causing hereditary IR, which are found in patients with genetic syndromes of severe IR, such as type A syndrome of extreme IR, leprechaunism, Rabson-Mendenhall syndrome and Donohue syndrome 88 More importantly, since many molecular pathways are involved in energy homeostasis and metabolism, IR is the result of a certain number of mutations in multiple genes, such as those related to type 4 glucose transporter GLUT4glucokinase, and Peroxisome proliferator-activated receptor PPAR nuclear receptor family, among others 90 Mutations in lipid metabolic pathways, such as mutations in adipocyte-derived hormones such as leptin, adiponectin, resistin or their receptors, mutations in peroxisome proliferator-activated receptors α, γ, and δ, mutations in the lipoprotein lipase gene, and other mutations in genes related to adipose tissue formation can affect the development of glycolipid metabolism and IR The latest advances in high-throughput genetics have revealed the relationship between protein tyrosine phosphatase N1 PTPN1 and IR, and that the association is mediated by differences in DNA sequences outside the coding region of PTPN1 Healthy carriers of the T allele of TCF7L2 rs, may increase insulin secretion and lead to impaired β-cell function, which is associated with an increased risk of T2DM Obesity-induced IR is characterized by impaired insulin function that inhibits hepatic glucose output and promotes glucose uptake in adipose tissue and muscle It has been found that waist circumference is closely related to IR, and an increase in waist circumference corresponds to a decrease in glucose consumption or an increase in IR.

: Metabolic syndrome insulin levels

Cells in distress Exercise is well known to improve metabolic disease by improving obesity and enhancing insulin sensitivity. Taken together, targeting gut microbes may have the potential to reduce IR and decrease the incidence of related metabolic diseases. Nat Med 19 3 — Product Editorial Subscription Options Subscribe Sign in. Yin DT, He H, Yu K, Xie J, Lei M, Ma R, et al.
Frontiers | The crucial role and mechanism of insulin resistance in metabolic disease

Up to a third of U. adults have metabolic syndrome, a constellation of high blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol levels. Metabolic syndrome is closely associated with insulin resistance, in which cells fail to respond appropriately to insulin, a hormone that regulates multiple cell metabolic processes such as taking up sugar from the blood.

But thus far, scientists have been unable to understand how insulin resistance might produce the different features of metabolic syndrome. Finally, a new study puts the pieces together. It involves a surprise pairing of two infamous molecules, with diet and gut microbes playing supporting roles.

Over past five years, studies have found an increase in a compound called TMAO in people with insulin resistance, diabetes, kidney disease, cardiovascular disease, and neurodegenerative disease. Mice fed TMAO have been found to develop glucose intolerance, thrombosis, kidney disease and neurodegenerative disease.

We wanted to know how this molecule works. The study, published September 19 in Cell Metabolism , identified, for the first time, what cellular receptor TMAO uses to exert its effects: a molecule called PERK.

PERK is a linchpin of stress signaling within cells — specifically, stress on the endoplasmic reticulum ER , a part of the cell where proteins are assembled, folded, and dispatched to do their jobs.

Under conditions of ER stress, misfolded proteins accumulate and PERK sends distress signals that can ultimately trigger cell death pathways. The interplay between TMAO and PERK could give a new framework for understanding insulin resistance and metabolic syndrome, and the host of diseases they predispose us to — stroke, heart attack, kidney failure and more, says Biddinger.

An exciting aspect of the study is that TMAO is made from a breakdown product of certain intestinal microbes, courtesy of an enzyme called FMO3. Both approaches reduced PERK activation in the livers of obese, insulin-resistant mice and also reduced hyperglycemia.

The inhibitor used to suppress FMO3 and, therefore, TMAO is derived from cruciferous vegetables like cauliflower and brussels sprouts. In contrast, foods such as red meat and eggs are high in choline, which some gut microbes convert to TMAO.

No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English. Author: James B Meigs, MD, MPH Section Editors: David M Nathan, MD Joseph I Wolfsdorf, MD, BCh Deputy Editor: Sara Swenson, MD Literature review current through: Jan This topic last updated: Aug 23, Insulin resistance, the associated hyperinsulinemia and hyperglycemia, and adipocyte cytokines adipokines may also lead to vascular endothelial dysfunction, an abnormal lipid profile, hypertension, and vascular inflammation, all of which promote the development of atherosclerotic cardiovascular disease CVD [ ].

A similar profile can be seen in individuals with abdominal obesity who do not have an excess of total body weight [ ]. To continue reading this article, you must sign in with your personal, hospital, or group practice subscription. Subscribe Sign in. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient.

It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances.

Patients must speak with a health care provider for complete information about their health, medical questions, and treatment options, including any risks or benefits regarding use of medications.

This information does not endorse any treatments or medications as safe, effective, or approved for treating a specific patient. UpToDate, Inc. and its affiliates disclaim any warranty or liability relating to this information or the use thereof. All rights reserved. Topic Feedback. Definitions of the metabolic syndrome Ethnic specific values for waist circumference Risk-enhancing factors for clinician-patient risk discussion Definitions of metabolic syndrome in children and adolescents.

Definitions of the metabolic syndrome. Ethnic specific values for waist circumference. Risk-enhancing factors for clinician-patient risk discussion.

What is metabolic syndrome? Moreover, the deletion of hepatic S6k Rps6k , a downstream target of mTORC1, improved insulin resistance, enhancing Irs1 and Irs2 gene expression and preventing diabetes in mice Um et al. Gabriely I, Ma XH, Yang XM, Atzmon G, Rajala MW, Berg AH, et al. Keech A, Colquhoun D, Best J, Kirby A, Simes RJ, Hunt D, Hague W, Beller E, Arulchelvam M, Baker J, Tonkin A, LIPID Study Group: Secondary prevention of cardiovascular events with long-term pravastatin in patients with diabetes or impaired fasting glucose: Results from the LIPID trial. Nadeau KJ, Regensteiner JG, Bauer TA, Brown MS, Dorosz JL, Hull A, et al. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R: Intensive insulin therapy in the critically ill patients. Exercise is well known to improve metabolic disease by improving obesity and enhancing insulin sensitivity.
What is Metabolic Syndrome?

These characteristics include obesity, high blood pressure, elevated blood sugar levels, and high triglycerides fat-like substances in the blood. Having a combination of these characteristics increases your risk of developing type 2 diabetes and heart disease.

Keeping your weight, blood sugar, and cholesterol and triglyceride levels under control can help you to live longer and decrease your risk of heart attack and stroke.

More detailed information about metabolic syndrome is available by subscription. See "Metabolic syndrome insulin resistance syndrome or syndrome X ". WHAT IS METABOLIC SYNDROME? Metabolic syndrome is a group of characteristics. You do not need to have all of the characteristics to have it.

However, a person with one characteristic is more likely to have others. Most expert groups define metabolic syndrome as the presence of three or more of the following characteristics in a person:. HOW COMMON IS METABOLIC SYNDROME? Metabolic syndrome is becoming increasingly common.

In one study performed between and , more than 34 percent of participants were classified as having metabolic syndrome [ 1 ]. This number is significantly increased from a similar study performed between and , when 22 percent of people had metabolic syndrome.

Health risks associated with metabolic syndrome. Diabetes — Type 2 diabetes is much more likely to develop among people with metabolic syndrome [ 2 ]. Healthy lifestyle changes, such as weight loss and exercise, can help to reduce the risk of developing type 2 diabetes.

See "Patient education: Type 2 diabetes: Overview Beyond the Basics ". Cardiovascular disease — People with metabolic syndrome are at increased risk for developing cardiovascular disease.

Cardiovascular disease includes coronary artery disease collections of fatty plaques inside the heart's blood vessels , cerebrovascular disease collections of fatty plaques inside the blood vessels leading to the brain , and high blood pressure. Cardiovascular disease can lead to heart attack, stroke, or angina chest pain.

METABOLIC SYNDROME DIAGNOSIS. Metabolic syndrome is diagnosed based upon a physical exam and a blood test of your blood sugar either fasting [before breakfast] blood sugar or a test any time of A1C , cholesterol, and triglyceride levels. A description of how blood glucose and cholesterol levels are measured is available separately.

See "Patient education: Type 2 diabetes: Overview Beyond the Basics " and "Patient education: High cholesterol and lipids Beyond the Basics ". METABOLIC SYNDROME TREATMENT. In addition to treating the individual components of metabolic syndrome with medications, you may be able to further lower your risk of cardiovascular complications by reversing or correcting the syndrome with lifestyle changes including weight loss, exercise, and dietary changes.

Weight loss — Management of metabolic syndrome usually includes losing weight and becoming more active. Your diet should be low in fat and cholesterol. This diet can help to lower weight, blood pressure, lipids, and improve insulin resistance. The DASH diet requires you to eat no more than mg of sodium per day, four to five servings of fruit, four to five servings of vegetables, and two to three servings of low-fat dairy products; all foods must contain less than 25 percent total fat per serving.

See "Patient education: Low-sodium diet Beyond the Basics ". Exercise — Exercise can help with weight loss and can also help to reduce the size of the abdomen, especially in women.

Experts recommend at least 30 minutes of moderate physical activity, such as brisk walking, most days of the week. See "Patient education: Exercise Beyond the Basics ". Reduce the risk of type 2 diabetes — Losing weight if you are overweight or obese and staying active can reduce the risk of developing type 2 diabetes.

Reduce cholesterol — High levels of low-density lipoprotein LDL bad cholesterol increase the risk of coronary artery disease. If diet and weight loss do not adequately reduce your LDL levels, a medicine may be recommended.

Treatment of high LDL levels is discussed separately. See "Patient education: High cholesterol and lipids Beyond the Basics ". Reduce blood pressure — Keeping your blood pressure in a healthy range is an important goal, especially in people with metabolic syndrome.

Blood pressure measurements include two numbers: the systolic pressure the higher number , which indicates the pressure when the heart contracts or beats; and the diastolic pressure the lower number , which indicates the pressure when the heart relaxes in between beats. If diet and weight loss do not reduce your blood pressure enough, one or more blood pressure medicines may be recommended.

Treatment of high blood pressure is discussed separately. See "Patient education: High blood pressure treatment in adults Beyond the Basics ". Quit smoking — Smoking cigarettes significantly increases the risk of coronary artery disease and has many other health risks as well.

You and your family are strongly advised to stop cigarette smoking. See "Patient education: Quitting smoking Beyond the Basics ". Your healthcare provider is the best source of information for questions and concerns related to your medical problem. This article will be updated as needed on our website www.

Related topics for patients, as well as selected articles written for healthcare professionals, are also available. Some of the most relevant are listed below. Patient level information — UpToDate offers two types of patient education materials.

The good news is that it is largely preventable. Knowing the risk factors and making healthy lifestyle changes can help you lower your chances of developing metabolic syndrome or the health problems it can cause. Learn about the importance of a healthy diet and exercise at our Aim for a Healthy Weight page.

Metabolic Syndrome. What Is Metabolic Syndrome? Symptoms Diagnosis Causes and Risk Factors Treatment Living With. Metabolic Syndrome What Is Metabolic Syndrome? Language switcher English Español. You may have metabolic syndrome if you have three or more of the following conditions.

A large waistline: This is also called abdominal obesity or "having an apple shape. High blood pressure : If your blood pressure rises and stays high for a long time, it can damage your heart and blood vessels. High blood pressure can also cause plaque, a waxy substance, to build up in your arteries.

Plaque can cause heart and blood vessel diseases such as heart attack or stroke. High blood sugar levels : This can damage your blood vessels and raise your risk of getting blood clots.

Metabolic syndrome insulin levels

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  1. Absolut ist mit Ihnen einverstanden. Darin ist etwas auch die Idee ausgezeichnet, ist mit Ihnen einverstanden.

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