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Insulin Resistance And Type 2 Diabetes

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Last Updated: 02 July 2021

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One in three Americans, half of those aged 60 and older, have silent blood sugar problem known as insulin resistance. Insulin resistance increases the risk for prediabetes, type 2 Diabetes and a host of other serious health problems, including heart attacks, strokes 2 and cancer. 3 insulin resistance is when cells in your muscles, body fat and liver start resisting or ignoring signal that hormone insulin is trying to send outwhich, is to grab glucose out of your bloodstream and put it into your cells. Glucose, also know as blood sugar, is the body's main source of fuel. We get glucose from grains, fruit, vegetables, dairy products, and drinks that bring break down into carbohydrates. While genetics, aging and ethnicity play roles in developing insulin sensitivity, driving forces behind insulin resistance include excess body weight, too much belly fat, lack of exercise, smoking, and even skimping on sleep. 4 as insulin resistance develop, your body fights back by producing more insulin. Over months and years, beta cells in your pancreas that are working so hard to make insulin wear out and can no longer keep pace with demand for more and more insulin. Then - years after insulin resistance silently begins - your blood sugar may begin to rise and you may develop prediabetes or type 2 Diabetes. You may also develop non - alcoholic fatty liver Disease, growing problem associated with insulin resistance that boosts your risk for liver damage and heart disease. 5 insulin resistance is usually triggered by a combination of factors linked to weight, age, genetics, being sedentary and smoking. - Large waist. Experts say the best way to tell whether youre at risk for insulin resistance involves tape measure and a moment of truth in front of the bathroom mirror. Waist that measures 35 inches or more for women, 40 or more for men 6 increase odds of insulin resistance and metabolic syndrome, which is also linked to insulin resistance. - You have additional signs of metabolic syndrome. According to the National Institutes of Health, 7 in addition to large waist, if you have three or more of following, you likely have metabolic syndrome, which creates insulin resistance. High triglycerides. Levels of 150 or higher, or taking medication to treat high levels of these blood fats. Low HDLs. Low - density lipoprotein levels below 50 for women and 40 for men - or taking medication to raise low high - density lipoprotein levels. High blood pressure. Readings of 130 / 85 mmHg or higher, or taking medication to control high blood pressure and high blood sugar. Levels of 100 - 125 mg / dl or over 125. High fasting blood sugar. Mildly high blood sugar may be an early sign of Diabetes. - You develop dark skin patches. If insulin resistance is severe, you may have visible skin changes. These include patches of darkened skin on the back of your neck or on your elbows, knees, knuckles or armpits. This discoloration is called acanthosis nigricans.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

What is insulin resistance?

If you have insulin resistance, you want to become oppositemore insulin sensitive. Physical activity makes you more sensitive to insulin, one reason why it is a cornerstone of Diabetes management. Dont wait until youre diagnosed with Diabetes to start moving more. The earlier you take action, better off youll be. Weight loss is important too, as is avoiding high blood sugar, reducing stress, and getting enough sleep. These lifestyle changes really work. Talk with your health care provider about how to get start.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Development

When cells cannot absorb glucose, levels of this sugar build up in the blood. If glucose, or blood sugar, levels are higher than usual but not high enough to indicate diabetes, doctors refer to this as prediabetes. Prediabetes often occurs in people with high insulin resistance. Around 1 in 3 people in the United States have prediabetes, according to figures from the Centers for Disease Control and Prevention. In this article, we look at current understanding of insulin resistance and explain its role as a risk factor for Diabetes and other conditions. We also describe signs and symptoms of insulin resistance and ways to avoid it. Insulin is essential for regulating the amount of glucose that circulates in the bloodstream. It induces cells to absorb glucose. Insulin is also a chemical messenger that instructs the liver to store some glucose, rather than releasing it into the bloodstream. Liver packages glucose for storage in the form of glycogen. Insulin usually helps the body maintain a good balance of energy, never allowing the level of blood glucose to spike for too long. Reasons for insulin resistance remain complex, and researchers continue to investigate. The following steps outline the medical community's current understanding of insulin resistance: body cells become less affected by insulin. This resistance initially causes the pancreas to secrete more insulin, in order to maintain safe blood sugar levels. Pancreas become unable to maintain release of extra insulin to compensate for cells increasing resistance. Consistently high levels of blood glucose develop, progressing into prediabetes and type 2 Diabetes if person do not adopt management strategies and receive treatment.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Risk factors

People with a cluster of risk factors including obesity, impaired fasting glucose, hypertension, low HDL Cholesterol, and elevated triglycerides are thought to have metabolic syndrome, reflecting underlying Insulin Resistance. Both metabolic syndrome and Insulin Resistance are factors in the development of type 2 Diabetes and cardiovascular disease. Several competing definitions of metabolic syndrome are in use, and each is differently linked to the presence of Insulin Resistance. These definitions include that of National Cholesterol Education Program Third Adult Treatment Panel, International Diabetes Federation, and European Group for Study of Insulin Resistance. The English definition requires presence of Insulin Resistance plus any two other metabolic traits; ATP III and IDF definitions require at least three metabolic traits but do not require presence of Insulin Resistance. In studies of ATP III metabolic syndrome, as many as half of subjects do not have Insulin Resistance. There is little population - base data comparing how well ATP III or IDF metabolic syndrome definitions identify subjects with Insulin Resistance or comparing how well ATP III, IDF, or EGIR metabolic syndrome definitions predict subsequent risk for incident Diabetes or CVD. In addition, while it has been implied that the presence of metabolic syndrome is surrogate for presence of Insulin Resistance, there is little data on Diabetes or CVD risk associated with metabolic syndrome in the absence of Insulin Resistance or in the presence of both metabolic syndrome and Insulin Resistance. With this background in mind, we performed analysis in the Framingham Offspring Study using three metabolic syndrome definitions to test the hypothesis that metabolic syndrome confers risk for subsequent development of Diabetes or CVD with or without concomitant Insulin Resistance.


Causes

Glucose sugar is the main source of energy for cells that make up muscles and other tissues. Glucose comes from two major sources: food and your liver. Sugar is absorbed into the bloodstream, where it enters cells with the help of insulin. Your liver stores and makes glucose. When your glucose levels are low, such as when you haven't eaten in a while, liver breaks down stored glycogen into glucose to keep your glucose level within normal range. In type 2 diabetes, this process doesn't work well. Instead of moving into your cells, sugar builds up in your bloodstream. As blood sugar levels increase, insulin - producing beta cells in the pancreas release more insulin, but eventually these cells become impaired and can't make enough insulin to meet the body's demands. In much less common type 1 diabetes, immune system mistakenly destroys beta cells, leaving the body with little to no insulin.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Prevention

It is not possible to influence some risk factors for Insulin Resistance and type 2 Diabetes, such AS family history and genetic makeup. However, person can take some steps to reduce chances of becoming Insulin resistant. Some of the same strategies are key to preventing heart disease and stroke. Also, American Heart Association reports that individuals can r educe their risk of type 2 Diabetes by making preventive lifestyle changes, primarily by losing weight and increasing physical activity. Muscles become more sensitive to Insulin after exercise, and person can reverse Insulin resistance with an active, healthy lifestyle. While diagnosis of Insulin Resistance or prediabetes might cause alarm, making rush lifestyle changes and expecting immediate results is not a sustainable way to proceed. Instead, increase levels of physical activity gradually, replace one item per meal with a healthful, low - carbohydrate option, and be sure to keep this up, week after week. The most effective way to reduce Insulin Resistance is to make slow, sustainable changes. Here, read about the best foods to eat and avoid to reverse prediabetes. Research, including that involving the landmark Diabetes Prevention Program, shows that lifestyle changes can reduce the risk of prediabetes progressing to Diabetes by over 58 percent. Start taking steps today to reduce Insulin Resistance and the risk of Diabetes.


What is insulin resistance?

The prevalence of type 2 diabetes is increasing to epidemic proportions worldwide. It has been estimated that the diabetic population will double from 150 to 300 million in the next 25 years. Furthermore, long - term complications associated with diabetes are major causes of morbidity and mortality, imposing a high financial burden on health care costs. Type 2 diabetes will certainly be one of the major diseases of the 21st century and should be recognized as a priority. It is now well established that the development of type 2 diabetes results from interaction between the genetic makeup of individuals and their environment. The development of obesity seems to be an important factor in the development of insulin resistance. If this insulin resistance occurs in the presence of genetically determined propensity to - cell dysfunction, glucose intolerance can occur. Although there is still disagreement over the relative contribution in alterations in insulin sensitivity versus - cell function in the development of diabetes, it is becoming clear that reductions in both processes have already occurred by the time hyperglycemia develop. Concepts for prevention of diabetes have been developed on the basis of better understanding of the pathophysiology of glucose intolerance and stimulated by the ever - increasing burden of disease. It has now been demonstrated that diabetes can be prevent, or at least delay, by nonpharmacological interventions, such as lifestyle modification including diet and exercise, and by pharmacological intervention, including metformin, acarbose, and troglitazone. The purpose of this article is to discuss mechanisms involved in prevention of type 2 diabetes by those different interventions. Is it through effect on insulin resistance and / or insulin secretion or through some other mechanisms? In the first part, we will briefly review the pathophysiology of type 2 diabetes. In the second part, we will describe major intervention trials on prevention of type 2 diabetes and discuss probable mechanisms involved in prevention of diabetes.


THE PATHOPHYSIOLOGY OF TYPE 2 DIABETES

If you are at risk for diabetes, you may be able to prevent or delay getting it. Most of the things that you need to do involve having a healthier lifestyle. So if you make these changes, you will get other health benefits as well. You may lower your risk of other diseases, and you will probably feel better and have more energy. Changes are losing weight and keeping it off. Weight control is an important part of diabetes prevention. You may be able to prevent or delay diabetes by losing 5 to 10 percent of your current weight. For example, if you weigh 200 pounds, your goal would be to lose between 10 to 20 pounds. And once you lose weight, it is important that you don't gain it back. Following a healthy eating plan. It is important to reduce the amount of calories you eat and drink each day, so you can lose weight and keep it off. To do that, your diet should include smaller portions and less fat and sugar. You should also eat a variety of foods from each food group, including plenty of whole grains, fruits, and vegetables. It's also a good idea to limit red meat, and avoid processed meats. Get regular exercise. Exercise has many health benefits, including helping you to lose weight and lower your blood sugar levels. These both lower your risk of type 2 diabetes. Try to get at least 30 minutes of physical activity 5 days a week. If you have not been active, talk with your health care professional to figure out which types of exercise are best for you. You can start slowly and work up to your goal. Don't smoke. Smoking can contribute to insulin resistance, which can lead to type 2 diabetes. If you already smoke, try to quit. Talk to your health care provider to see whether there is anything else you can do to delay or to prevent type 2 diabetes. If you are at high risk, your provider may suggest that you take one of few types of diabetes medicine.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Acknowledgements

As indicated in Table 1, two groups were very closely matched by age and BMI. However, individuals with type 2 diabetes had increased waist / hip ratio and total fat mass, latter mainly due to increased truncal obesity. Vo 2 max per total body weight was decreased in diabetics compared with that in control subjects; however, difference was not significant when VO 2 max was calculated against kilograms of LBM. Plasma triglyceride concentration was increased in patients compared with controls, but lipid content in lipoprotein subfractions obtained after ultracentrifugation was similar in the two groups. Patients were mildly hyperglycemic and had fasting hyperinsulinemia. Early Insulin response and total incremental Insulin release during OGTT tend to be lower in diabetic patients despite greater increases in plasma Glucose concentration. Plasma Insulin levels and rates of Glucose Infusion during various stages of hyperinsulinemic clamps are shown in Table 2. To maintain normoglycemia during low - dose Insulin clamp, Glucose had to be infused at a higher rate in control than in diabetic subjects. Corresponding M - values during high - dose Insulin Infusion rate were 8. 3 0. 7 vs. 4. 6 0. 4 mU / kg body weightmin. These differences remain significant when calculated against kilograms of LBM. M - value correlates inversely with fasting plasma concentration of Glucose, total body fat mass, truncal fat mass, and total abdominal fat area, and directly with VO 2 max. In multivariate analysis, truncal fat mass was the strongest determinant of M - value and, together with VO 2 max explains 52% of its variation. Under basal conditions, substrate oxidation rates and plasma FFA levels were similar in patients and control subjects; however, during high - dose Insulin clamp, fat oxidation rates and plasma FFA levels were significantly higher in diabetic patients, and Glucose oxidation rates were lower. In rat muscle, Insulin and Glucose have been shown to increase concentration of malonyl CoA by increasing cytosolic concentration of citrate, allosteric activator of acetyl CoA carboxylase, and precursor of its substrate, cytosolic acetyl CoA. In this study, concentrations of citrate, malate, and malonyl CoA were similar in the muscles of patients and control individuals under basal conditions. During high - dose Insulin clamp, increased in muscle citrate, malate, and sum of citrate and malate in muscle were all less in patients than in control subjects. However, increase in malonyl CoA concentration during high - dose Insulin clamp was nearly the same in the two groups. Whole - body fatty acid oxidation rates during clamps correlate inversely with malonyl CoA levels and sum of citrate Plus malate in all subjects. Anthropometric and biochemical variables of morbidly obese patients with high Insulin resistance and diabetes and lean healthy controls are summarized in Table 1. Plasma fasting Insulin, Glucose levels and HOMA values were seen to be significantly higher in the obese population compared to the lean group.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Type 2 Diabetes Mellitus

Insulin is a hormone produced in the pancreas by special cells, called beta cells. Pancreas is below and behind the stomach. Insulin is needed to move blood sugar into cells. Inside cells, glucose is stored and later used for energy. When you have type 2 Diabetes, your fat, liver, and muscle cells do not respond correctly to insulin. This is called insulin resistance. As a result, blood sugar does not get into these cells to be stored for energy. When sugar cannot enter cells, high level of sugar builds up in the blood. This is called hyperglycemia. The body is unable to use glucose for energy. This leads to symptoms of type 2 Diabetes. Type 2 Diabetes usually develops slowly over time. Most people with disease are overweight or obese when they are diagnose. Increased fat makes it harder for your body to use insulin in the correct way. Type 2 Diabetes can also develop in people who are not overweight or obese. This is more common in older adults. Family history and genes play a role in type 2 Diabetes. Low activity level, poor diet, and excess body weight around the waist increase your chance of getting disease. Your health care provider may suspect that you have Diabetes if your blood sugar level is higher than 200 milligrams per deciliter or 11. 1 mmol / L. To confirm diagnosis, one or more of the following tests must be done. Fasting blood glucose level - Diabetes is diagnosed if it is 126 mg / dL or higher two different times. Hemoglobin A1C test - Diabetes is diagnosed if the test result is 6. 5% or higher. Oral glucose tolerance test - Diabetes is diagnosed if the glucose level is 200 mg / dL or higher 2 hours after drinking a special sugar drink. Overweight children who have other risk factors for Diabetes, starting at age 10 and repeating every 2 years. Overweight Adults who have other risk factors, such as high blood pressure, or having a mother, father, sister or brother with Diabetes. Overweight women who have other risk factors, such as high blood pressure, who are planning to become pregnant Adults starting at age 45 every 3 years, or at a younger age if person has risk factors. If you have been diagnosed with type 2 Diabetes, you need to work closely with Your provider. See your provider as often as you instruct. This may be every 3 months. Following exams and tests will help you and your provider monitor your diabetes and prevent problems. Check the skin, nerves, and joints of your feet and legs. Check if your feet are getting numb. Have your blood pressure checked at least once a year. Have your A1C test every 6 months if your diabetes is well control. Have a test every 3 months if your diabetes is not well control. Have your cholesterol and triglyceride levels checked once a year. Get tests at least once a year to make sure your kidneys are working well.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

The Role of Insulin

Insulin is cod on the short arm of chromosome 11 7 and synthesise in cells of Pancreatic islets of Langherhans as its precursor, proinsulin. Proinsulin is synthesise in ribosomes of rough endoplasmic reticulum from mRNA as pre - proinsulin. Pre - proinsulin is formed by sequential synthesis of signal peptide, B chain, connecting peptide and then chain comprising a single chain of 100 amino acids. Removal of signal peptide forms proinsulin, which acquires its characteristic 3 dimensional structure in the endoplasmic reticulum. Secretory vesicles transfer proinsulin from RER to Golgi apparatus, whose aqueous zinc and calcium rich environment favours formation of soluble zinc - containing proinsulin hexamers. 6 As immature storage vesicles form from Golgi, enzymes acting outside Golgi convert proinsulin to Insulin and C - peptide. 8 Insulin forms zinc - containing hexamers which are insoluble, precipitating as chemically stable crystals at pH 5. 5 When mature granules are secreted into circulation by exocytosis, Insulin, and equimolar ratio of C - peptide are release. Proinsulin and zinc typically comprise no more than 6% of islet cell secretion. 6 Insulin secretion from islet cells into portal veins is characteristically pulsatile, reflecting summation of coordinate secretory bursts from millions of islet cells. Ultradian oscillatory pattern of Insulin release, in addition to post meal variation, has been report. 9 in response to stimulus such as glucose, Insulin secretion is characteristically biphasic, with an initial rapid phase of Insulin secretion, followed by less intense but more sustained release of hormone. 10 Insulin secretion may be influenced by alterations in synthesis at level of gene transcription, translation, and post - translational modification in Golgi as well as by factors influencing Insulin release from secretory granules. Longer - term modification may occur via influences on cell mass and differentiation. 11 give insulin a pivotal role in glucose utilisation and metabolism, It is not surprising that glucose has multiple influences on Insulin biosynthesis and secretion. However, other factors such as amino acids, fatty acids, acetylcholine, pituitary adenylate cyclase - activating polypeptide, glucose - dependent insulinotropic polypeptide, glucagon - like peptide - 1, and several other agonists, together in combination, also influence these processes. 10 increased levels of glucose induce first phase of glucose - mediate Insulin secretion by release of Insulin from secretory granules in cell. Glucose entry into cell is sensed by glucokinase, which phosphorylates glucose to glucose - 6phosphate, generating ATP. 12 Closure of K + - ATP - dependent channels results in membrane depolarization and activation of voltage dependent calcium channels leading to an increase in intracellular calcium concentration; this triggers pulsatile Insulin secretion. 13 Augmentation of this response occurs by both K + - ATP channel - independent Ca 2 + - dependent pathway and K + - ATP channel - independent Ca 2 + - independent pathways of glucose action. 10 Other mediators of Insulin release include activation of phospholipases and protein kinase C and by stimulation of adenylyl cyclase activity and activation of cell protein kinase, which potentiate Insulin secretion. This latter mechanism may be activated by hormones, such as vasoactive intestinal peptide, PACAP, GLP - 1, and GIP.


Do You Have Insulin Resistance?

An increase in adipose tissue, especially that in upper body or android deposition, was first associated with Diabetes and vascular disease by French endocrinologist Jean Vague in 1956. 94 Insulin Resistance increases with increasing body mass Index, waist circumference and in particular, waist - hip ratio. 95 These reflect increased adiposity, especially increased levels of visceral adipose tissue. Visceral Adipose tissue refers to intra - abdominal fat around the intestines and correlates with liver fat. Visceral Adipose tissue has metabolic characteristics which differ from those of subcutaneous fat. It is more metabolically active with regard to Free Fatty acid turnover; increased flux of Free Fatty acids promotes Insulin Resistance at cellular level and increases Hepatic VLDL production. 35 Omental pre - Adipocytes have increased 11 - hydroxysteroid dehydrogenase Type 1 activity, initially thought to promote Insulin Resistance by effects of locally produced active glucocorticoid, via conversion of cortisone to cortisol, though the significance of these findings in vivo is debate. 96 Adipose tissue produces a number of cytokines which have been associated with Insulin Resistance, including those with pro - inflammatory activity eg TNF, interleukins, and PAI - 1. There are regional differences in adipocyte cytokine production. Interestingly, recent reports suggest improvements in Insulin Resistance by high dose aspirin, supporting the authors ' hypothesis regarding the role of serine kinase IkB kinase - as intracellular mediator of Insulin Resistance in muscle. Muscle Insulin Resistance is associated with increased intramyocellular triglyceride, derived from Adipose tissue lipolysis. 97 Insulin Resistance seen in obesity is believed to involve primarily muscle and liver, with increased adipocyte - derive Free Fatty acids promoting triglyceride accumulation in these tissues. 97 This is more likely where adipocytes are Insulin Resistant. 32 Free Fatty acid flux is greater from visceral Adipose tissue and more likely in those individuals with genetically mediated adipocyte Insulin Resistance. 98 Whilst individual differences in effects of increasing adiposity exist, weight gain worsens and weight loss improves Insulin Resistance in those so predispose.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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