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What Is Insulin Sensitivity And Resistance?

The Causes Of Insulin Resistance In Type 1 Diabetes, Type 2 Diabetes And Prediabetes (video)

The Causes Of Insulin Resistance In Type 1 Diabetes, Type 2 Diabetes And Prediabetes (video)

Most people believe that people with type 1 diabetes are not insulin resistant simply because they are not overweight. This could not be farther from the truth. While insulin resistance affects many overweight individuals, many people with type 1 diabetes remain skinny their entire lives despite a large degree of insulin resistance (1–3). Over the past decade, I have helped many people with type 1 diabetes measure, track and reverse insulin resistance. In practice, 100% of all my clients with type 1 diabetes suffer from insulin resistance despite the assumption that they were insulin sensitive. By measuring their baseline insulin resistance, we were able to identify an impaired ability to utilize glucose as a fuel, and through dedicated diet modification and frequent exercise, some of my clients have reduced their insulin usage by as much as 60%. If you have type 1 diabetes, do not be fooled into thinking that you are insulin sensitive simply because you are skinny. Insulin resistance is a hidden condition, and affects both normal weight and overweight individuals (1–3). What Causes Insulin Resistance? Insulin resistance underlies all forms of diabetes, and is a condition which primarily affects your muscles, liver and adipose tissue. Many people think that diabetes is caused by an excess intake of sugar and candy starting from a young age. While eating artificial sweeteners and drinking soda can certainly increase your risk for the development of insulin resistance and diabetes, in most cases diabetes is caused by excessive FAT intake. The most important thing you can do as a person with diabetes is understand the following: Diabetes is caused by a fat metabolism disorder, which results in a glucose metabolism disorder. At the heart of all forms of diabetes is insu Continue reading >>

Assessment Of Insulin Sensitivity/resistance

Assessment Of Insulin Sensitivity/resistance

Go to: Hyperinsulinemic euglycemic clamp (HEC) is known to be the “gold standard” for the measurement of insulin sensitivity. However, the realization that it is time and money consuming led to the development of a simplified approach in quantification of insulin sensitivity. Various indices of insulin sensitivity/resistance using the data from oral glucose tolerance test (OGTT) were proposed in last 20 years. There are two groups of insulin sensitivity indices: (1) Indices calculated by using fasting plasma concentrations of insulin, glucose and triglycerides, (2) indices calculated by using plasma concentrations of insulin and glucose obtained during 120 min of a standard (75 g glucose) OGTT [Tables 1 and 2]. Former group include homeostasis model assessment-insulin resistance (HOMA-IR), QUIKI INDEX, and McAuley index while latter include, Matsuda, Belfiore, Cederholm, Avignon and Stumvoll index [Tables 1 and 2]. These indices are conveniently used in epidemiological and clinical studies to predict diabetes development in a non-diabetic population. Their use in clinical practice is limited because of the absence of reference values for normal and impaired insulin sensitivity. For the clinical uses HOMA-IR, QUIKI, and Matsuda are suitable while HES, McAuley, Belfiore, Cederholm, Avignon and Stumvoll index are suitable for epidemiological/research purposes [Tables 1 and 2]. Insulin resistance is accepted to be a major risk factor in the etiology of type 2 diabetes mellitus, hypertension, dyslipidemia, atherosclerotic vascular disease, and may be a risk factor for coronary heart disease and stroke as well.[1] Several risk factors (e.g. obesity, physical inactivity, body fat distribution, age and hyperinsulinemia) may be considered markers of insulin resistance. Insul Continue reading >>

Increasing Insulin Sensitivity

Increasing Insulin Sensitivity

Insulin is a hormone that is normally released by the beta cells of the pancreas. When a person’s pancreas cannot produce enough insulin to sustain good health, insulin can be injected into the body with a needle, inhaled with an inhaler, or infused with a pump. One of the main functions of insulin is to lower blood glucose levels by enabling glucose to enter the cells of the body, where it is used for energy or stored for future use. A person who is insulin-sensitive needs only a relatively small amount of insulin to keep blood glucose levels in the normal range and to keep the body’s cells supplied with the glucose they need. A person who is insulin-resistant, on the other hand, needs a lot more insulin to get the same blood-glucose-lowering effects. Insulin resistance is associated with numerous health risks. For one thing, it causes hyperinsulinemia, or high circulating insulin levels, which may be directly damaging to blood vessels. Hyperinsulinemia is also associated with high blood pressure, heart disease and heart failure, obesity (particularly abdominal obesity), osteoporosis (thinning bones), and certain types of cancer, such as colon, breast, and prostate cancer. In contrast, having low circulating insulin levels is associated with greater longevity; most centenarians without diabetes have low circulating insulin levels. Insulin resistance is a hallmark of Type 2 diabetes, but it can occur in Type 1 diabetes as well. In fact, there is a growing number of people who are said to have “double diabetes” because, in addition to having Type 1 diabetes, they also have the insulin resistance characteristic of Type 2. The good news is that you can lower your level of insulin resistance — and raise your level of insulin sensitivity — by modifying your lifes Continue reading >>

Resistance Training, Insulin Sensitivity And Muscle Function In The Elderly

Resistance Training, Insulin Sensitivity And Muscle Function In The Elderly

Ageing is associated with a loss in both muscle mass and in the metabolic quality of skeletal muscle. This leads to sarcopenia and reduced daily function, as well as to an increased risk for development of insulin resistance and type 2 diabetes. A major part, but not all, of these changes are associated with an age-related decrease in the physical activity level and can be counteracted by increased physical activity of a resistive nature. Strength training has been shown to improve insulin-stimulated glucose uptake in both healthy elderly individuals and patients with manifest diabetes, and likewise to improve muscle strength in both elderly healthy individuals and in elderly individuals with chronic disease. The increased strength is coupled to improved function and a decreased risk for fall injuries and fractures. Elderly individuals have preserved the capacity to improve muscle strength and mass with training, but seem to display a reduced sensitivity towards stimulating protein synthesis from nutritional intake, rather than by any reduced response in protein turnover to exercise. View Full Text Continue reading >>

Twice-weekly Progressive Resistance Training Decreases Abdominal Fat And Improves Insulin Sensitivity In Older Men With Type 2 Diabetes

Twice-weekly Progressive Resistance Training Decreases Abdominal Fat And Improves Insulin Sensitivity In Older Men With Type 2 Diabetes

OBJECTIVE—To evaluate the influence of a twice-weekly progressive resistance training (PRT) program, without a concomitant weight loss diet, on abdominal fat and insulin sensitivity in older men with type 2 diabetes. RESEARCH DESIGN AND METHODS—Nine older men (aged 66.6 ± 3.1) with type 2 diabetes participated in a 16-week PRT supervised program (50–80% of the one repetition maximum), for all main muscle groups. Basal glycemia, HbA1c, diet, habitual physical activity, body composition, and upper/lower maximal strength were measured. Insulin sensitivity was determined according to Bergman’s minimal model procedure and abdominal fat was obtained by computed tomography. The measurements were taken 4 weeks before training (−4), immediately before training (0), and at 8-week intervals (i.e., weeks 8 and 16) during the 16-week training period. RESULTS—No significant variation was observed in any of the above selected parameters during the 4-week control period. After PRT, both leg and arm maximal strength increased significantly by 17.1 and 18.2%, respectively. Visceral and subcutaneous abdominal fat decreased significantly by 10.3% (from 249.5 ± 97.9 to 225.6 ± 96.6 cm3, P < 0.01) and by 11.2% (from 356.0 ± 127.5 to 308.6 ± 118.8 cm3, P < 0.01), respectively, while no changes were observed in body mass. PRT significantly increased insulin sensitivity by 46.3% (from 2.0 ± 1.2 to 2.8 ± 1.6 · 104 · min−1 · μU−1 · ml−1, P < 0.01), whereas it significantly decreased (−7.1%, P < 0.05) fasting blood glucose (from 146.6 ± 28.3 to 135.0 ± 29.3 mg/dl). Finally, a 15.5% increase in energy intake (from 2,287.1 ± 354.7 to 2,619.0 ± 472.1 kcal/day, P < 0.05) was observed. CONCLUSIONS—Two sessions per week of PRT, without a concomitant weight loss diet Continue reading >>

Insulin And Insulin Resistance - The Ultimate Guide

Insulin And Insulin Resistance - The Ultimate Guide

Insulin is an important hormone that controls many processes in the body. However, problems with this hormone are at the heart of many modern health conditions. Sometimes our cells stop responding to insulin like they are supposed to. This condition is termed insulin resistance, and is incredibly common. In fact, a 2002 study showed that 32.2% of the US population may be insulin resistant (1). This number may rise to 70% in obese adult women and over 80% in some patient groups (2, 3). About a third of obese children and teenagers may also have insulin resistance (4). These numbers are scary, but the good news is that insulin resistance can be dramatically improved with simple lifestyle measures. This article explains what insulin resistance is, why you should care and how you can overcome it. Insulin is a hormone secreted by an organ called the pancreas. Its main role is to regulate the amount of nutrients circulating in the bloodstream. Although insulin is mostly implicated in blood sugar management, it also affects fat and protein metabolism. When we eat a meal that contains carbohydrates, the amount of blood sugar in the bloodstream increases. This is sensed by the cells in the pancreas, which then release insulin into the blood. Then insulin travels around the bloodstream, telling the body's cells that they should pick up sugar from the blood. This leads to reduced amounts of sugar in the blood, and puts it where it is intended to go, into the cells for use or storage. This is important, because high amounts of sugar in the blood can have toxic effects, causing severe harm and potentially leading to death if untreated. However, due to various reasons (discussed below), sometimes the cells stop responding to the insulin like they are supposed to. In other words, they Continue reading >>

Effects Of Tumour Necrosis Factor Antagonists On Insulin Sensitivity/resistance In Rheumatoid Arthritis: A Systematic Review And Meta-analysis

Effects Of Tumour Necrosis Factor Antagonists On Insulin Sensitivity/resistance In Rheumatoid Arthritis: A Systematic Review And Meta-analysis

Abstract Beyond the joints, TNFi (tumour necrosis factor inhibitor) therapy may confer systemic benefits in rheumatoid arthritis (RA). Several studies have investigated the role of TNFi on insulin resistance/sensitivity (IR/IS). This question is of general interest given the emerging evidence linking inflammation and insulin resistance. The main aim of this review was to summarise the published data and to determine the effects of TNFi on IR/IS. We searched the PubMed and ISI Web of Knowledge databases for studies which examined the effects of TNFi on IR/IS. The studies were assessed independently by two reviewers according to a pre-specified protocol. The data on Homeostatic Model Assessment for Insulin resistance (HOMA) and Quantitative Insulin Sensitivity Check Index (QUICKI) were pooled and reported as standard difference in means (SDM) with 95% confidence interval (CI) using a random-effects model. A total of eight studies with 260 subjects met the selection criteria. The duration of the studies was from 8 weeks to 12 months. There was statistically significant reduction in HOMA index in six out of eight studies and four reported significant increment in QUICKI. The pooled analysis revealed significant reduction in HOMA [SDM-0.148, 95%CI[-0.278 to -0.017], p=0.026] and increment in QUICKI [SDM 0.312, 95%CI[0.019 to 0.606], p=0.037] with TNFi. There is emerging evidence to support that TNFi therapy improves IS and reduces IR in RA. Further, well conducted trials are needed to determine if such effects translate to lower incidence of diabetes in RA or other autoimmune conditions on biologic therapy. Figures Citation: Burska AN, Sakthiswary R, Sattar N (2015) Effects of Tumour Necrosis Factor Antagonists on Insulin Sensitivity/Resistance in Rheumatoid Arthritis: A Sys Continue reading >>

Insulin Resistance Insulin Sensitivity

Insulin Resistance Insulin Sensitivity

As a Type-1 Diabetic and due to the manner in which I learned to manage it, Insulin Resistance became a passionate topic for me as it is a fundamental element of metabolic control. I learned that the lower the insulin resistance, the less insulin I had to inject and the better I felt. However, it wasn’t until two and a half decades later that I discovered that there was actually a technical term for this metabolic relationship; Insulin Resistance. What is insulin? Insulin is a hormone that enables the metabolism (“burn rate”) of glucose. Insulin is produced by a portion of the pancreas and is secreted into the blood stream. It is produced in direct response to the level of glucose in the blood stream to regulate a near constant blood-glucose level. As glucose rises, more insulin is produced to burn the glucose into energy, as blood-glucose decreases, less insulin is produced. What is Glucose? Glucose is the simple sugar that is biology’s fuel. What is insulin resistance? Insulin resistance is an extremely common condition affecting almost every American, however it is rarely diagnosed. Most commonly, when it is diagnosed it is labeled under various other terms, including chronic fatigue syndrome. It is important to understand that insulin resistance is by degree and that everyone has it and that it is continuously variable and that it is lifestyle related and that it is reversible and that it is not genetic or something you catch or something you get and are stuck with. It is something to overcome. There are two primary lifestyle elements that influence insulin resistance: food and exercise. Insulin resistance is variable in step with each of these, however, it is possible to become insulin sensitive (opposite of insulin resistant) with food alone. The object is Continue reading >>

Insulin Resistance

Insulin Resistance

Practice Essentials Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. Insulin resistance has also been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis. The syndromes of insulin resistance actually make up a broad clinical spectrum, which includes obesity, glucose intolerance, diabetes, and the metabolic syndrome, as well as an extreme insulin-resistant state. Many of these disorders are associated with various endocrine, metabolic, and genetic conditions. These syndromes may also be associated with immunological diseases and may exhibit distinct phenotypic characteristics. [1, 2, 3, 4, 5, 6, 7, 8] The metabolic syndrome —a state of insulin-resistance that is also known as either syndrome X or the dysmetabolic syndrome—has drawn the greatest attention because of its public health importance. In addition to hypertension, findings can include central obesity, peripheral arterial disease, type A syndrome, type B syndrome, ancanthosis nigricans, polycystic ovary syndrome, and other insulin-resistant states. In clinical practice, no single laboratory test is used to diagnose insulin resistance syndrome. Diagnosis is based on clinical findings corroborated with laboratory tests. Individual patients are screened based on the presence of comorbid conditions. Lab tests include the plasma glucose level, the fasting insulin level, and a lipid profile, among others. Treatment involves pharmacologic therapy to reduce insulin resistance, along with surgical management of underlying causes if appropriate. Comorbid conditions should be evaluated and addressed; this is generally feasible on an outpatient basis, though some patients wi Continue reading >>

Assessing Insulin Sensitivity

Assessing Insulin Sensitivity

References: McAuley KA, Williams SM, Mann JI, Walker RJ, Lewis-Barned NJ, Temple LA, Duncan AW (2001) Diagnosing insulin resistance in the general population. Diabetes Care 24:460-464. Background: The concept of insulin resistance is relatively easy to understand, but determining precisely who is insulin resistant is more complicated. The relationship between glucose and insulin is quite complex and involves the interaction of many metabolic and regulatory factors. Normal insulin sensitivity varies widely and is influenced by age, ethnicity, and obesity. Simply put, not all people with impaired insulin sensitivity are necessarily suffering from a disorder, and pregnancy is a perfect example of this. A World Health Organization consensus group recently concluded that the insulin sensitivity index (SI) of the lowest 25% of a general population can be considered insulin resistant. The European Group for the Study of Insulin Resistance took a more restricted view, defining insulin resistance as the SI of the lowest 10% of a non-obese, nondiabetic, normotensive Caucasian population. Richard Legro and his associates also used the SI of the lowest 10% of an obese, non-PCOS population to define insulin resistance. Ideally, we should be deriving the normal SI range from a population of women who are not obese, have regular menstrual cycles, are not suffering from hirsutism, and have normal circulating androgen levels. Choosing the best assessment technique The hyperinsulinemic-euglycemic clamp technique is the most scientifically sound technique for measuring insulin sensitivity, and it's against this standard that all other tests are usually compared. Because this and similar "clamp" techniques are expensive, time consuming, and labor intensive, they are not very practical in a Continue reading >>

Insulin Sensitivity After Maximal And Endurance Resistance Training

Insulin Sensitivity After Maximal And Endurance Resistance Training

Hansen, Elisabeth1,2; Landstad, Bodil J3,4; Gundersen, Kjell T2; Torjesen, Peter A5; Svebak, Sven1 Hansen, E, Landstad, BJ, Gundersen, KT, Torjesen, PA, and Svebak, S. Insulin sensitivity after maximal and endurance resistance training. J Strength Cond Res 26(2): 327–334, 2012—The purpose of the study was to compare the effects of maximal resistance training (MRT) vs. endurance resistance training (ERT) on improvements in insulin levels and glucose tolerance in overweight individuals at risk of developing type 2 diabetes. Eighteen participants with baseline values suggesting impaired glucose tolerance were randomly assigned to 1 of 2 groups. Group 1 engaged in supervised MRT (Bernstein inverted pyramid system: 5 × 3–4, 60–85% 1 repetition maximum [1RM]), 3 d·wk−1 over 4 months, whereas members of group 2 acted as controls. Later, group 2 engaged in supervised ERT (3 × 12–15, 45–65% 1RM), 3 d·wk−1 over a 4 month period with the 2 prebaselines as controls. Both interventions consisted of 8 exercises that included the entire body. Glucose (fasting and 2-hour test), insulin and C-peptide measures were assessed from pre to post in both groups. The MRT led to reduced blood levels of 2-hour glucose (p = 0.044) and fasting C-peptide (p = 0.023) and decreased insulin resistance (p = 0.040). The ERT caused a significant reduction in the blood levels of insulin (p = 0.023) and concomitant positive effects on % insulin sensitivity (p = 0.054) and beta-cell function (p = 0.020). The findings indicate that both MRT and ERT lead to decreased insulin resistance in people with a risk of developing type 2 diabetes; MRT led to a greater increase in glucose uptake capacity (in muscles), whereas ERT led to greater insulin sensitivity, supporting the recommendation of bot Continue reading >>

A Practical Guide To Carb Tolerance And Insulin Sensitivity

A Practical Guide To Carb Tolerance And Insulin Sensitivity

One of the biggest reasons why people go Paleo is the metabolic benefits. Most people find Paleo to be very therapeutic for a whole cluster of carb-related problems: high blood sugar (or the rollercoaster of highs and lows), insulin resistance, and all the related issues. These issues can make weight loss difficult or impossible, but on the flip side, addressing them through diet can make it easier and more pleasant than you ever thought could happen! On the other hand, though, there are a lot of myths and half-truths floating around about diet, exercise, and carb metabolism. So here’s a quick review of what it all means, and the evidence supporting various different complementary strategies for improving your carb tolerance (preview: it’s so much more than dietary carbs). Note: This article is not written for diabetics. Diabetes is a very complicated disease and strategies that are right for other people might not be appropriate. If you have diabetes, see a doctor! What Is “Carb Tolerance”/Insulin Sensitivity? (If you already know how insulin and glucose work, this section has nothing new for you; just skip down to the next one) Very simply put, insulin sensitivity (or “carb tolerance” in everyday language) is a healthy hormonal state that allows your body to digest and store carbohydrates without a problem. In healthy people, here’s how it works: You eat something with carbs (let’s say a potato, but it could be anything). Your digestive system breaks down the starch in that potato into glucose. Glucose is a simple sugar – this is the form of carbohydrate that you’ll either use for energy or store as fat. Your blood sugar temporarily rises as the glucose enters the bloodstream. This is not a big problem, because… Insulin (produced in the pancreas) Continue reading >>

How Can We Measure Insulin Sensitivity/resistance?

How Can We Measure Insulin Sensitivity/resistance?

Insulin resistance represents a major public health problem, as it plays a major role in the pathophysiology of type 2 diabetes mellitus; it is also associated with increased cardiovascular risk and atherogenic dyslipidaemia, and is a central component of the cluster of metabolic abnormalities that comprise the metabolic syndrome. Thus, the development of tools to quantify insulin sensitivity/resistance has been the main objective of a number of studies. Insulin resistance can be estimated with the use of several biological measurements that evaluate different aspects of this complex situation. To that end, it requires various resources, ranging from just a single fasting blood sample for simple indices, such as the HOMA or QUICKI, to a research setting in which to perform the gold-standard hyperinsulinaemic–euglycaemic clamp test. The choice of method for evaluating insulin resistance depends on the nature of the information required (classification of individual subjects, group comparisons, precise measurement of either global, muscle or liver insulin sensitivity/resistance) and on the available resources. The aim of this review is to analyze the most frequently used assay methods in an attempt to evaluate when and why these methods may be useful. The full text of this article is available in PDF format. La résistance à l’insuline représente un problème majeur de santé publique puisqu’elle joue un rôle central dans la physiopathologie du diabète de type 2, est associée à une augmentation du risque cardiovasculaire et est un élément central d’un ensemble d’anomalies métaboliques qui définissent le syndrome métabolique. Ainsi, de nombreuses études se sont attachées à développer des outils pour apprécier et quantifier la sensibilité/résista Continue reading >>

How Can We Measure Insulin Sensitivity/resistance?

How Can We Measure Insulin Sensitivity/resistance?

Abstract Insulin resistance represents a major public health problem, as it plays a major role in the pathophysiology of type 2 diabetes mellitus; it is also associated with increased cardiovascular risk and atherogenic dyslipidaemia, and is a central component of the cluster of metabolic abnormalities that comprise the metabolic syndrome. Thus, the development of tools to quantify insulin sensitivity/resistance has been the main objective of a number of studies. Insulin resistance can be estimated with the use of several biological measurements that evaluate different aspects of this complex situation. To that end, it requires various resources, ranging from just a single fasting blood sample for simple indices, such as the HOMA or QUICKI, to a research setting in which to perform the gold-standard hyperinsulinaemic-euglycaemic clamp test. The choice of method for evaluating insulin resistance depends on the nature of the information required (classification of individual subjects, group comparisons, precise measurement of either global, muscle or liver insulin sensitivity/resistance) and on the available resources. The aim of this review is to analyze the most frequently used assay methods in an attempt to evaluate when and why these methods may be useful. Continue reading >>

Homeostastic Model Assessment And Insulin Sensitivity/resistance

Homeostastic Model Assessment And Insulin Sensitivity/resistance

Homeostasis is the manifestation of a large network of integrated metabolic reactions and signaling pathways designed to maintain life and function in a stable manner. Insulin is an integral part of this regulatory network and affects virtually all its parts. The actions of insulin vary in time (1) as well as in the various tissues it affects as demonstrated, for example, by selective receptor deletion studies (2). Moreover, insulin individually affects a large number of reactions within these tissues. Lack of insulin, or of its action(s), results in diabetes. This has historically been viewed from the perspective of glucose metabolism, although, as pointed out by McGarry (3), a similar spectrum of deficiencies would have been identified first if lipids had been the primary focus of investigation. Insulin action as an entity is therefore, necessarily, ill-defined. It is embedded within the network of reactions and signals where it plays critical regulatory roles. In some sense, measuring insulin action must be equally tenuous. When, where, and how it is measured is a matter of physiology, but also of history. Clinically then, resistance to insulin action was first defined on the backdrop of glucose metabolism (4). Specifically, diabetes was divided into insulin-sensitive and -insensitive types. Insulin insensitivity or resistance rose into more prominence when it was associated with other risk factors for the development of type 2 diabetes, such as obesity, dyslipidemia, hypertension, and hypercoagulopathy, grouped under the term hyperinsulinemic/insulin resistance syndrome (X) or currently, the metabolic syndrome. Collectively, this group of pathologies increased the risk of developing diabetes and was associated also with an increased risk of cardiovascular disease (5 Continue reading >>

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