Insulin Resistance
Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults.[1] Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose.[2] In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose. People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome. Insuli Continue reading >>
High Insulin Levels Tied To Obesity Pathway
DALLAS – August 25, 2014 – UT Southwestern Medical Center researchers have identified a crucial link between high levels of insulin and pathways that lead to obesity, a finding that may have important implications when treating diabetes. Researchers with UT Southwestern’s Touchstone Diabetes Centerfound that giving mice high levels of insulin, which is typically done to counter the effects of diabetes or insulin resistance in Type 2 diabetes, also fosters processes that lead to obesity. The discovery was made by studying mice engineered to lack receptors for a hormone called glucagon. Glucagon spurs the liver’s production of glucose into the bloodstream and thus maintains the fuel supply for the brain. Insulin blocks the secretion of glucagon, opposes glucagon action on the liver, and instructs the body to take up glucose from the blood. Type 2 diabetics cannot respond properly to insulin and have uncontrolled glucagon production, thereby causing their livers to overproduce glucose, contributing to high blood-sugar levels. Insulin is often given to people with type 2 diabetes to try to overcome insulin-resistance and lower the levels of glucose in the bloodstream. But insulin also signals the body to produce fat, so when given the high levels of insulin needed to control excess glucose, mice become fat, explained corresponding author Dr. Michael Roth, Professor of Biochemistry at UT Southwestern and a member of the Touchstone Diabetes Center. “We found that mice lacking the receptor for glucagon cannot get fat unless they are given the high levels of insulin found in mice (and humans) that have type 2 diabetes,” said Dr. Roth, who holds the Diane and Hal Brierley Distinguished Chair in Biomedical Research. “This result suggests that the high levels of insu Continue reading >>
High Insulin Levels Could Result In Obesity
Study sheds new light on the link between high insulin levels and weight gain…. While the dominating opinion is that rising insulin is a result of obesity and insulin resistance, a new study provides evidence that it appears to be the other way around. According to the study, researchers found that when we eat too much, obesity may actually develop as a result of chronically high insulin levels. To prove this, the team used mice to show that animals with persistently lower insulin stay trim even as they indulge themselves on a high-fat, all-you-can-eat buffet. These results provide evidence that it is circulating insulin that drives obesity in mammals. Study author James Johnson of the University of British Columbia added that the results are also consistent with clinical studies showing that long-term insulin use by people with diabetes tends to come with weight gain. One of insulin’s functions is management of the utilization of fat as an energy source. And because insulin controls the central metabolic processes, failure of insulin production can lead to diabetes type 1 or diabetes type 2. In this study, Johnson and his colleagues used mice because they have two insulin genes: insulin1, which shows up primarily in the pancreas, and insulin2, in the brain and the pancreas. By eliminating insulin2 altogether and varying the number of good copies of insulin1, the team produced mice that varied only in their fasting blood insulin levels. When the mice were presented with high-fat food, those with one copy and lower fasting insulin were completely protected from obesity, even without any loss of appetite. They also had lower levels of inflammation and less fat in their livers. These differences "reprogrammed" the animals’ fat tissue to burn more energy. Johnson stat Continue reading >>
Body Fat Distribution And Insulin Levels In Obese Children
Obesity is associated with metabolic disturbances, depending on regional body fat distribution. In adults, central pattern is associated wiht known cardiovascular risk factors, insulin resistnace and hyperinsulinemia. Theaim of the study was to determine the pattern of body fat distribution in children and adolescents obese patients and to evaluate the differences in oral glucose tolerance test (O.G.T.T.) and insulin responseMat. and Meth: 39 obese patients 15 male and 24 female, age x 11 03 y. ± 3.2 were studied. Body mass index (B.M.I.): 31.14±4.96 kgr/m2. Tripceps, subescapular, suprailiac bicipital and medial calf skinfold thiknesses were measured to determine the pattern of body fat distribution. The insulin response durign O.G.T.T. was evaluated by calculating the area under the curve. Results: The central adiposity pattern was present in 59% (23/39) of patients, and the generalized one in 41% (16/39). There were not significantly differences between the two groups in B.M.I. and sex, but age was lesser in the generalized group(p<0.01). Glucose levels during O.G.T.T. were similar in both group. Insulin levels weer significantly higher in the central obesity: 487±200 vs. generalized obesity above. 278±133 (p< 0.001)Conslusions: Results show a significant association between central pattern and hyperinsulinemia in children obesity. Early identification would be important for prevention estategies. Continue reading >>
Your Weight And Diabetes
Diabetes is a group of disorders characterized by chronic high blood glucose levels (hyperglycemia) due to the body's failure to produce any or enough insulin to regulate high glucose levels. There are two main types of diabetes. Type 1 diabetes, which often occurs in children or adolescents, is caused by the body's inability to make insulin or type 2 diabetes, which occurs as a result of the body's inability to react properly to insulin (insulin resistance). Type 2 diabetes is more prevalent than type 1 diabetes and is therefore seen in roughly 90% of all diabetes cases. Type 2 diabetes is predominantly diagnosed after the age of forty, however, it is now being found in all age ranges, including children and adolescents. The impact of diabetes goes beyond chronic hyperglycemia. Diabetes is the leading cause of blindness (diabetic retinopathy), end stage kidney diseases (diabetic nephropathy) and non-traumatic lower extremity amputations (diabetic neuropathy) in working-age adults. People with diabetes are also two to four times more likely to experience cardiovascular complications and strokes. Diabetes and its related complications result in an estimated 200,000+ deaths each year, making diabetes one of the major causes of mortality in the U.S. In 2012, the NIH reported an estimated 29.1 million Americans (9.3% of the population) living with diabetes. Of these, an estimated 8.1 million persons were unaware that they had the disease. How does my weight relate to type 2 diabetes? There are many risk factors for type 2 diabetes such as age, race, pregnancy, stress, certain medications, genetics or family history, high cholesterol and obesity. However, the single best predictor of type 2 diabetes is overweight or obesity. Almost 90% of people living with type 2 diabetes a Continue reading >>
Mechanisms Of Obesity-associated Insulin Resistance: Many Choices On The Menu
Abstract Obesity-associated insulin resistance is a major risk factor for type 2 diabetes and cardiovascular disease. In the past decade, a large number of endocrine, inflammatory, neural, and cell-intrinsic pathways have been shown to be dysregulated in obesity. Although it is possible that one of these factors plays a dominant role, many of these factors are interdependent, and it is likely that their dynamic interplay underlies the pathophysiology of insulin resistance. Understanding the biology of these systems will inform the search for interventions that specifically prevent or treat insulin resistance and its associated pathologies. The number of obese individuals worldwide has reached 2.1 billion, leading to an explosion of obesity-related health problems associated with increased morbidity and mortality (Li et al. 2005; Olshansky 2005). Obese individuals develop resistance to the cellular actions of insulin, characterized by an impaired ability of insulin to inhibit glucose output from the liver and to promote glucose uptake in fat and muscle (Saltiel and Kahn 2001; Hribal et al. 2002). Insulin resistance is a key etiological factor for type 2 diabetes mellitus (T2DM), which has reached epidemic proportions: In the United States, ∼6% of the current adult population is diagnosed with this disease. An additional 41 million people are prediabetic, with a constellation of insulin resistance, hypertension, and dyslipidemia that puts them at increased risk for cardiovascular morbidity and mortality (Zimmet et al. 2001; American Diabetes Association diabetes statistics at Lifestyle changes, while desirable, have proven difficult to achieve. Thus, a better understanding of the molecular mechanisms underlying insulin resistance will be required to combat the epidemics Continue reading >>
Insulin Resistance Syndrome
Insulin resistance can be linked to diabetes, hypertension, dyslipidemia, cardiovascular disease and other abnormalities. These abnormalities constitute the insulin resistance syndrome. Because resistance usually develops long before these diseases appear, identifying and treating insulin-resistant patients has potentially great preventive value. Insulin resistance should be suspected in patients with a history of diabetes in first-degree relatives; patients with a personal history of gestational diabetes, polycystic ovary syndrome or impaired glucose tolerance; and obese patients, particularly those with abdominal obesity. Present treatment consists of sensible lifestyle changes, including weight loss to attain healthy body weight, 30 minutes of accumulated moderate-intensity physical activity per day and increased dietary fiber intake. Pharmacotherapy is not currently recommended for patients with isolated insulin resistance. Obesity, type 2 diabetes mellitus (formerly known as non–insulin-dependent diabetes), hypertension, lipid disorders and heart disease are common in most Western societies and are collectively responsible for an enormous burden of suffering. Many people have more than one—and sometimes all—of these conditions, leading to the hypothesis that the coexistence of these diseases is not a coincidence, but that a common underlying abnormality allows them to develop. In 1988 it was suggested that the defect was related to insulin, and the insulin resistance syndrome was first described.1 It is estimated that this syndrome affects 70 to 80 million Americans.2 Insulin stimulates glucose uptake into tissues, and its ability to do so varies greatly among individual persons. In insulin resistance, tissues have a diminished ability to respond to the actio Continue reading >>
Massive Weight Loss Does Not Restore Normal Insulin Secretory Pulses In Obese Patients With Type 2 (non-insulin-dependent) Diabetes Mellitus.
Abstract To study the effects of massive weight loss on insulin secretion, we analysed the oscillations of fasting peripheral insulin levels in obese patients who underwent vertical banded gastroplasty as treatment for morbid obesity. Patients were studied before and 6 months after surgery. Serial measurements of plasma free insulin levels were obtained in duplicates from 0 to 60 min at one-minute intervals. Insulin levels were then analysed by autocorrelation and Fourier transformation. In normal controls and obese patients, the first oscillatory insulin component was detected between 10 and 14 min. Compared to obese controls (n = 4), overt Type 2 diabetic patients (n = 4) had reduced amplitudes of insulin pulses and no oscillatory component. These defects were not as pronounced in patients with impaired glucose tolerance (IGT) after an oral glucose tolerance test (OGTT) (n = 5). When detected, the periodicity of the oscillations occurred at different periods. In 3/5 IGT patients, the first positive peak of correlation was found at 13.3 +/- 2.3 min. Weight loss (mean +/- SD) after 6 months was 24.3 +/- 3.7 for subjects with normal glucose tolerance (NGT), 37.9 +/- 9 for those with IGT and 29.8 +/- 5 kgs for Type 2 diabetic subjects. After weight loss, insulin oscillatory activity was detected in 4/5 IGT patients, with a period of 13 +/- 3 min. Weight loss did not reverse the defects observed in obese diabetic patients despite a significant reduction in peripheral insulin levels from 28.6 +/- 6 to 15.6 +/- 6 mU/l (p < 0.05). Insulin values remained higher than in obese controls (7.82 +/- 2, p < 0.05), and Type 2 patients remained mildly hyperglycaemic. These findings indicate that beta-cell activity is abnormal in Type 2 diabetic patients. The absence of modification af Continue reading >>
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Insulin Resistance In Nondiabetic Morbidly Obese Patients: Effect Of Bariatric Surgery
Abstract Objective: To evaluate insulin action on substrate use and insulinemia in nondiabetic class III obese patients before and after weight loss induced by bariatric surgery. Research Methods and Procedures: Thirteen obese patients (four men/nine women; BMI = 56.3 ± 2.7 kg/m2) and 13 lean subjects (five men/eight women; BMI = 22.4 ± 0.5 kg/m2) underwent euglycemic clamp, oral glucose tolerance test, and indirect calorimetry. The study was carried out before (Study I) and after (∼40% relative to initial body weight; Study II) weight loss induced by Roux-en-Y Gastric bypass with silastic ring surgery. Results: The obese patients were insulin resistant (whole-body glucose use = 19.7 ± 1.5 vs. 51.5 ± 2.4 μmol/min per kilogram fat-free mass, p < 0.0001) and hyperinsulinemic in the fasting state (332 ± 86 vs. 85 ± 5 pM, p < 0.0001) and during the oral glucose tolerance test compared with the lean subjects. Fasting plasma insulin normalized after weight loss, whereas whole-body glucose use increased (35.5 ± 3.7 μmol/min per kilogram fat-free mass, p < 0.05 vs. Study I). The higher insulin clearance of obese did not change during the follow-up period. Insulin-induced glucose oxidation and nonoxidative glucose disposal were lower in the obese compared with the lean group (all p < 0.05). In Study II, the former increased slightly, whereas nonoxidative glucose disposal reached values similar to those of the control group. Fasting lipid oxidation was higher in the obese than in the control group and did not change significantly in Study II. The insulin effect on lipid oxidation was slightly improved (p = 0.01 vs. Study I). Discussion: The rapid weight loss after surgery in obese class III patients normalized insulinemia and improved insulin sensitivity almost entirel Continue reading >>
Food Order Impacts Glucose And Insulin Levels
Eating protein and vegetables before carbohydrates leads to lower post-meal glucose and insulin levels in obese patients with type 2 diabetes, Weill Cornell Medical College researchers found in a new study. This finding, published June 23 in the journal Diabetes Care, might impact the way clinicians advise diabetic patients and other high-risk individuals to eat, focusing not only on how much, but also on when carbohydrates are consumed. “We’re always looking for ways to help people with diabetes lower their blood sugar,” said senior author Dr. Louis Aronne, the Sanford I. Weill Professor of Metabolic Research and a professor of clinical medicine at Weill Cornell Medical College, the study’s principal investigator. “We rely on medicine, but diet is an important part of this process, too. Unfortunately, we’ve found that it’s difficult to get people to change their eating habits. “Carbohydrates raise blood sugar, but if you tell someone not to eat them – or to drastically cut back – it’s hard for them to comply,” added Aronne, who is also director of the Comprehensive Weight Control Center at Weill Cornell. “This study points to an easier way that patients might lower their blood sugar and insulin levels.” Patients with type 2 diabetes typically use a finger prick test to check their glucose levels throughout the day. Maintaining normal levels, specifically after meals, is of the utmost importance, because if a diabetics’ blood-sugar level is consistently high or frequently spikes, they risk complications of their disease, including hardening of the arteries and death from heart disease. This study looked to validate and advance previous research that showed eating vegetables or protein before carbohydrates leads to lower post-meal glucose le Continue reading >>
High Insulin Levels Could Lead To Obesity
An unexpected discovery has shown that certain widespread beliefs about healthy eating habits may be false, and actually causing people to put on weight. The finding came from a researcher at the University of British Columbia and was published in Cell Metabolism. The study set out to observe the role of insulin, which is hormone that permits the body to store blood sugar so that it can be used as energy later on. A lack of insulin causes diabetes, and, according to a different study in the same journal, impaired brain insulin action may be the cause of the unrestrained lipolysis which results in, and worsens, type 2 diabetes. After analyzing the role of insulin in animals, James Johnson, an associate professor or cellular and physiological sciences, discovered that too much insulin may be detrimental. Johnson split mice into two groups and provided both with a high-fat diet. One group, the control group, consisted of normal mice and the other consisted of mice which were bred to have only half the regular amount of insulin. Results showed that the normal mice became overweight, just as the scientist anticipated. However, the mice that had low levels of insulin did not gain weight due to the fact that their fat cells burned more energy while storing less. The mice that remained skinny had less swelling and had livers that were in better health. This meant, according to Johnson, that obesity resulted from the additional insulin that was made in the normal mice by the high-fat diet. In other words, mice, as well as humans, may produce more insulin than necessary. The research indicates that people can maintain a healthy weight by constantly bringing the levels of insulin back to a healthy minimum. This can be done by increasing the time between meals and eliminating snack Continue reading >>
[plasma Levels Of Insulin And Leptin In Patients With Morbid Obesity And Anorexia Nervosa After Weight Loss Or Gain, Respectively].
Abstract The present study was conducted in order to analyze the relationship existing between leptin and insulin levels in massive weight loss and weight recovery. Thirteen patients with severe obesity, 14 patients with anorexia nervosa and 13 healthy control subjects were studied. The patients with severe obesity underwent a vertical banded gastroplasty followed by an 800 kcal/day diet for 12 weeks. They were evaluated prior to (body mass index [BMI] 51.2 +/- 8.8 Kg/m2) and after drastic weight loss (BMI 40.6 +/- 6.7 Kg/m2). Patients with anorexia nervosa were treated exclusively with nutritional therapy during 12 weeks, and they were evaluated at their lowest weight status (BMI 16.2 +/- 2.2 Kg/m2) and after weight recovery (BMI 17.9 +/- 2.3 Kg/m2). The BMI of the normal subjects was in the normal range of 20 to 27 Kg/m2 (average 22.8 +/- 2.6 Kg/m2). BMI, percentage of body fat, waist circumference, and serum levels of leptin, insulin, and C-peptide were determined in each patient and normal subject. In severely obese patients, serum leptin and insulin decreased significantly after drastic weight reduction (leptin: from 51.8 +/- 22.3 to 23.7 +/- 10.2 ng/ml; insulin: from 27.1 +/- 13.3 to 17.2 +/- 7.2 mU/ml). In patients with anorexia nervosa, the mean serum leptin levels were significantly higher after weight recovery (5.5 +/- 3.2 vs 7.6 +/- 6 ng/ml). Serum leptin in the severe obesity group correlated positively with BMI, percentage body fat and waist circumference before and after weight loss. In those patients suffering from anorexia nervosa, serum leptin correlated positively with the BMI, percentage of body fat, and waist circumference in the low weight state and after weight recovery. In addition, their serum insulin correlated with BMI and waist circumference a Continue reading >>
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Obesity Workup
Approach Considerations Standard laboratory studies in the evaluation of obesity should include the following: Other tests are performed as indicated by clinical findings. For example, the 24-hour urinary free-cortisol test is needed only when Cushing syndrome or other hypercortisolemic states are clinically suspected. However, approximately 4% of patients with Cushing syndrome have normal urinary free-cortisol values. Lipid panel At minimum, test fasting cholesterol, triglycerides, and high-density lipoprotein cholesterol (HDL-C) levels. These levels may be normal, or the typical dyslipidemia associated with cardiometabolic syndrome may be found. This dyslipidemia is characterized by reduced HDL-C and elevated fasting triglyceride concentrations; however, increased low-density lipoprotein cholesterol (LDL-C) and normal to marginally increased total cholesterol are not uncommon among obese individuals. Liver and thyroid function tests Liver function tests yield normal results in most obese patients. However, elevated transaminase levels may indicate nonalcoholic steatohepatitis (NASH) or fatty infiltration of the liver). Thyroid function test results are also typically normal, but checking them to detect primary hypothyroidism (characterized by increased serum thyrotropin and normal or reduced thyroxine and/or triiodothyronine levels) is worthwhile. Screening with a serum thyrotropin level is usually sufficient. Of importance, hypothyroidism itself rarely causes more than mild obesity. Glucose and insulin studies Obesity is associated with insulin resistance and increased serum levels of fasting insulin and C-peptide serum levels. However, insulin levels are normal in many persons who are obese. All patients with obesity should be screened for diabetes. Additional infor Continue reading >>
Leptin Levels And Insulin Sensitivity In Obese And Non-obese Patients With Polycystic Ovary Syndrome
The study was conducted to assess leptin levels and insulin sensitivity in obese and non-obese patients with polycystic ovary syndrome (PCOS). Twenty-two women with PCOS and 19 control healthy women were included in the study, divided into obese and non-obese groups. Leptin was determined using Linco Research radioimmunoassay while insulin sensitivity was calculatedfrom intravenous glucose tolerance tests with frequent blood sampling using MINMOD analysis. Significantly higher basal leptin levels were found in obese compared to non-obese PCOS (31.76 ± 3.06 vs. 10.42 ± 2.31 ng/ml; p < 0.05) as well as in obese in comparison to non-obese controls(29.16 ± 5.06 vs 8.51 ± 0.88 ng/ml; p < 0.05). A negative correlation was found between insulin sensitivity and leptin levels in both obese (r = -0.2480; p > 0.05) and non-obese PCOS groups (t = -0.4620; p > 0.05). In conclusion, high serum leptin, insulin and testosterone levels together with reduced insulin sensitivity were found in obese PCOS women, suggesting that high leptin levels could be a characteristic of the obese PCOS phenotype. Continue reading >>
Role Of Ghrelin, Leptin And Insulin Resistance In Development Of Metabolic Syndrome In Obese Patients
1Department of Internal Medicine, Faculty of Medicine, Taif University and Tanta University, Egypt 2Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz and Tanta University, Egypt 3Department of Clinical Pathology, Faculty of Medicine, Azhar University, Egypt Citation: Mohamed WS, Hassanien MA, Sayed Abokhosheim KEL (2014) Role of Ghrelin, Leptin and Insulin Resistance in Development of Metabolic Syndrome in Obese Patients. Endocrinol Metab Synd 3:122. doi: Copyright: © 2014 Mohamed WS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Endocrinology & Metabolic Syndrome Abstract Objective: Obesity and its complications including metabolic syndrome (MetS) have been increased in children and adolescents recently. Leptin is known to play an important role in the pathogenesis of obesity. The objective of this study was to evaluate the relationship between Leptin, Ghrelin and Insulin resistance in the development of metabolic syndrome in obese persons. Methods: this study was carried out on fifty obese persons. All patients have BMI ≥ 30 Kg/m2. Twenty of them have metabolic syndrome. Body Mass Index (BMI), Waist Circumference (WC), and blood pressure were measured. Fasting Plasma Glucose (FBG), two hours Post Prandial Blood Glucose (PPBG), Glycated hamoglobin A1C (HbA1c), triglyceride (TG), Total Cholesterol (TC), high and low density lipoprotein cholesterol (HDL-C and LDL-C), serum Leptin, Ghrelin and Insulin were done. HOMA-IR and HOMA- β were calculated. Results: SBP, DBP, FBS, PPBG, HbA1c, HOMA-IR and HOMA-β were signific Continue reading >>
