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Predicting insulin resistance using the triglyceride-to-high-density lipoprotein cholesterol ratio in Taiwanese adults
Jui-Kun Chiang, Ning-Sheng Lai, Jiunn-Kae Chang, Malcolm Koo
Cardiovascular Diabetology , 2011, DOI: 10.1186/1475-2840-10-93
Abstract: A total of 812 subjects were recruited from at the time of their general health examination at the Buddhist Dalin Tzu Chi General Hospital, Taiwan. Demographic information and clinical characteristics were obtained. Insulin resistance was defined by the homeostasis model assessment for insulin resistance (HOMA-IR). Simple and multiple logistic regression analyses were used to obtain probabilities of insulin resistance (HOMA-IR > 2) using TG/HDL-C with (Model 2) and without (Model 1) other clinical variables. A receiver operating characteristic (ROC) analysis was conducted to evaluate the ability of the two models to correctly discriminate between subjects of low and elevated HOMA-IR.Female sex, greater waist circumferences, and higher ALT levels were significantly associated with the risk of elevated HOMA-IR in addition to TG/HDL-C in the multiple logistic regression (Model 2). The area under the ROC curve (AUC) of Model 2 was 0.71 [95% CI = 0.67-0.75] and was significantly higher (P = 0.007) than the AUC 0.66 [95% CI = 0.62-0.71] of Model 1.The diagnostic accuracy of insulin resistance, defined by HOMA-IR, using TG/HDL-C can be significantly enhanced by including three additional clinically available factors - sex, waist circumferences, and ALT levels.Metabolic syndrome is characteristically defined as a clustering condition of cardiovascular risk factors including hyperglycemia, dyslipidemia, hypertension, and central obesity [1]. Its occurrence is strongly associated with increased risk in the development of diabetes and cardiovascular disease. A recent meta-analysis of 87 prospective observational studies reported that metabolic syndrome was associated with a two-fold increase in cardiovascular disease outcomes and a 50% increase in risk of all-cause mortality [2].The pathophysiology of the metabolic syndrome remains a subject of controversy but many of its features are associated with insulin resistance. It is typically defined as decreased sensitivity or respo
Insulin resistance increases the occurrence of new cardiovascular events in patients with manifest arterial disease without known diabetes. The SMART study
Sandra N Verhagen, Annemarie MJ Wassink, Yolanda van der Graaf, Petra M Gorter, Frank LJ Visseren, the SMART Study Group
Cardiovascular Diabetology , 2011, DOI: 10.1186/1475-2840-10-100
Abstract: Prospective cohort study in 2611 patients with manifest arterial disease without known diabetes. Homeostasis model of insulin resistance (HOMA-IR) was used to quantify insulin resistance. The relation of HOMA-IR with cardiovascular events (vascular death, myocardial infarction or stroke) and all cause mortality was assessed with Cox regression analysis. In additional models adjustments were performed for the single components constituting the metabolic syndrome and for inflammation.HOMA-IR increases with the number of metabolic syndrome components (mean HOMA-IR ± SD in groups with 0, 1, 2, 3, 4 and 5 metabolic syndrome components: 1.4 ± 0.7; 1.8 ± 1.2; 2.4 ± 1.5; 3.1 ± 1.8; 4.0 ± 2.6; and 5.6 ± 3.6 respectively). High HOMA-IR was independently associated with an increased risk of cardiovascular events (tertile 2 vs. 1 HR 1.92; 95%CI 1.20-3.08) (tertile 3 vs.1 HR 1.78; 95%CI 1.10-2.89) and with all cause mortality (tertile 2 vs. 1 HR 1.80; 95%CI 1.04-3.10) (tertile 3 vs.1 HR 1.56; 95%CI 0.88-2.75). These relations were not influenced by the individual components of metabolic syndrome or by inflammation.In patients with manifest arterial disease without known diabetes, insulin resistance increases with the number of metabolic syndrome components, and elevated insulin resistance increases the risk of new cardiovascular events.Both insulin resistance and metabolic syndrome are recognized as important factors in the development of cardiovascular disease [1,2]. Obesity-induced insulin resistance is considered to be the major driver of the clustering of interrelated metabolic disturbances (e.g. dyslipidemia, hyperglycemia, elevated blood pressure)[3], often referred to as metabolic syndrome [4], thereby leading to an increased cardiovascular risk. Although insulin resistance may be the unifying pathophysiological mechanism underlying the metabolic syndrome [5], there is uncertainty regarding the independent role of insulin resistance in the development of atherosclerotic v
Breastfeeding and Its Prospective Association with Components of the GH-IGF-Axis, Insulin Resistance and Body Adiposity Measures in Young Adulthood – Insights from Linear and Quantile Regression Analysis  [PDF]
Anke L. B. Günther, Helena Walz, Anja Kroke, Stefan A. Wudy, Christina Riedel, Rüdiger von Kries, Gesa Joslowski, Thomas Remer, Guo Cheng, Anette E. Buyken
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0079436
Abstract: Background Breastfeeding may lower chronic disease risk by long-term effects on hormonal status and adiposity, but the relations remain uncertain. Objective To prospectively investigate the association of breastfeeding with the growth hormone- (GH) insulin-like growth factor- (IGF) axis, insulin sensitivity, body composition and body fat distribution in younger adulthood (18–37 years). Design Data from 233 (54% female) participants of a German cohort, the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study, with prospective data on infant feeding were analyzed. Multivariable linear as well as quantile regression were performed with full breastfeeding (not: ≤2, short: 3–17, long: >17 weeks) as exposure and adult IGF-I, IGF binding proteins (IGFBP) -1, -2, -3, homeostasis model assessment of insulin resistance (HOMA-IR), fat mass index, fat-free mass index, and waist circumference as outcomes. Results After adjustment for early life and socio-economic factors, women who had been breastfed longer displayed higher adult IGFBP-2 (ptrend = 0.02) and lower values of HOMA-IR (ptrend = 0.004). Furthermore, in women breastfeeding duration was associated with a lower mean fat mass index (ptrend = 0.01), fat-free mass index (ptrend = 0.02) and waist circumference (ptrend = 0.004) in young adulthood. However, there was no relation to IGF-I, IGFBP-1 and IGFBP-3 (all ptrend>0.05). Associations for IGFBP-2 and fat mass index were more pronounced at higher, for waist circumference at very low or high percentiles of the distribution. In men, there was no consistent relation of breastfeeding with any outcome. Conclusions Our data suggest that breastfeeding may have long-term, favorable effects on extremes of adiposity and insulin metabolism in women, but not in men. In both sexes, breastfeeding does not seem to induce programming of the GH-IGF-axis.
Insulin Resistance in Liver Diseases
M Irshad,Khushboo Irshad,Prashant Nag
Macedonian Journal of Medical Sciences , 2011,
Abstract: Present report gives a brief and consolidated review of insulin resistance developed in chronic liver diseases. Insulin resistance remains an important feature of chronic liver diseases and progresses disease towards fibrogenesis. Of hepatitis viral infections, hepatitis C virus (HCV) was reported to have a significant role in inducing insulin resistance. Both viral particles as such, as well its structural components induce insulin resistance. Hepatitis C virus core protein, specially, causes insulin resistance via its direct action on insulin signaling cascade as well as by inducing over expression of certain cytokines including TNF-alpha. Insulin resistance has a direct relation with liver steatosis and oxidative stress. Both steatosis and oxidative stress enhances insulin resistance and vice-a-versa. Insulin resistance has widespread implications on metabolism and needs its correction before planning therapeutic regimen in liver diseases.
Insulin Resistance: Causes And Metabolic Implications
OG Igharo, K Ikeke, AE Ubhenin
Benin Journal of Postgraduate Medicine , 2009,
Abstract: Insulin is an anabolic hormone that plays key roles in glucose metabolism. Insulin resistance is a decreased biological response to normal concentration of circulating insulin. In insulin resistance, normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells results in hydrolysis of stored triglycerides, which elevates free fatty acids in the blood plasma. In muscles, it reduces glucose uptake, whereas in the liver, it reduces glucose storage with both effects serving to elevate blood glucose. High plasma levels of Insulin and glucose due to Insulin resistance often lead to metabolic syndrome and type 2 diabetes mellitus. The cause of the vast majority of cases of insulin resistance remains unknown. However, it is claimed that insulin resistance might be caused by a high carbohydrate diet. Studies have shown that glucosamine (often prescribed for joint problems) may cause Insulin resistance. It is also reported that insulin resistance occurrence in a population increased as sugar consumption and addition of high fructose corn syrup to diets increased. Physical inactivity and obesity have been implicated as factors, which aggravate insulin resistance. The presumption that a defect in specific gene may cause insulin resistance is still under investigation.
Idiopathic Hirsutism and Insulin Resistance  [PDF]
Afsaneh Talaei,Zahra Adgi,Mahnaz Mohamadi Kelishadi
International Journal of Endocrinology , 2013, DOI: 10.1155/2013/593197
Abstract: Background and Objectives. Polycystic ovary syndrome (PCOS) and idiopathic hirsutism (HI) are the two most common causes of hirsutism. Insulin resistance plays a key role in PCOS, but there are not enough data showing that patients with HI also have insulin resistance. This study was designed to evaluate the presence of insulin resistance in women with HI. Methods. Based on a cross-sectional study, two groups of age-BMI matched, hirsute women were compared to age-BMI matched, nonhirsute women. Sixty nonobese women with PCOS, thirty nonobese women with HI, and sixty nonobese control women were included in the study. Samples of hormones including androgens were measured. Insulin resistance based on homeostasis model assessment of insulin resistance (HOMA-IR) was compared between three groups by the Kruskal-Wallis test. Results. Patients with PCOS had significantly higher basal insulin level ( versus ?μIu/mL) and HOMA-IR score ( versus ) than patients with HI ( ). Patients with HI also had significantly higher basal insulin level and HOMA-IR score than control group ( ). Conclusion. Our data suggest that both PCOS and HI are associated with insulin resistance and these patients are more insulin resistant than healthy control people. 1. Introduction Hirsutism, the presence of terminal hairs in females in a male-like pattern, is a common clinical condition which affects 5–10% of women of reproductive age. Hirsutism is extremely distressing for patients and has a significant negative impact on their psychosocial development [1]. Polycystic ovary syndrome (PCOS) and idiopathic hirsutism (HI) are the two most common causes of hirsutism [2]. PCOS is the most common endocrinopathy in women which is characterized by hyperandrogenemia and chronic anovulation [3]. Women with PCOS demonstrate marked clinical heterogeneity; the commonly associated features such as hirsutism, acne, polycystic-appearing ovaries, obesity, and acanthosis nigricans are neither uniform nor universal [4]. Insulin resistance and compensated hyperinsulinemia are the most features of PCOS [5]. According to some studies, the prevalence of diabetes, hypertension, hyperlipidemia, and cardiovascular disease is much more in PCOS patients than in general population [6]. Regarding the role of insulin resistance in PCOS, insulin resistance-lowering drugs are usually used to manage PCOS [7–9]. Rotterdam criteria have been generally used to describe PCOS, based on the exclusion of other androgen excess disorders and the presence of any two of oligoovulation or anovulation, clinical and/or biochemical
Adipokines and Hepatic Insulin Resistance  [PDF]
Yu Li,Lin Ding,Waseem Hassan,Daoud Abdelkader,Jing Shang
Journal of Diabetes Research , 2013, DOI: 10.1155/2013/170532
Abstract: Obesity is a major risk factor for insulin resistance and type 2 diabetes. Adipose tissue is now considered to be an active endocrine organ that secretes various adipokines such as adiponectin, leptin, resistin, tumour necrosis factor- , and interleukin-6. Recent studies have shown that these factors might provide a molecular link between increased adiposity and impaired insulin sensitivity. Since hepatic insulin resistance plays the key role in the whole body insulin resistance, clarification of the regulatory processes about hepatic insulin resistance by adipokines in rodents and human would seem essential in order to understand the mechanism of type 2 diabetes and for developing novel therapeutic strategies to treat it. 1. Introduction In many developed and developing countries, obesity has reached epidemic proportions, resulting in an increasing prevalence of type 2 diabetes characterized by insulin resistance of peripheral tissues such as liver, muscle, and fat which cannot be overcome by hypersecretion of pancreatic beta cells [1]. One survey conducted in 2000 revealed that more than 150 million people in the world suffered from type 2 diabetes [2] and 80% of these cases were related to obesity. Because various studies have demonstrated that hepatic insulin resistance plays a central role in the development of type 2 diabetes and obesity is centrally involved in increasing the clinical risk of diabetes, visceral adipose tissue is now thought to provide a link between obesity and hepatic insulin resistance. Adipose tissue was traditionally regarded as a passive energy reservoir. However, since the discovery of leptin and subsequent identification of other adipose tissue-derived cytokines (e.g., adiponectin and resistin) in the last two decades [3], it became clear that adipose tissue is an active endocrine organ. Obese adipose tissue also secretes various inflammatory cytokines, such as interleukin-6 (IL-6) and tumour necrosis factor- (TNF- ) [4]. All of these cytokines, termed adipokines, act in an autocrine, paracrine, or endocrine fashion to control various metabolic functions. Some of these adipokines have been implicated in the development of hepatic insulin resistance. Indeed, they may act locally or distally to alter insulin sensitivity in insulin-targeted organs such as liver which is also discussed in detail by Marra and Bertolani [5] previously or may act through neuroendocrine, autonomic, or immune pathways. For example, activation of proinflammatory pathways in adipose tissue is known to interfere with insulin signaling and induce
Insulin Resistance: From Theory To Practice  [cached]
Srinivas Kakkilaya Bevinje
Online Journal of Health & Allied Sciences , 2006,
Abstract: Insulin resistance is at the core of the well recognised metabolic syndrome and possibly many other ailments commonly seen in the modern society. While the quantification of insulin resistance remains a difficult task, the problems associated with it are increasing in epidemic proportions. Need of the hour therefore is to develop concise dietary and pharmacological guidelines for for prevention and management of insulin resistance
Microarray Evidences the Role of Pathologic Adipose Tissue in Insulin Resistance and Their Clinical Implications  [PDF]
Sandeep Kumar Mathur,Priyanka Jain,Prashant Mathur
Journal of Obesity , 2011, DOI: 10.1155/2011/587495
Abstract: Clustering of insulin resistance and dysmetabolism with obesity is attributed to pathologic adipose tissue. The morphologic hallmarks of this pathology are adipocye hypertrophy and heightened inflammation. However, it's underlying molecular mechanisms remains unknown. Study of gene function in metabolically active tissues like adipose tissue, skeletal muscle and liver is a promising strategy. Microarray is a powerful technique of assessment of gene function by measuring transcription of large number of genes in an array. This technique has several potential applications in understanding pathologic adipose tissue. They are: (1) transcriptomic differences between various depots of adipose tissue, adipose tissue from obese versus lean individuals, high insulin resistant versus low insulin resistance, brown versus white adipose tissue, (2) transcriptomic profiles of various stages of adipogenesis, (3) effect of diet, cytokines, adipokines, hormones, environmental toxins and drugs on transcriptomic profiles, (4) influence of adipokines on transcriptomic profiles in skeletal muscle, hepatocyte, adipose tissue etc., and (5) genetics of gene expression. The microarray evidences of molecular basis of obesity and insulin resistance are presented here. Despite the limitations, microarray has potential clinical applications in finding new molecular targets for treatment of insulin resistance and classification of adipose tissue based on future risk of insulin resistance syndrome.
Body trunk fat and insulin resistance in post-pubertal obese adolescents
Santos, Luana Caroline dos;Cintra, Isa de Pádua;Fisberg, Mauro;Martini, Lígia Araújo;
Sao Paulo Medical Journal , 2008, DOI: 10.1590/S1516-31802008000200004
Abstract: context and objective: insulin resistance is a metabolic disorder commonly associated with excess body fat accumulation that may increase chronic disease risk. the present study was undertaken to evaluate the relationship between body composition and insulin resistance among obese adolescents. design and setting: cross-sectional study, at the adolescence center, pediatric department, universidade federal de s?o paulo. methods: body composition was assessed using dual-energy x-ray absorptiometry. dietary intake was evaluated using a three-day dietary record. the biochemical evaluation comprised glucose, insulin, serum lipid, leptin and ghrelin measurements. insulin resistance was calculated by means of the homeostasis model assessment of insulin resistance (homa-ir). results: forty-nine post-pubertal obese adolescents participated in the study: 12 boys and 37 girls of mean age 16.6 (1.4) years and mean body mass index (bmi) of 35.0 (3.9) kg/m2. the mean glucose, insulin and homa values were 90.3 (6.4) mg/dl, 16.6 (8.1) μiu/ml and 3.7 (1.9), respectively. hyperinsulinemia and insulin resistance were observed in 40.2% and 57.1% of the subjects, respectively. adolescents with insulin resistance had higher bmi and body trunk fat. there was a trend towards higher leptin concentration in obese individuals with insulin resistance. insulin resistance was positively correlated with body trunk fat, bmi, body fat mass (kg), leptin and body fat percentage. furthermore, there was a negative correlation between homa-ir and lean body mass. the body composition predicted 30% of the homa-ir levels, according to linear regression models. conclusion: body trunk fat was significantly associated with insulin resistance, demonstrating the clinical importance of abdominal obesity during adolescence.
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