Insulin resistance at the crossroads of metabolic syndrome: Systemic analysis using microarrays

Kim, Eun-Jung

doi:10.1002/biot.201000048

Cited by 16 publications

(12 citation statements)

References 76 publications

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“…Some genetic work has recently shown promise. Although far from clinical use, microarray analysis of genes in muscle, adipose tissue and the liver shows alterations in the setting of IR [62] . Serum genetic markers may lead to future genetic techniques to detect and monitor IR.…”

Section: Assessment Of Insulin Resistancementioning

confidence: 99%

Assessing and treating insulin resistance in women with polycystic ovarian syndrome

Traub¹

2011

WJD

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Polycystic ovarian syndrome (PCOS) is a highly pre valent hormonal and metabolic disorder among repro ductive aged women worldwide. Women with PCOS have widely varying phenotypes and seek medical care for differing reasons. In addition to concern for men strual cycle function, ovulation, hirsutism and acne, many PCOS women have abnormal glucose metabolism. While diabetes mellitus and impaired glucose tolerance are easily diagnosed, the diagnosis of and concern for insulin resistance as a precursor disorder is under appreciated. Insulin resistance may be the first im portant marker of metabolic disease in PCOS women at risk for metabolic syndrome and coronary artery di sease.

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Section: Assessment Of Insulin Resistancementioning

confidence: 99%

Assessing and treating insulin resistance in women with polycystic ovarian syndrome

Traub¹

2011

WJD

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“…Most of these studies have focused on identifying the transcriptional changes underlying the pathophysiology of obesity, as well as the anti-obesity effects of dietary, pharmacological, and behavioral interventions (Sun 2007). In a consequence, thousands of genes differentially expressed between lean and obese individuals have been identified, including those related to the hepatic glucose and lipid metabolism, insulin signaling, inflammation, coagulation, cell adhesion, oxygen stress, and activity of chaperone (Sharma et al 2006; Greco et al 2008; Kim 2010; Naik et al 2013). On the contrary, a limited number of muscle transcriptomic studies have been reported so far.…”

Section: Introductionmentioning

confidence: 99%

“…In one series of them, a short-term feeding of mice with HFD changed the expression of more than 1,000 genes in the skeletal muscle (de Wilde et al 2008), but an 8-week HFD feeding induced rather small alterations in the muscle transcriptome, with up-regulation of only Fatty acid oxidation pathway (de Wilde et al 2009). Others studies revealed, however, that overall gene expression in muscle, involved in fatty acid oxidation and biosynthesis, was either decreased or obesity unresponsive (Kim 2010). …”

Section: Introductionmentioning

confidence: 99%

Mitochondrial-related proteomic changes during obesity and fasting in mice are greater in the liver than skeletal muscles

Nesteruk

Hennig

Mikula

et al. 2013

Funct Integr Genomics

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Although mitochondrial dysfunction is implicated in the pathogenesis of obesity, the molecular mechanisms underlying obesity-related metabolic abnormalities are not well established. We performed mitochondrial quantitative proteomic and whole transcriptome analysis followed by functional annotations within liver and skeletal muscles, using fasted and non-fasted 16- and 48-week-old high-fat diet (HFD)-fed and normal diet-fed (control group) wild-type C56BL/6J mice, and hyperphagic ob/ob and db/db obese mice. Our study identified 1,675 and 704 mitochondria-associated proteins with at least two peptides in liver and muscle, respectively. Of these, 221 liver and 44 muscle proteins were differentially expressed (adjusted p values ≤ 0.05) between control and all obese mice, while overnight fasting altered expression of 107 liver and 35 muscle proteins. In the liver, we distinguished a network of 27 proteins exhibiting opposite direction of expression changes in HFD-fed and hyperphagic mice when compared to control. The network centered on cytochromes P450 3a11 (Cyp3a11) and 4a14 (Cyp4a14), and fructose-bisphosphate aldolase B (Aldob) proteins which bridged proteins cluster involved in Metabolism of xenobiotics with proteins engaged in Fatty acid metabolism and PPAR signaling pathways. Functional annotations revealed that most of the hepatic molecular alterations, which characterized both obesity and fasting, related to different aspects of energy metabolism (such as Fatty acid metabolism, Peroxisome, and PPAR signaling); however, only a limited number of functional annotations could be selected from skeletal muscle data sets. Thus, our comprehensive molecular overview revealed that both obesity and fasting states induce more pronounced mitochondrial proteome changes in the liver than in the muscles.Electronic supplementary materialThe online version of this article (doi:10.1007/s10142-013-0342-3) contains supplementary material, which is available to authorized users.

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“…A multidisciplinary research effort involving a combination of clinical, biochemical and omics approaches appears mandatory to increase knowledge in the complexity of biological traits and processes associated with obesity [5]. Through probing of the transcriptional activity of tissues, the techniques allowing systematic analysis of AT gene expression have proved useful at identifying master genes [6] and regulatory networks involved in human obesity and related disorders [7]. Moreover, mRNAs are molecular species easily and evenly amplified.…”

Section: Introductionmentioning

confidence: 99%

Determinants of Human Adipose Tissue Gene Expression: Impact of Diet, Sex, Metabolic Status, and Cis Genetic Regulation

et al. 2012

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Weight control diets favorably affect parameters of the metabolic syndrome and delay the onset of diabetic complications. The adaptations occurring in adipose tissue (AT) are likely to have a profound impact on the whole body response as AT is a key target of dietary intervention. Identification of environmental and individual factors controlling AT adaptation is therefore essential. Here, expression of 271 transcripts, selected for regulation according to obesity and weight changes, was determined in 515 individuals before, after 8-week low-calorie diet-induced weight loss, and after 26-week ad libitum weight maintenance diets. For 175 genes, opposite regulation was observed during calorie restriction and weight maintenance phases, independently of variations in body weight. Metabolism and immunity genes showed inverse profiles. During the dietary intervention, network-based analyses revealed strong interconnection between expression of genes involved in de novo lipogenesis and components of the metabolic syndrome. Sex had a marked influence on AT expression of 88 transcripts, which persisted during the entire dietary intervention and after control for fat mass. In women, the influence of body mass index on expression of a subset of genes persisted during the dietary intervention. Twenty-two genes revealed a metabolic syndrome signature common to men and women. Genetic control of AT gene expression by cis signals was observed for 46 genes. Dietary intervention, sex, and cis genetic variants independently controlled AT gene expression. These analyses help understanding the relative importance of environmental and individual factors that control the expression of human AT genes and therefore may foster strategies aimed at improving AT function in metabolic diseases.

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Insulin resistance at the crossroads of metabolic syndrome: Systemic analysis using microarrays

Cited by 16 publications

References 76 publications

Assessing and treating insulin resistance in women with polycystic ovarian syndrome

Assessing and treating insulin resistance in women with polycystic ovarian syndrome

Mitochondrial-related proteomic changes during obesity and fasting in mice are greater in the liver than skeletal muscles

Determinants of Human Adipose Tissue Gene Expression: Impact of Diet, Sex, Metabolic Status, and Cis Genetic Regulation

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