Microarray Evidences the Role of Pathologic Adipose Tissue in Insulin Resistance and Their Clinical Implications. (28th April 2011)

• Record Type: Journal Article
• Authors: Mathur, Sandeep Kumar; Jain, Priyanka; Mathur, Prashant
• Other Names: Brinton Eliot Academic Editor.
• Is Part Of: Journal of obesity. Volume 2011(2011)
• Publication Date: 2011-04-28
• Subjects: Obesity -- Periodicals; Obesity; Obesity; Electronic journals; Periodicals; Periodicals; 616.398
• DOI: 10.1155/2011/587495
• Languages: English
• ISSNs: 2090-0708

Abstract

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.