Abstract
The increased prevalence of obesity and type 2 diabetes (T2D) has become an important factor affecting the health of the human. Obesity is commonly considered as a major risk factor for the development of T2D. However, the molecular mechanisms of the disease relations are not well discovered yet. In this study, the combination of multiple differential expression profiles and a comprehensive biological network of obesity and T2D allowed us to identify and compare the disease-responsive active modules and subclusters. The results demonstrated that the connection between obesity and T2D mainly relied on several pathways involved in the digestive metabolism, immunization, and signal transduction, such as adipocytokine, chemokine signaling pathway, T cell receptor signaling pathway, and MAPK signaling pathways. The relationships of almost all of these pathways with obesity and T2D have been verified by the previous reports individually. We also found that the different parts in the same pathway are activated in obesity and T2D. The association of cancer, obesity, and T2D was identified too here. As a conclusion, our network-based method not only gives better support for the close connection between obesity and T2D, but also provides a systemic view in understanding the molecular functions underneath the links. It should be helpful in the development of new therapies for obesity, T2D, and the associated diseases.
Highlights
A sedentary life-style coupled with calorie-dense dietary behavior of contemporary human causes the accumulation of body fat
The latest National Health and Nutrition Examination Survey (NHANES) program estimated that the prevalence of obesity in adults has reached 36% in the United State [2], while the global incidence of diabetes mellitus is expected to increase to 366 million cases by the year 2030 [3]
Very few disease genes have been reported in both obesity and diabetes, such as PPARG [8, 9] and UCP3 [10]
Summary
A sedentary life-style coupled with calorie-dense dietary behavior of contemporary human causes the accumulation of body fat. The prevalence of obesity increased rapidly in industrialized societies with its undesirable consequences such as type 2 diabetes (T2D), high blood pressure, and heart diseases [1]. It has been reported that the altered glucose and lipid metabolism in liver, skeletal muscles, and adipose tissues with the disorganized insulin signals lead to the systemic and chronic inflammation [4, 5]. They recognized that the obesity-caused metabolic inflammation could connect obesity to the insulin resistance (IR), which is associated with T2D [6, 7]. The molecular mechanism in the association between obesity and diabetes is still far from being fully understood
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