Abstract
Type-2 diabetes and obesity are among the leading human diseases and highly complex in terms of diagnostic and therapeutic approaches and are among the most frequent and highly complex and heterogeneous in nature. Based on epidemiological evidence, it is known that the patients suffering from obesity are considered to be at a significantly higher risk of type-2 diabetes. There are several pieces of evidence that support the hypothesis that these diseases interlinked and obesity may aggravate the risk(s) of type-2 diabetes. Multi-level unwanted alterations such as (epi-) genetic alterations, changes at the transcriptional level, and altered signaling pathways (receptor, cytoplasmic, and nuclear level) are the major sources that promote several complex diseases, and such a heterogeneous level of complexity is considered as a major barrier in the development of therapeutics. With so many known challenges, it is critical to understand the relationships and the shared causes between type-2 diabetes and obesity, and these are difficult to unravel and understand. For this purpose, we have selected publicly available datasets of gene expression for obesity and type-2 diabetes, have unraveled the genes and the pathways associated with the immune system, and have also focused on the T-cell signaling pathway and its components. We have applied a simplified computational approach to understanding differential gene expression and patterns and the enriched pathways for obesity and type-2 diabetes. Furthermore, we have also analyzed genes by using network-level understanding. In the analysis, we observe that there are fewer genes that are commonly differentially expressed while a comparatively higher number of pathways are shared between them. There are only 4 pathways that are associated with the immune system in case of obesity and 10 immune-associated pathways in case of type-2 diabetes, and, among them, only 2 pathways are commonly altered. Furthermore, we have presented SPNS1, PTPN6, CD247, FOS, and PIK3R5 as the overexpressed genes, which are the direct components of TCR signaling.
Highlights
Type 2 diabetes (T2D) is a global epidemic that is strongly correlated with obesity [1, 2]
The data have been collected from the public database, and we have performed a comparative analysis in terms of altered gene expression patterns and their respective functions
In terms of the altered functions, they share 14 pathways, and the T2D- and obesity-specific pathways have 17 and 18 (Figure 1B, Table 1), respectively. It appears that there are only a few genes that are differentially expressed in both cases, while in terms of biological functions, a large number of pathways are affected, which means that T2D and obesity share more biological functions in terms of alterations and their source of alterations, i.e., differentially expressed genes (DEGs) are not shared at a large scale
Summary
Type 2 diabetes (T2D) is a global epidemic that is strongly correlated with obesity [1, 2]. There are a number of works where the crosstalk between the immune system and metabolism have been presented alongside evidence that supports the hypothesis that these diseases are interlinked and that obesity may aggravate the risk(s) of T2D [5,6,7,8] In such cases, it is critical to understand multi-level unwanted alterations such as (epi-)genetic alterations, changes at the transcriptional level, and altered signaling pathways (receptor, cytoplasmic, and nuclear level). It is critical to understand multi-level unwanted alterations such as (epi-)genetic alterations, changes at the transcriptional level, and altered signaling pathways (receptor, cytoplasmic, and nuclear level) These are the major sources that promote a number of complex diseases and such heterogeneous complexities are considered the major barrier in the development of therapeutic approaches. It is crucial to understand and unravel the relationships and the common causes between type-2 diabetes and obesity [9,10,11,12,13]
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