Abstract
The prevalence and the incidence of type 2 diabetes (T2D), representing >90% of all cases of diabetes, are increasing rapidly worldwide. Identification of individuals at high risk of developing diabetes is of great importance, as early interventions might delay or even prevent full-blown disease. T2D is a complex disease caused by multiple genetic variants in interaction with lifestyle and environmental factors. Cardiovascular disease (CVD) is the major cause of morbidity and mortality. Detailed understanding of molecular mechanisms underlying in CVD events is still largely missing. Several risk factors are shared between T2D and CVD, including obesity, insulin resistance, dyslipidemia, and hyperglycemia. CVD can precede the development of T2D, and T2D is a major risk factor for CVD, suggesting that both conditions have common genetic and environmental antecedents and that they share “common soil”. We analyzed the relationship between the risk factors for T2D and CVD based on genetics and population-based studies with emphasis on Mendelian randomization studies.
Highlights
Type 2 diabetes (T2D) has reached epidemic proportions
The authors found in their Mendelian randomization (MR) analysis that host genetic-driven increase in gut production of the short-chain fatty acids (SCFAs) butyrate was associated with improved insulin secretion
In an MR study by Malik et al [74] including 255,714 European ancestry participants without a history of Cardiovascular disease (CVD), the risk of incident CVD increased by 49%, coronary artery disease (CAD) by 50%, and stroke by 44% for every 10 mm Hg increase in genetically proxied systolic blood pressure
Summary
Type 2 diabetes (T2D) has reached epidemic proportions. According to the evaluation of the International Diabetes Federation, the number of individuals with diabetes will increase from 463 million adults in 2019 to 700 million by 2045 (https://www.idf.org/ access on 20 July2021) [1]. Several risk factors are shared between T2D and CVD, such as obesity, insulin resistance, dyslipidemia, and hyperglycemia [7]. A defect in insulin-mediated control of glucose metabolism in different tissues, prominently in muscle, adipose tissue, and liver, is one of the earliest manifestations of T2D and CVD. These diseases share intertwined metabolic abnormalities, including obesity, hyperinsulinemia, hyperglycemia, and hyperlipidemia [21]. Insulin resistance in different tissues is caused mainly by environmental and lifestyle factors, whereas only a few genetic variants for the risk of T2D identified in GWAS studies are associated with insulin resistance. This finding supports the notion that decreased insulin secretion is more important than decreased insulin sensitivity for the conversion to T2D
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