Genetic links between diabetes mellitus and coronary atherosclerosis

Abstract

Diabetes mellitus is one of the most common endocrine disorders. It affects almost 6% of the world's population, and its prevalence continues to increase. The causes of diabetes mellitus are multifactorial, and in the general population both genetic and environmental factors contribute evenly to its development. Several genes have been consistently associated with type 2 diabetes mellitus; however, it is not clear how many of those translate into increased cardiovascular disease risk. Recent evidence suggests that genetic variation at the CALPN10, FABP4, GK, GST, PPARA, and PPARG loci may confer higher cardiovascular disease risk in patients with type 2 diabetes mellitus. However, the evidence is scattered and inconclusive and its translation into practical clinical testing will require studies properly designed to examine not only simple genetic associations but also gene-gene and gene-environment interactions.

Metabolic syndrome and coronary artery disease in young Egyptians presenting with acute coronary syndrome

“…This was in agreement with other authors who reported a prevalence of 72% in patients with acute coronary syndrome [22]. Moreover, others reported a prevalence of 46% in patients presenting with ACS in six Middle Eastern arabian countries [23].…”

Metabolic syndrome, platelet activation and the development of transient ischemic attack or thromboembolic stroke

“…A number of both genetic and environmental factors are thought to influence the development of metabolic syndrome although obesity and insulin resistance remains at the core of the etiology [27,49]. Importantly, not all obese individuals develop metabolic syndrome and not all metabolic syndrome patients are viscerally obese although these cases are in the minority [24].…”

Cardiovascular Disease Risk Factors in Youth With Diabetes Mellitus

“…20,406 Similarly, genetic variation in CALPN10, FABP4, GK, GST, PPARA, and PPARG may be associated with increased CVD risk in people with T2DM, but the evidence is inconclusive. 407 Family history of premature CVD is an established and independent risk factor for the development of CVD. 408,409 For example, the AHA scientific statement on cardiovascular risk reduction in high-risk pediatric populations 4 identifies a family history of premature coronary artery disease in expanded firstdegree pedigrees (corresponding to male family members <55 years of age and female family members <65 years of age) as a risk factor for CVD in patients with T1DM and T2DM.…”