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Metabolic syndrome, diabetes and atherosclerosis: influence of gene-environment interaction
1CNR Institute of Clinical Physiology, G. Pasquinucci Hospital, Via Aurelia Sud, Massa, Italy. andreas@ifc.cnr.it
Insights
Gene-environment interactions influence susceptibility to cardiovascular disease (CVD), metabolic syndrome, and type 2 diabetes. Understanding these links can personalize prevention strategies for better cardiovascular risk management.
Area of Science:
- Cardiovascular disease research
- Metabolic syndrome
- Diabetes pathogenesis
- Gene-environment interactions
Background:
- Cardiovascular disease (CVD) is a leading cause of mortality globally, despite diagnostic advances.
- Metabolic syndrome, characterized by visceral obesity, insulin resistance, dyslipidemia, and hypertension, is a key risk factor for type 2 diabetes and atherosclerotic CVD.
- Inter-individual variations in disease susceptibility and onset age suggest a complex interplay between genetic and environmental factors.
Purpose of the Study:
- To review current knowledge on gene-environment interactions in the pathogenesis of metabolic syndrome, diabetes, and CVD.
- To highlight specific genes (e.g., PPAR-gamma, ADH1C, APOE, GSTs) modified by diet and lifestyle.
- To explore the role of xenobiotic metabolizing enzymes and environmental toxicants in CVD development.
Main Methods:
- Literature review focusing on gene-environment interactions.
- Analysis of studies examining specific genes (PPAR-gamma, ADH1C, APOE, GSTs) and their modification by diet, alcohol, and smoking.
- Examination of research on genetic variants of xenobiotic metabolizing enzymes and environmental toxicants.
Main Results:
- Certain genes (PPAR-gamma, ADH1C, APOE, GSTs) are significantly influenced by dietary habits, alcohol consumption, and smoking.
- Limited understanding exists regarding the role of genetic variants in xenobiotic metabolism and their interaction with environmental toxicants in CVD.
- Individual differences in detoxifying environmental toxicants may play a crucial role in CVD development.
Conclusions:
- Gene-environment interactions are critical in the development of metabolic syndrome, diabetes, and CVD.
- Further research into environmental toxicants and detoxification pathways is needed for "environmental cardiology".
- This knowledge is vital for improving cardiovascular risk stratification and developing personalized intervention programs.
Abstract:
Despite remarkable progress in diagnosis and understanding of risk factors, cardiovascular disease (CVD) remains still the leading cause of morbidity and mortality in the world's developed countries. The metabolic syndrome, a cluster of risk factors (visceral obesity, insulin resistance, dyslipidaemia, and hypertension), is increasingly being recognized as a new risk factor for type 2 diabetes and atherosclerotic cardiovascular disease. Nevertheless, there is wide variation in both the occurrence of disease and age of onset, even in individuals who display very similar risk profiles. There is now compelling evidence that a complex interplay between genetic determinants and environmental factors (still largely unknown) is the reason for this large inter-individual variation in disease susceptibility. The purpose of the present review is to describe the current status of our knowledge concerning the gene-environment interactions potentially implicated in the pathogenesis of metabolic syndrome, diabetes and cardiovascular disease. It focuses predominantly on studies of genes (peroxisome proliferator-activated receptor-gamma, alcohol dehydrogenase type 1C, apolipoprotein E, glutathione S-transferases T1 and M1) that are known to be modified by dietary and lifestyle habits (fat diet, intake of alcohol and smoking habit). It also describes the limited current understanding of the role of genetic variants of xenobiotic metabolizing enzymes and their interactions with environmental toxicants. Additional studies are needed in order to clarify whether inter-individual differences in detoxification of environmental toxicants may have an essential role in the development of CVD and contribute to the emerging field of "environmental cardiology". Such knowledge may be particularly relevant for improving cardiovascular risk stratification and conceiving the development of "personalized intervention program".
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