Gene–Nutrient Interactions in the Metabolic Syndrome

Abstract

The metabolic syndrome (MetS) is a very common disease associated with an increased risk of type 2 diabetes mellitus and cardiovascular disease. The diverse clinical characteristics of the MetS illustrate the complexity of the disease process, which involves several dysregulated metabolic pathways. Thus, multiple genetic targets must be involved in the pathogenesis and progression of the disease. Research indicates a major role for genetic susceptibility to the MetS. However, the human genome has not changed markedly in the last decade but the prevalence of the condition has increased exponentially, illustrating the importance of gene–environmental interactions. Dietary fat is an important environmental factor which can modify the development of the MetS. Genetic background can interact with habitual dietary fat composition, affecting predisposition to the MetS. Recent research indicates that currently ineffective therapeutic dietary recommendations may require a ‘personalised nutrition’ approach, wherein the genetic profile may determine the responsiveness of patients to specific dietary fatty acid interventions. Understanding the biological impact of gene–nutrient interactions will provide a key insight into the pathogenesis and progression of diet-related polygenic disorders, including the MetS. This review will explore the interactions between genetic background and dietary exposure/nutritional therapy.

A CLA enriched diet improves organ damage associated with the metabolic syndrome in spontaneous hypertensive rats

“…This phenomenon could explain the absence of excessive fat in the hepatocytes of animals that received dietary CLA. Similarly, studies at the molecular level suggest that there are regulatory genes that can be triggered by dietary fatty acids (Belury et al, 2002;Phillips et al, 2008). Probably the lack of hepatic steatosis in the parenchyma of the animals that received the CLA was caused by regulatory genes activated in the presence of polyunsaturated fatty acids, such as p65 and NFkBα (Belury et al, 2002;Chen 2004;Phillips et al, 2008); however, it is necessary to pursue additional studies to support this.…”

“…Because resistance to insulin also results in the relative non-suppression of adipocyte hormonesensitive lipase, there is a further enhancement of lipolysis and increased FFA concentration. Thus, a vicious circle of lipolysis, increased FFA, insulin resistance, and inflammation is formed (Dandona et al, 2005;Roche, 2005;Phillips et al, 2008).…”

Dietary Patterns and Metabolic Syndrome in Children and Adolescents: A Systematic Review

“…Given the role of gene-nutrient interaction in the occurrence and prevention of MetS, the association between MetS and ethnic groups and culture and changes in food preferences, food availability, and the dietary pattern over time (36)(37)(38), it is recommended to provide new dietary patterns that would obtain their main components from the mentioned healthier diets such as MDP or DASH and have more complementary items that are derived from the regional studies of each population as well as the findings of recent studies. Thus, taking such dietary patterns in early life, which should be updated frequently, would properly prevent the increasing occurrence of MetS both during childhood and adulthood.…”

Cardiometabolic Syndrome

“…Recent research indicates that currently ineffective therapeutic dietary recommendations may require a 'personalised nutrition' approach, wherein the genetic profile may determine the responsiveness of patients to specific dietary fatty acid interventions [98].…”