Genetics, genomics, and diet interactions in obesity in the Latin American environment

Abstract

Obesity is a chronic disease characterized by abnormal or excessive fat accumulation that could impact an individual’s health; moreover, the World Health Organization (WHO) has declared obesity a global epidemic since 1997. In Latin America, in 2016, reports indicated that 24.2% of the adult population was obese. The environmental factor or specific behaviors like dietary intake or physical activity have a vital role in the development of a condition like obesity, but the interaction of genes could contribute to that predisposition. Hence, it is vital to understand the relationship between genes and disease. Indeed, genetics in nutrition studies the genetic variations and their effect on dietary response; while genomics in nutrition studies the role of nutrients in gene expression. The present review represents a compendium of the dietary behaviors in the Latin American environment and the interactions of genes with their single nucleotide polymorphisms (SNPs) associated with obesity, including the risk allele frequencies in the Latin American population. Additionally, a bibliographical selection of several studies has been included; these studies examined the impact that dietary patterns in Latin American environments have on the expression of numerous genes involved in obesity-associated metabolic pathways.

Crosstalk between Gut Microbiota and Epigenetic Markers in Obesity Development: Relationship between Ruminococcus, BMI, and MACROD2/SEL1L2 Methylation

“…There are various factors that have been shown to play a role in the pathophysiology and pathogenesis of obesity such as genetic susceptibility, dietary patterns, ethnic differences, antibiotic intake, and environmental factors. The environmental factors include increased energy intake, reduced consumption of high-fiber foods, and reduced physical activity due to a sedentary lifestyle [ 3 ]. Moreover, it has been reported that gut microbiota and their metabolites can modulate the pathogenesis of obesity and metabolic traits [ 4 ].…”

RNA-seq transcriptome profiling of pigs’ liver in response to diet with different sources of fatty acids

“…Bile acids in high concentrations are toxic (Jung et al, 2006). The CYP2B6 enzyme is involved in the reduction of bile acid toxicity, and the downregulation of the CYP7A1 enzyme is involved in the decrease in bile acid biosynthesis and is found in the endoplasmic reticulum of hepatocytes (Jung et al, 2006;Guevara-Ramírez et al, 2022). The CYP7A1 protein is of great importance in the metabolism of steroids, cholesterol, and other lipids (Guevara-Ramírez et al, 2022).…”

NOS1AP Gene Variants and Their Role in Metabolic Syndrome: A Study of Patients with Schizophrenia

“…It is believed that genes with different functional characteristics are involved in the development of MetS. Products of some genes play a role in the body’s energy metabolism, including, in particular, lipid metabolism: the apolipoprotein A5 gene ( ApoA5 ), the fat mass and obesity-associated gene ( FTO ), the fatty acid-binding protein 2 gene ( FABP2 ), the adipose triglyceride lipase gene ( ATGL ), the adiponectin gene ( ADIPOQ ), the adiponectin receptor gene ( ADIPOR2 ), and others [ 23 ]. Products of other genes are responsible for the formation of appetite and eating behavior ( TMEM18 , NEGR1 , and BDNF ) and are involved in inflammatory processes (potassium channel tetramerization domain-containing 15 [ KCTD15 ], MAF , and MAP2K5 ) [ 24 ].…”

“…At the same time, genes directly associated with mental disorders and genes responsible for metabolism regulation are considered potential markers of MetS in schizophrenia. According to a systematic review, for FTO and leptin and leptin receptor genes ( LEP and LEPR ), for the methylenetetrahydrofolate reductase ( MTHFR ) gene, and for the serotonin receptor 2C gene ( HTR2C ), there is strong evidence of association with MetS in schizophrenia patients [ 23 ]. In our previous papers, it has been demonstrated that polymorphisms in insulin-induced gene 2 ( INSIG2 ), LEP , FTO , dopamine D2 receptor ( DRD2 ), and 5-HT receptor genes may contribute to the development of metabolic disorders in schizophrenia [ 25 , 26 , 27 , 28 ].…”