Impact of NMT1 Gene Polymorphisms on Features of the Metabolic Syndrome among Severely Obese Patients.
The NMT1 gene, located on chromosome 17, encodes the enzyme N-myristoyltransferase 1 (NMT1). It catalyzes the irreversible reaction of myristoylation, which makes a specific covalent linkage between myristic acid, a 14-carbon saturated fatty acid, and the NH2-terminal glycine of a protein. For many proteins, myristoylation is essential for stability and functions, such as protein-protein interactions, membrane attachment and cellular localization.
To our knowledge, the present study is the first to present data suggesting a potential role for NMT1 in lipoprotein and cholesterol metabolism, and it is particularly relevant as plasma lipid alterations are major elements of obesity and associated health risk factors.
Knowing that NMT1 is overexpressed and hypermethylated in VAT of MetS+ compared to MetS- obese patients, the current study reveals the associations between SNPs within this gene and obesity-related metabolic complications. Additionally, the data related to gene methylation and expression levels suggest potential mechanisms linking NMT1 gene variations to MetS risk factors.
Insulin resistant adipose tissue with limited expandability and lipid storage capacity eventually
leads to systemic insulin resistance, involving of course other important sites of glucose uptake such as skeletal muscle, due to excessive postprandial non-esterified fatty acid spillover to non adipose tissues and inflammatory mechanisms. Hyperglycemia and dyslipidemia eventually emerge as major consequences of these alterations. Similar mechanisms may also partly apply to
hypertension which is related to obesity and insulin resistance.
Obes Res Open J. 2015; 2(4): 101-110. doi: 10.17140/OROJ-2-116
