Epigenetics of diabetes Type 2 have shown that miRNAs have pivotal roles in many different gene regulatory pathways. A subset of miRNAs has been shown to be involved in metabolic regulation of glucose homeostasis and in epigenetics of diabetes type 2. Pancreatic islet-specific miR-375 inhibits insulin secretion in mouse pancreatic β-cells by inhibiting the expression of the protein myotrophin. An overexpression of miR-375 can completely suppress glucose-induced insulin secretion, while inhibition of native miR-375 will increase insulin secretion. In another study, increasing the level of miR-9, a different miRNA, resulted in a severe defect in glucose-stimulated insulin release. This happens because miR-9 down-regulated the transcription
Epigenetics of diabetes Type 2 re-methylated to form methionine, be taken into the cysteine biosynthetic pathway, or be freed into the extracellular medium. When a person lacks sulfur in their diet, it prompts the body to use methionine and form cysteine. This in turn increases the risk of a person contracting type 2 diabetes later in life. The reason behind this turns out to be rather simple. Methionine directly affects S-adenosyl methionine (SAM) levels. SAM is the substance that provides the methyl groups for DNA methylation. A shortage of SAM leads to an inability to develop proper methylation patterns, and is thought to be an