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However, single nucleotide polymorphism (SNP) is one of many mechanisms that leads to increased risk for type 2 diabetes. To locate genes and loci that are responsible for the risk of type 2 diabetes, genome wide association studies (GWAS) was utilized to compare the genomes of diabetic patient group and the non-diabetic control group. [4]
Maturity-onset diabetes of the young (MODY) refers to any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production. [1] Along with neonatal diabetes , MODY is a form of the conditions known as monogenic diabetes.
The PPARGC1A gene regulates genes involved in energy metabolism. [1] [2] Since type 2 diabetes is characterized by chronic hyperglycaemia as a result of impaired pancreatic beta cell function [3] and insulin resistance in peripheral tissues, [4] it was thought that the gene might be downregulated in type 2 diabetes patients through DNA methylation.
Low IGF-1 levels are shown to increase the risk of developing type 2 diabetes and insulin resistance. [67] On the other hand, a high IGF-1 bioavailability in people with diabetes may delay or prevent diabetes-associated complications, as it improves impaired small blood vessel function. [67] IGF-1 has been characterized as an insulin sensitizer ...
MODY 2 or GCK-MODY is a form of maturity-onset diabetes of the young. [1] It is due to any of several mutations in the GCK gene on human chromosome 7 for glucokinase. [2] Glucokinase serves as the glucose sensor for the pancreatic beta cell. Normal glucokinase triggers insulin secretion as the glucose exceeds about 90 mg/dl (5 mM).
Studies with monkeys show that injecting high-insulin-producing forms of these cells into the animals can “cure” type-1 diabetes for about six months. Human trials are underway.
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