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The GLUT1 protein that transports glucose across the blood brain barrier is encoded by the SLC2A1 gene, located on chromosome 1. [8] In GLUT1 deficiency syndrome, one of the two genes is damaged by a mutation and an insufficient amount protein is made. As a result, insufficient glucose is passing the blood brain barrier.
If a reduction in the amount of glucose-6-phosphate dehydrogenase or alteration of structure occurs due to the mutations of the G6PD gene, the enzyme loses its protective role and leads to the accumulation of reactive oxygen species and thus damages red blood cells. [6]
Induced mutations are alterations in the gene after it has come in contact with mutagens and environmental causes. Induced mutations on the molecular level can be caused by: Chemicals Hydroxylamine; Base analogues (e.g., Bromodeoxyuridine (BrdU)) Alkylating agents (e.g., N-ethyl-N-nitrosourea (ENU). These agents can mutate both replicating and ...
Inflammation-induced ROS that cause DNA damage can trigger apoptosis, [52] [53] but may also cause cancer if repair and apoptotic processes are insufficiently protective. [ 45 ] Bile acids , stored in the gall bladder, are released into the small intestine in response to fat in the diet.
Due to environmental conditions such as climate, diet, oxygen levels, light cycles, and mutagens or chemicals which are strongly related to disease susceptibility, genes expression can vary. [ 5 ] [ 6 ] The timing and duration of exposure to such elements is a critical factor as well as it can significantly impact the phenotypic response of an ...
Mutations of the gene for this enzyme can cause unusual forms of diabetes or hypoglycemia. Glucokinase (GK) is a hexokinase isozyme, related homologously to at least three other hexokinases. [4] All of the hexokinases can mediate phosphorylation of glucose to glucose-6-phosphate (G6P), which is the first step of both glycogen synthesis and ...
These loss-of-function mutations result in a glucokinase molecule that is less sensitive or less responsive to rising levels of glucose. The beta cells in MODY 2 have a normal ability to make and secrete insulin, but do so only above an abnormally high threshold (e.g., 126–144 mg/dl, or 7-8 mM).
These reactive oxygen species and their reaction products, such as the hydroxyl radical, are very harmful to cells, as they oxidize proteins and cause mutations in DNA. This cellular damage may contribute to disease and is proposed as one cause of aging .