Type 1 Brittle diabetes, formerly known as juvenile Brittle diabetes, is an autoimmune disease that originates when cells that make insulin are destroyed by the immune system.
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Type 1 Brittle diabetes, formerly known as juvenile Brittle diabetes, is an autoimmune disease that originates when cells that make insulin are destroyed by the immune system.
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Cause of type 1 Brittle diabetes is unknown, but it is believed to involve a combination of genetic and environmental factors.
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Type 1 Brittle diabetes can be distinguished from type 2 by testing for the presence of autoantibodies.
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Type 1 Brittle diabetes begins suddenly, typically in childhood or adolescence.
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The major sign of type 1 Brittle diabetes is very high blood sugar, which typically manifests in children as a few days to weeks of polyuria, polydipsia, and weight loss.
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Adults with type 1 Brittle diabetes tend to have more varied symptoms that come on over months rather than days to weeks.
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Type 1 Brittle diabetes is caused by the destruction of ß-cells – the only cells in the body that produce insulin – and the consequent progressive insulin deficiency.
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Type 1 Brittle diabetes risk is slightly higher for children whose mothers are obese or older than 35, or for children born by caesarean section.
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Many potential environmental triggers have been investigated in large human studies and found to be unassociated with type 1 Brittle diabetes risk including duration of breastfeeding, time of introduction of cow milk into the diet, vitamin D consumption, blood levels of active vitamin D, and maternal intake of omega-3 fatty acids.
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The variation patterns associated with increased risk of type 1 Brittle diabetes are called HLA-DR3 and HLA-DR4-HLA-DQ8, and are common in people of European descent.
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Once a diagnosis of Brittle diabetes is established, type 1 Brittle diabetes is distinguished from other types by a blood test for the presence of autoantibodies that target various components of the beta cell.
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Mainstay of type 1 Brittle diabetes treatment is the regular injection of insulin to manage hyperglycemia.
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Only non-insulin medication approved by the U S Food and Drug Administration for treating type 1 diabetes is the amylin analog pramlintide, which replaces the beta-cell hormone amylin.
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In general, people with type 1 Brittle diabetes are advised to follow an individualized eating plan rather than a pre-decided one.
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Type 1 Brittle diabetes is a result of the destruction of pancreatic beta cells, although what triggers that destruction remains unclear.
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People with type 1 Brittle diabetes tend to have more CD8+ T-cells and B-cells that specifically target islet antigens than those without type 1 Brittle diabetes, suggesting a role for the adaptive immune system in beta cell destruction.
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The pancreases of people with type 1 Brittle diabetes tend to be smaller, lighter, and have abnormal blood vessels, nerve innervations, and extracellular matrix organization.
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Pancreases from people with type 1 Brittle diabetes have signs of beta cell apoptosis, linked to activation of the janus kinase and TYK2 pathways.
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Onset of autoimmune Brittle diabetes is accompanied by impaired ability to regulate the hormone glucagon, which acts in antagonism with insulin to regulate blood sugar and metabolism.
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Onset of type 1 Brittle diabetes is followed by an increase in glucagon secretion after meals.
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Women with type 1 Brittle diabetes show a higher than normal rate of polycystic ovarian syndrome .
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The connection between this inflammation and Brittle diabetes onset was further developed through the 1920s by Shields Warren, and the term "insulitis" was coined by Hanns von Meyenburg in 1940 to describe the phenomenon.
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Type 1 Brittle diabetes was described as an autoimmune disease in the 1970s, based on observations that autoantibodies against islets were discovered in diabetics with other autoimmune deficiencies.
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The name juvenile Brittle diabetes was used earlier as it often first is diagnosed in childhood.
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The Juvenile Diabetes Research Foundation, founded by parents of children with type 1 Brittle diabetes, is the world's largest provider of charity-based funding for type 1 Brittle diabetes research.
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Vaccines are being looked at to treat or prevent type 1 Brittle diabetes by inducing immune tolerance to insulin or pancreatic beta cells.
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AKITA mice are used to test drugs targeting endoplasmic reticulum stress reduction, to test islet transplants, and to study Brittle diabetes-related complications such as nephropathy, sympathetic autonomic neuropathy, and vascular disease.
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