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| == '''[[Diabesity]]''' ==
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| ''by [[User:Gareth Leng|Gareth Leng]], [[User:Hannah Frost|Hannah Frost]], [[User:Luke Kennedy Burke|Luke Kennedy Burke]], [[User:Charlie Player|Charlie Player]] and [[User:Katie Rowland|Katie Rowland]]
| | <small> |
| | | ==Footnotes== |
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| The term '''diabesity''' was coined by [https://vpn.ucsf.edu/oby/journal/v19/n3/full/,DanaInfo=www.nature.com+oby2010334a.html Ethan Sims] in 1973, to describe the close relationship between [[diabetes mellitus type 2]] (T2DM) and [[obesity]]. Their findings suggested that by overfeeding young men, with no previous family history of diabetes, the initial signs of diabetes were induced. This excess consuption led to increases in [[insulin]] production, plasma [[glucose]], [[triglycerides]] and eventually impaired glucose tolerance; all signs predisposing one to T2DM and obesity<ref>
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| Sims EAH ''et al.'' (1973) Endocrine and metabolic effects of experimental obesity in man, ''Recent Prog Horm Res'' 29:457–96</ref><ref>Haslam DW, James WP (2005) Obesity''Lancet'' 366:1197–209</ref>
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| T2DM is a disorder where cells fail to take up glucose from the blood. Glucose is the fuel for respiration which produces energy for our cells to function properly. Diabetes mellitus is the foremost cause of kidney failure ([[diabetic nephropathy]]), blindness ([[diabetic retinopathy]]), and amputation in adults ([[diabetic neuropathy]]). People with this disease lack the ability to utilize the hormone [[insulin]]. Insulin is produced by the [[pancreas]] after a meal inresponse to increased concentrations of glucose in the blood. The insulin signal attaches to specific receptors on the surface of target cells, causing them to switch on their glucose-transporting machinery. People with T2DM have normal or even elevated levels of insulin in their blood, and normal insulin receptors, but the binding of insulin to its receptors does not turn on the glucose-transporting machinery.
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| Proteins called [[IRS proteins]] (insulin receptor substrate) bind with the insulin receptor inside the cell. The receptor responds by adding a phosphate group onto the IRS molecules. This rouses the IRS molecules into action, and they activate a variety of processes, including an enzyme that turns on the glucose transporter machinery. When the IRS genes are deliberately inactivated in [[transgenic]] “knockout” mice, T2DM results. However, there are no IRS gene mutations in inherited T2DM; the IRS genes are normal. This suggests that in T2DM something is impeding with the action of the IRS proteins. An estimated 80% of those who develop T2DM are obese.
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| ===Visceral fat accumulation and type 2 diabetes===
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| Excess visceral adipose tissue increases the risk for T2DM. Excess fat within the [[abdomen]], known as [[visceral adiposity]], creates a serious health risk of metabolic complications independent from accumulation of adipose tissue in other regions: visceral adiposity is related with an increase in ''[[insulin resistance]]'', whereas abdominal subcutaneous fat is not. (''Insulin resistance'' describes the impaired ability of insulin to suppress hepatic glucose output and promote glucose disposal in the periphery.) As T2DM gets worse, patients have higher blood sugar levels ([[hyperglycaemia]]) because the [[pancreatic beta cells]] are unable to make enough insulin. In insulin resistance, normal amounts of insulin are unable to produce a normal response from adipose, muscle and liver cells. Cnop ''et al.'' showed that visceral fat is the best predictor of insulin sensitivity whilst subcutaneous fat establishes leptin levels <ref>Cnop''et al.'' (2002) The concurrent accumalation of intra-adominal and subcutaneous fat explains the association between insulin resistance and plasma leptin concentrations. ''Diabetes'' 51:1005-15</ref>
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| In 1994, a new hormone was found, called [[leptin]], that provides feedback to the brain of the level of fat in the body. Leptin suppresses appetite, but most obese people have very high leptin levels, as leptin is secreted by adipose cells. Therefore, obesity is not generally caused by a deficiency in leptin; instead there seems to be a defect in leptin signalling. Adipocytes also produce an array of other peptides including [[adiponectin]], [[resistin]] and [[TNF alpha]]. They act on peripheral tissues and thereby affect insulin sensitivity and the processes involved in substrate metabolism.
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| ''[[Diabesity|.... (read more)]]''
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| ! style="text-align: center;" | [[Diabesity#References|notes]]
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| {{reflist|2}} | | {{reflist|2}} |
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| | </small> |
Latest revision as of 10:19, 11 September 2020
The Irvin pin. The eyes have always been red, but there are
urban legends about the meanings of other colors.
A pin from another company, possibly Switlik or Standard Parachute. This style is common in catalogs and auctions of military memorabilia.
The Caterpillar Club is an informal association of people who have successfully used a parachute to bail out of a disabled aircraft. After authentication by the parachute maker, applicants receive a membership certificate and a distinctive lapel pin.
History
Before April 28, 1919 there was no way for a pilot to jump out of a plane and then to deploy a parachute. Parachutes were stored in a canister attached to the aircraft, and if the plane was spinning, the parachute could not deploy. Film industry stuntman Leslie Irvin developed a parachute that the pilot could deploy at will from a back pack using a ripcord. He joined the Army Air Corps parachute research team, and in April 1919 he successfully tested his design, though he broke his ankle during the test. Irvin was the first person to make a premeditated free fall jump from an airplane. He went on to form the Irving Airchute Company, which became a large supplier of parachutes. (A clerical error resulted in the addition of the "g" to Irvin and this was left in place until 1970, when the company was unified under the title Irvin Industries Incorporated.) The Irvin brand is now a part of Airborne Systems, a company with operations in Canada, the U.S. and the U.K.[1].
An early brochure [2] of the Irvin Parachute Company credits William O'Connor 24 August 1920 at McCook Field near Dayton, Ohio as the first person to be saved by an Irvin parachute, but this feat was unrecognised. On 20 October 1922 Lieutenant Harold R. Harris, chief of the McCook Field Flying Station, jumped from a disabled Loening W-2A monoplane fighter. Shortly after, two reporters from the Dayton Herald, realising that there would be more jumps in future, suggested that a club should be formed. 'Caterpillar Club' was suggested because the parachute canopy was made of silk, and because caterpillars have to climb out of their cocoons and fly away. Harris became the first member, and from that time forward any person who jumped from a disabled aircraft with a parachute became a member of the Caterpillar Club. Other famous members include General James Doolittle, Charles Lindbergh and (retired) astronaut John Glenn.
In 1922 Leslie Irvin agreed to give a gold pin to every person whose life was saved by one of his parachutes. By 1945 the number of members with the Irvin pins had grown to over 34,000. In addition to the Irvin Air Chute Company and its successors, other parachute manufacturers have also issued caterpillar pins for successful jumps. Irvin/Irving's successor, Airborne Systems Canada, still provides pins to people who made their jump long ago and are just now applying for membership. Another of these is Switlik Parachute Company, which though it no longer makes parachutes, still issues pins.
