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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]]
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| | | ==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== | |
| 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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Latest revision as of 10:19, 11 September 2020
Nuclear weapons proliferation is one of the four big issues that have held back worldwide deployment of peaceful nuclear power. This article will address the proliferation questions raised in Nuclear power reconsidered.
As of 2022, countries with nuclear weapons have followed one or both of two paths in producing fissile materials for nuclear weapons: enrichment of uranium to very high fractions of U-235, or extraction of fissile plutonium (Pu-239) from irradiated uranium nuclear reactor fuel. The US forged the way on both paths during its World War II Manhattan Project. The fundamental aspects of both paths are well understood, but both are technically challenging. Even relatively poor countries can be successful if they have sufficient motivation, financial investment, and, in some cases, direct or illicit assistance from more technologically advanced countries.
The International Non-proliferation Regime
The International Atomic Energy Agency (IAEA) has a vigorous program to prevent additional countries from acquiring nuclear weapons. The Treaty on the Non-Proliferation of Nuclear Weapons (NPT) is the cornerstone arrangement under which strategic rivals can trust, by independent international verification, that their rivals are not developing a nuclear weapons threat. The large expense of weapons programs makes it very unlikely that a country would start its own nuclear weapons program, if it knows that its rivals are not so engaged. With some notable and worrying exceptions, this program has been largely successful.
Paths to the Bomb
It is frequently claimed that building a civil nuclear power program adds to the weapons proliferation risk. There is an overlap in the two distinct technologies, after all. To build a bomb, one needs Highly Enriched Uranium (HEU) or weapons-grade plutonium (Pu-239).
Existing reactors running on Low Enriched Uranium (LEU, under 5% U-235) or advanced reactors running on High Assay LEU (HALEU,up to 20% U-235) use the same technology that can enrich uranium to very high levels, but configured differently. Enrichment levels and centrifuge configurations can be monitored using remote cameras, on-site inspections, and installed instrumentation -- hence the value of international inspections by the IAEA. Using commercial power reactors as a weapons plutonium source is an extremely ineffective, slow, expensive, and easily detectable way to produce Pu. Besides the nuclear physics issues, refueling pressurized water reactors is both time-consuming and obvious to outside observers. That is why the US and other countries developed specialized Pu production reactors and/or uranium enrichment to produce fissile cores for nuclear weapons.
Future Threats and Barriers
Minimizing the risk of future proliferation in states that want to buy nuclear reactors or fuel might require one or more barriers:
1) Insisting on full transparency for all nuclear activities in buyer states, including monitoring and inspections by the International Atomic Energy Agency (IAEA).
2) Limiting fuel processing to just a few supplier states that already have weapons or are approved by the IAEA.
3) Ensuring that fuel at any stage after initial fabrication has an isotopic composition unsuitable for weapons. "Spiking" the initial fuel with non-fissile isotopes, if necessary.
4) Limiting the types of reactors deployed to buyer states. In general, breeders are less secure than burners. Sealed reactor modules are more secure than reactors with on-site fuel processing.
5) Providing incentives and assurances for buyer states to go along with all of the above.
6) Application of diplomatic pressure, sanctions, and other economic measures to non-compliant states.
7) Agreement that any reactor declared rogue by the IAEA will be "fair game" for any state feeling threatened.