Re: [新聞轉載]病毒與兒童型糖尿病可能有關
為什麼不是糖尿病提高了感染腸病毒的機率?
沒有糖尿病的兒童其胰臟組織就不會感染腸病毒?
※ 引述《abc0.bbs@ptt.cc (洛磯山的壯麗)》之銘言：
> http://news.bbc.co.uk/chinese/trad/hi/newsid_7920000/newsid_7927500/7927513.stm
> 病毒可能「導致兒童患糖尿病」
> 兒童糖尿病患者需要不斷進行胰島素注射
> 英國的科研人員說，一種常見的病毒可能是許多糖尿病病例──尤其是兒童糖尿病的患病
> 原因。
> 在60%患有1型糖尿病兒童的胰臟組織發現了腸道病毒的跡象，而沒有糖尿病的兒童幾乎不
> 存在這一現象。
> 在40%患有2型糖尿病成年人的胰島素生產細胞上也發現了被這一病毒感染的跡象。
> 這個發表在醫學雜誌《糖尿病》上的研究結果增加了研製有關疫苗的可能性。
> 儘管基因在糖尿病患病原因中起重要作用已經廣為人知，但過去幾十年來，醫學界也在考
> 慮外界因素以及病毒感染的可能性。
> 得出這一最新研究結果的是蘇格蘭格拉斯哥的病理學家艾倫?弗裡斯醫生。過去25年來，
> 他從全英國收集了大量在被診斷患有1型糖尿病後不到一年去世的兒童的肌體組織樣本。
> 腸道病毒是一種常見病毒，其感染症狀是嘔吐與腹瀉。弗裡斯醫生認為，腸道病毒很可能
> 是導致糖尿病的原因之一，只不過迄今科學技術還無法將其檢測出來。
> 「重要發現」
> 在英格蘭半島醫學院還有布萊頓大學的研究人員協助下，弗裡斯醫生對從72個死於糖尿病
> 的兒童患者身體解剖中留取的組織樣本和另外50個沒有糖尿病的兒童組織樣本進行了對比
> 與研究。
> 他在糖尿病患者兒童的組織樣本中，尤其是胰島素生產細胞中發現了腸道病毒的跡象。
> 英國糖尿病協會主席弗雷姆醫生說，這一研究成果是在瞭解引發糖尿病潛在原因方面「向
> 前邁進的一大步」。
> 他說，下一步將是查出這些病毒以及它們在人體內的活動，這將有利於我們找出預防1型
> 糖尿病的方法。
> 資助這次科研行動的英國少年糖尿病基金會負責人阿丁頓說，這一研究成果極為重要，因
> 為1型糖尿病患者數量每年都在增加，而迄今為止我們對此毫無辦法。
> http://news.bbc.co.uk/2/hi/health/7926026.stm
> Virus 'triggers child diabetes'
> By Emma Wilkinson
> BBC News health reporter
> Advertisement
> Dr Alan Foulis speaks about the research
> A common virus may be the trigger for the development of many cases of
> diabetes, particularly in children, UK researchers have reported.
> Signs of enteroviruses were found in pancreatic tissue from 60% of children
> with type 1 diabetes, but in hardly any children without the disease.
> They also found that 40% of adults with type 2 diabetes had signs of the
> infection in insulin-producing cells.
> The study published in Diabetologia raises the possibility of a vaccine.
> Although genetics is known to play a fairly substantial role in a person's
> risk of developing diabetes, environmental factors must also be involved and
> the idea of a viral cause of diabetes has been considered for decades.
> Type 1 diabetes is a life- threatening condition that requires a life-time of
> painful finger prick blood testing and insulin injections
> Karen Addington, JDRF
> The latest study was made possible by a pathologist in Glasgow who for 25
> years collected tissue samples from children across the UK who had died less
> than 12 months after being diagnosed with type 1 diabetes.
> Dr Alan Foulis believed that enteroviruses - a common family of viruses which
> cause symptoms such as vomiting and diarrhoea - would be present but until
> recently the technology was not sensitive enough to detect them.
> Along with colleagues from the south west-based Peninsula Medical School and
> the University of Brighton, he has now been able to look for evidence of the
> enteroviruses in tissue samples routinely taken during autopsy in 72 children
> and compare that with samples from 50 children without the condition.
> In those with diabetes who had signs of the virus, it was specifically found
> in the insulin-producing beta cells.
> Immune trigger
> The researchers suggest that, in children with a genetic predisposition to
> type 1 diabetes - an autoimmune disease in which beta cells in the pancreas
> are destroyed - enterovirus infection can trigger the immune reaction that
> kicks off the disease process.
> With type 2 diabetes - the type often linked to obesity in adults - the
> researchers speculate that the infection affects the ability of the cells to
> make insulin, which in combination with the greater demand for insulin in
> obese people, is enough to set off the disease.
> The next steps to identify the viruses and find out what they are doing to
> the infected beta cells will be hugely exciting and will take us a step
> closer to preventing type 1 diabetes
> Dr Iain Frame, Diabetes UK
> At the same time, a separate study, published in Science, by researchers at
> Cambridge University, found four rare mutations in a gene which reduce the
> risk of developing type 1 diabetes.
> It also backs the viral theory because the gene in question is involved in
> the immune response to infection with enteroviruses.
> There are 100 different strains of enterovirus, so although the results open
> the way for the development of a vaccine, researchers still have to pin down
> which types are involved.
> The study's author, Professor Noel Morgan from the Peninsula Medical School,
> said the results showed the underlying infection with enteroviruses was not a
> "rare event".
> "The next stages of research - to identify which enteroviruses are involved,
> how the beta-cells are changed by infection and the ultimate goal to develop
> an effective vaccine - will lead to findings which we hope will drastically
> reduce the number of people around the world who develop type 1 diabetes, and
> potentially type 2 diabetes as well," he added.
> Dr Iain Frame, director of research at Diabetes UK, said the study was "a big
> step forward" in understanding the potential triggers for the disease.
> "We've known for some time that type 1 diabetes cannot be explained by
> genetics alone and that other, environmental triggers may also play a part.
> "The next steps to identify the viruses and find out what they are doing to
> the infected beta cells will be hugely exciting and will take us a step
> closer to preventing Type 1 diabetes."
> Karen Addington, chief executive of the Juvenile Diabetes Research
> Foundation, who funded the research, said the findings were important as the
> incidence of type 1 diabetes is increasing every year and there is currently
> no way to prevent it.
> "Type 1 diabetes is a life- threatening condition that requires a life-time
> of painful finger prick blood testing and insulin injections," she pointed
> out.
> http://www.ncbi.nlm.nih.gov/pubmed/19266182
> Diabetologia. 2009 Mar 6. [Epub ahead of print]
> The prevalence of enteroviral capsid protein vp1 immunostaining in
> pancreatic islets in human type 1 diabetes.
> Richardson SJ, Willcox A, Bone AJ, Foulis AK, Morgan NG.
> Institute of Biomedical and Clinical Sciences, Peninsula Medical School,
> John, Bull Building, Tamar Science Park, Plymouth, PL6 8BU, UK.
> AIMS/HYPOTHESIS: Evidence that the beta cells of human patients with type
> 1 diabetes can be infected with enterovirus is accumulating, but it remains
> unclear whether such infections occur at high frequency and are important in
> the disease process. We have now assessed the prevalence of enteroviral
> capsid protein vp1 (vp1) staining in a large cohort of autopsy pancreases of
> recent-onset type 1 diabetic patients and a range of controls. METHODS:
> Serial sections of paraffin-embedded pancreatic autopsy samples from 72
> recent-onset type 1 diabetes patients and up to 161 controls were
> immunostained for insulin, glucagon, vp1, double-stranded RNA activated
> protein kinase R (PKR) and MHC class I. RESULTS: vp1-immunopositive cells
> were detected in multiple islets of 44 out of 72 young recent-onset type 1
> diabetic patients, compared with a total of only three islets in three out of
> 50 neonatal and paediatric normal controls. vp1 staining was restricted to
> insulin-containing beta cells. Among the control pancreases, vp1
> immunopositivity was also observed in some islets from ten out of 25 type 2
> diabetic patients. A strong correlation was established between islet cell
> vp1 positivity and PKR production in insulin-containing islets of both type 1
> and type 2 diabetic patients, consistent with a persistent viral infection of
> the islets. CONCLUSIONS/INTERPRETATION: Immunoreactive vp1 is commonly found
> in the islets of recent-onset type 1 diabetes patients, but only rarely in
> normal paediatric controls. vp1 immunostaining was also observed in some
> islets of type 2 diabetes patients, suggesting that the phenomenon is not
> restricted to type 1 diabetes patients.
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