NUTRITIONAL INTERVENTION TO PREVENT TYPE 1 DIABETES PILOT TRIAL (NIP)

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 1型糖尿病（T1 D）是由基因-环境相互作用引起的器官特异性自身免疫引起的。遗传学被相当好地描述，与人类白细胞抗原HLA-DR 3和DR 4具有高风险关联。还有一个或多个难以捉摸的“环境”因素，我们仍然不明白。 有观察表明，接受omega-3脂肪酸补充剂的儿童患T1 D的风险较低。Omega-3脂肪酸可能在怀孕期间，婴儿期或两者都有积极的影响。 我们假设，补充二十二碳六烯酸（DHA），一种ω-3脂肪酸，将防止T1 D遗传风险儿童的自身抗体发展。我们认为，这种假定的保护机制是由于DHA介导的炎症反应的抑制。我们认为，有T1 D风险的参与者具有增加的促炎环境，并提出DHA给药将导致炎症相关因子的抑制。 这将阻断与遗传风险受试者中随后发生自身免疫相关的早期事件。 本研究是一项双组、多中心、随机、双盲对照临床试验。 研究药物是二十二碳六烯酸（DHA），一种omega-3多不饱和22碳脂肪酸。安慰剂是中性植物对照油。 将90名受试者的样本量随机分配至2组（对照组的实验治疗），数量大致相等。大约一半的研究参与者将每天接受DHA研究物质，另一半将接受对照。 研究的总长度为3年。所有母亲将每3个月进行一次随访。哺乳期的母亲将每3个月进行一次随访，直到婴儿1岁。 婴儿将每6个月随访一次，持续3年。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Type 1 Diabetes (T1D) is caused by organ specific autoimmunity resulting from a gene-environment interaction. The genetics are fairly well delineated, with a high-risk association with the human leukocyte antigen HLA-DR3 and DR4. There are also one or more elusive "environmental" factors that we still do not understand. Observations have been made that children who have received omega-3 fatty acid supplementation have a lower risk of T1D. Omega-3 fatty acids could have a proactive effect that may occur during pregnancy, during infancy or both. We hypothesize that supplementation with docosahexaenoic acid (DHA), an omega-3 fatty acid; will prevent autoantibody development in children at genetic risk for T1D. We propose that the mechanism for this putative protection is due to DHA mediated suppression of the inflammatory response. We suggest that participant at risk for T1D have an increased proinflammatory environment, and propose that DHA administration will result in the inhibition of inflammation-related factors. This would block the early events associated with the subsequent development of autoimmunity in genetically at-risk subjects. The study is a two-arm multicenter, randomized, double-masked controlled clinical trial. The study drug is docosahexaenoic acid (DHA), an omega-3, polyunsaturated, 22-carbon fatty acid. The placebo is neutral vegetable control oil. A sample size of 90 participants will be randomly assigned in approximately equal number to the 2 groups (experimental treatment of control group). About half of the study participants will receive the DHA study substance daily and the other half will receive the control. The total length of the study is 3 years. All mothers will have follow up every 3 months. Nursing mothers will have follow up every 3 months until the infant is 1 year old. Infants will have follow up every 6 months for 3 years.