Division of Pediatric Diabetes/Endocrinology, Harold Hamm Diabetes Center, Children's Hospital, The University of Oklahoma Health Sciences Center, 1200 Children's Ave Suite 4D, Oklahoma City, OK, 73104, USA.
Curr Diab Rep. 2020 Aug 7;20(9):45. doi: 10.1007/s11892-020-01328-6.
This review examines the impact of early life exposures on glucose metabolism in the offspring and explores potential metabolic mechanisms leading to type 2 diabetes in childhood.
One in five adolescents is diagnosed with prediabetes. Recent studies have elucidated the impact of early exposures such as maternal diabetes, but also hyperglycemia below the threshold of gestational diabetes, obesity, hyperlipidemia, and paternal obesity on the future metabolic health of the offspring. Mechanisms affecting the developmental programing of offspring toward type 2 diabetes include epigenetic modifications, alterations in stem cell differentiation, metabolome and microbiome variation, immune dysregulation, and neonatal nutrition. The risk of type 2 diabetes in offspring is increased not only by diabetes exposure in utero but also by exposure to a heterogeneous milieu of factors that accompany maternal obesity that provoke a vicious cycle of metabolic disease. The key period for intervention to prevent type 2 diabetes is within the first 1000 days of life.
本综述探讨了生命早期暴露对后代葡萄糖代谢的影响，并探讨了导致儿童 2 型糖尿病的潜在代谢机制。
五分之一的青少年被诊断患有前驱糖尿病。最近的研究阐明了早期暴露（如母体糖尿病，但也包括妊娠期糖尿病阈值以下的高血糖、肥胖、血脂异常和父体肥胖）对后代未来代谢健康的影响。影响后代 2 型糖尿病发育编程的机制包括表观遗传修饰、干细胞分化改变、代谢组和微生物组变化、免疫失调和新生儿营养。后代患 2 型糖尿病的风险不仅增加了宫内糖尿病暴露，还增加了伴随母体肥胖的异质因素暴露，这些因素引发了代谢性疾病的恶性循环。预防 2 型糖尿病的干预关键时期是生命的头 1000 天内。
