High Fat Programming of β-Cell Failure
High Fat Programming of β-Cell Failure
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DOI：
10.1007/978-90-481-3271-3_5
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发表时间：
2010-01-01
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影响因子：
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通讯作者：
Cerf, Marlon E.
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文献类型：
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作者：
Cerf, Marlon E.
高饱和脂肪摄入会导致胰岛素抵抗、β细胞衰竭和2型糖尿病。编程会改变后代的生理和新陈代谢，产生直接和持久的影响。妊娠期和哺乳期母亲的营养影响后代的发育和健康。母亲在妊娠期和/或哺乳期摄入的高饱和脂肪饮食是一种营养损害，可引起后代生理和代谢方面的致糖尿病变化。高脂肪编程是由母体在妊娠期和/或哺乳期摄入高饱和脂肪引起的，并对后代早期的生理和代谢进行编程。这种最近采用的发展规划形式反映了富裕国家和发展中国家的社会情况。高脂肪编程诱导新生儿和断奶后代β细胞发育和功能的不利变化。这些变化的特征是β细胞发育和功能受损，维持β细胞表型的关键因子表达改变。高脂肪编程很可能导致β细胞衰竭，最终导致2型糖尿病。
High saturated fat intake contributes to insulin resistance, beta-cell failure, and type 2 diabetes. Developmental programming refers to a stimulus or insult during critical periods of life which includes fetal and subsequent early neonatal life. Programming alters offspring physiology and metabolism with both immediate and lasting consequences. Maternal nutrition in gestation and lactation shapes offspring development and health. A high saturated fat diet ingested by mothers during gestation and/or lactation is a form of nutritional insult that induces diabetogenic changes in offspring physiology and metabolism. High fat programming is induced by maternal high saturated fat intake during defined periods of gestation and/or lactation and programs the physiology and metabolism of the offspring in early life. This more recently adopted form of developmental programming reflects society in both affluent and developing countries. High fat programming induces adverse changes in beta-cell development and function in neonatal and weanling offspring. These changes are characterized by compromised beta-cell development and function, evident by altered expression of key factors that maintain the beta-cell phenotype. High fat programming is likely to result in beta-cell failure and eventual type 2 diabetes.