Caribbean Institute for Health Research, The University of the West Indies, Mona, Jamaica.
UWI Solutions for Developing Countries, The University of the West Indies, Mona, Jamaica.
J Dev Orig Health Dis. 2022 Dec;13(6):750-756. doi: 10.1017/S2040174422000034. Epub 2022 Mar 1.
Adults who had non-edematous severe acute malnutrition (SAM) during infancy (i.e., marasmus) have worse glucose tolerance and beta-cell function than survivors of edematous SAM (i.e., kwashiorkor). We hypothesized that wasting and/or stunting in SAM is associated with lower glucose disposal rate (M) and insulin clearance (MCR) in adulthood.We recruited 40 nondiabetic adult SAM survivors (20 marasmus survivors (MS) and 20 kwashiorkor survivors (KS)) and 13 matched community controls. We performed 150-minute hyperinsulinaemic, euglycaemic clamps to estimate M and MCR. We also measured serum adiponectin, anthropometry, and body composition. Data on wasting (weight-for-height) and stunting (height-for-age) were abstracted from the hospital records.Children with marasmus had lower weight-for-height -scores (WHZ) (-3.8 ± 0.9 vs. -2.2 ± 1.4; < 0.001) and lower height-for-age -scores (HAZ) (-4.6 ± 1.1 vs. -3.4 ± 1.5; = 0.0092) than those with kwashiorkor. As adults, mean age (SD) of participants was 27.2 (8.1) years; BMI was 23.6 (5.0) kg/m. SAM survivors and controls had similar body composition. MS and KS and controls had similar M (9.1 ± 3.2; 8.7 ± 4.6; 6.9 ± 2.5 mg.kg.min respectively; = 0.3) and MCR. WHZ and HAZ were not associated with M, MCR or adiponectin even after adjusting for body composition.Wasting and stunting during infancy are not associated with insulin sensitivity and insulin clearance in lean, young, adult survivors of SAM. These data are consistent with the finding that glucose intolerance in malnutrition survivors is mostly due to beta-cell dysfunction.
患有婴儿期非水肿性严重急性营养不良（SAM）的成年人（即消瘦型）的葡萄糖耐量和胰岛β细胞功能比水肿性 SAM 幸存者（即夸希奥科营养不良）差。我们假设 SAM 中的消瘦和/或发育迟缓与成年后较低的葡萄糖处置率（M）和胰岛素清除率（MCR）有关。我们招募了 40 名非糖尿病成年 SAM 幸存者（20 名消瘦型 SAM 幸存者（MS）和 20 名夸希奥科营养不良幸存者（KS））和 13 名匹配的社区对照者。我们进行了 150 分钟的高胰岛素、正常血糖钳夹实验来估计 M 和 MCR。我们还测量了血清脂联素、人体测量学和身体成分。消瘦（身高体重比）和发育迟缓（年龄身高比）的数据从医院记录中提取。患有消瘦型的儿童体重身高比评分（WHZ）较低（-3.8 ± 0.9 比-2.2 ± 1.4；<0.001），身高年龄比评分（HAZ）也较低（-4.6 ± 1.1 比-3.4 ± 1.5；=0.0092）。作为成年人，参与者的平均年龄（SD）为 27.2（8.1）岁；BMI 为 23.6（5.0）kg/m。SAM 幸存者和对照组的身体成分相似。MS 和 KS 与对照组的 M（9.1 ± 3.2；8.7 ± 4.6；6.9 ± 2.5 mg.kg.min 分别；=0.3）和 MCR 相似。WHZ 和 HAZ 与 M、MCR 或脂联素无关，即使在调整身体成分后也是如此。婴儿期的消瘦和发育迟缓与瘦、年轻的 SAM 幸存者的胰岛素敏感性和胰岛素清除率无关。这些数据与营养不良幸存者的葡萄糖耐量主要归因于胰岛β细胞功能障碍的发现一致。
