Metabolic Syndrome--Prepubertal African Amer./Caucasian

代谢综合症——青春期前的非洲裔美国人/白种人

• 批准号: 7371142
• 负责人: MELINDA S SOTHERN
• 金额: $ 52.88万
• 依托单位: LSU HEALTH SCIENCES CENTER
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-05-16 至 2010-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7371142
• 关键词: 9 year old; Adult; African; African American; Birth Weight; Blood Pressure; Body fat; Body mass index; Caucasians; Caucasoid Race; Child; Childhood; Chronic Disease; Deposition; Development; Diabetes Mellitus; Early Diagnosis; Energy Metabolism; Environment; Environmental Risk Factor; Ethnic Origin; Fatty acid glycerol esters; Genetic; Hypotension; Indirect Calorimetry; Invasive; Link; Lipids; Lipoproteins; Liver; Low Birth Weight Infant; Measures; Metabolic; Metabolic syndrome; Muscle; NMR Spectroscopy; Non-Insulin-Dependent Diabetes Mellitus; Nuclear Magnetic Resonance; Obesity; Personal Satisfaction; Phenotype; Physiological; Play; Population; Research; Research Personnel; Rest; Risk Factors; Role; Sampling; Serum; Skeletal Muscle; Syndrome; Techniques; Testing; Triglycerides; Work; Youth; abdominal fat; cardiovascular disorder risk; critical developmental period; density; disorder prevention; ethnic minority population; experience; insulin sensitivity; intravenous glucose tolerance test; low density lipoprotein triglyceride; obesity risk; oxidation; programs; respiratory

DESCRIPTION (provided by applicant): Recent research indicates that the metabolic syndrome develops during childhood and is associated with several early risk factors including low (<= 10th percentile body mass index [BMI-USCDC]) or high (>= 90th percentile [BMI-USCDC]) birth weight. However, markers that precede the syndrome and mechanisms that explain these relationships have yet to be identified. These mechanisms may originate in the intrauterine environment, be exacerbated in susceptible populations, such as African Americans and, be further promoted by an early "obesigenic" environment. Thus, we propose that young African American children with low or high birth weight may be predisposed genetically and behaviorally to the early manifestation of subtle, non-symptomatic metabolic abnormalities that work synergistically to create a metabolic syndrome phenotype. The metabolic abnormalities increasing the propensity to type 2 diabetes may originate earlier than previously proposed. In adults insulin sensitivity is correlated negatively with lipid depots in the skeletal muscle (intramyocellular lipids = IMCL) and in the liver long before the development of diabetes. Noninvasive techniques for examining the relationship of skeletal muscle and liver lipids to insulin sensitivity have not been applied to prepubertal African American youth. How early and to what extent metabolic abnormalities occur in children and whether it is more prevalent in African American vs. Caucasian children are unknown. We therefore propose to: 1) Explore the potential markers and mechanisms of impaired insulin sensitivity in pre-pubertal (7-9 years) African American and Caucasian children with low or high birth weight. 2) Determine the relationship of birth weight and ethnicity to insulin sensitivity in these youth. We aim to explore potential markers and mechanisms of the impaired insulin sensitivity observed in 7-9 y prepubertal children by examining the relationships between insulin sensitivity and ectopic fat deposition i.e. triglyceride content in skeletal muscle and liver, abdominal fat (independent of ectopic fat), resting energy metabolism (REE and respiratory quotient [RQ] [fat oxidation] and cardiovascular disease risk factors lipid profiles and blood pressure). Insulin Sensitivity will be measured by Frequently Sampled Intravenous Glucose Tolerance Test (FSIGTT), triglyceride contents in skeletal muscle and liver by Nuclear Magnetic Resonance pectroscopy (ill-MRS) and energy metabolism by ventilated hood indirect calorimetry. A secondary aim is to examine he relationship of birth weight and ethnicity (African American vs. Caucasian) to insulin sensitivity in children, 7-9 years (with and without adjusting for total body fat and/or ectopic fat).

描述（由申请人提供）：最近的研究表明，代谢综合征在儿童期发生，并与几个早期风险因素相关，包括低（<=第10百分位体重指数[BMI-USCDC]）或高（>=第90百分位[BMI-USCDC]）出生体重。然而，在综合征之前的标记物和解释这些关系的机制尚未确定。这些机制可能起源于子宫内环境，在易感人群中加剧，如非洲裔美国人，并进一步促进早期的“obesigenic”环境。因此，我们提出，低或高出生体重的年轻非洲裔美国儿童可能在遗传和行为上倾向于早期表现出微妙的，无症状的代谢异常，协同工作，创造一个代谢综合征表型。增加2型糖尿病倾向的代谢异常可能比以前提出的更早发生。在成年人中，胰岛素敏感性与骨骼肌（肌细胞内脂质= IMCL）和肝脏中的脂质贮库呈负相关，早在糖尿病发生之前。用于检查骨骼肌和肝脏脂质与胰岛素敏感性关系的非侵入性技术尚未应用于青春期前的非洲裔美国青年。代谢异常在儿童中发生的时间有多早，程度有多严重，以及它在非洲裔美国儿童中是否比白人儿童更普遍尚不清楚。因此，我们建议：1）探索青春期前（7-9岁）低或高出生体重的非洲裔美国人和白人儿童胰岛素敏感性受损的潜在标志物和机制。2)确定这些青年的出生体重和种族与胰岛素敏感性的关系。我们的目的是通过检查胰岛素敏感性与异位脂肪沉积（即骨骼肌和肝脏中的甘油三酯含量、腹部脂肪）之间的关系，探索在7-9岁青春期前儿童中观察到的胰岛素敏感性受损的潜在标志物和机制。（与异位脂肪无关），静息能量代谢（REE和呼吸商[RQ] [脂肪氧化]和心血管疾病风险因素血脂谱和血压）。将通过频繁采样静脉葡萄糖耐量试验（FSIGTT）测量胰岛素敏感性，通过核磁共振光谱（ill-MRS）测量骨骼肌和肝脏中的甘油三酯含量，通过通风罩间接热量测定法测量能量代谢。第二个目的是检查出生体重和种族（非洲裔美国人与高加索人）与7-9岁儿童胰岛素敏感性的关系（调整和不调整全身脂肪和/或异位脂肪）。