Fasting Plasma Glucose Levels Within the Normoglycemic Range in Childhood as a Predictor of Prediabetes and Type 2 Diabetes in Adulthood

Nguyen, Quoc Manh; Srinivasan, Sathanur R.; Xu, Jihua; Chen, Wei; Berenson, Gerald S.

doi:10.1001/archpediatrics.2009.268

Cited by 78 publications

(85 citation statements)

References 24 publications

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“…In response to a glucose challenge, the ACI strain shows only a slight increase in plasma insulin levels, with a very low IGI, indicating decreased beta cell function. In addition to being glucose intolerant, the ACI is the only strain to exhibit increased fasting glucose levels, a known predictor of T2D (51,52). In contrast to the ACI, the WKY strain shows elevated fasting insulin and an increased insulin response to a glucose challenge, as previously demonstrated (35,63).…”

Section: Discussionsupporting

confidence: 54%

Fine-mapping diabetes-related traits, including insulin resistance, in heterogeneous stock rats

Woods

Holl

Oreper³

et al. 2012

Physiological Genomics

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(T2D) is a disease of relative insulin deficiency resulting from both insulin resistance and beta cell failure. We have previously used heterogeneous stock (HS) rats to fine-map a locus for glucose tolerance. We show here that glucose intolerance in the founder strains of the HS colony is mediated by different mechanisms: insulin resistance in WKY and an insulin secretion defect in ACI, and we demonstrate a high degree of variability for measures of insulin resistance and insulin secretion in HS rats. As such, our goal was to use HS rats to fine-map several diabetes-related traits within a region on rat chromosome 1. We measured blood glucose and plasma insulin levels after a glucose tolerance test in 782 male HS rats. Using 97 SSLP markers, we genotyped a 68 Mb region on rat chromosome 1 previously implicated in glucose and insulin regulation. We used linkage disequilibrium mapping by mixed model regression with inferred descent to identify a region from 198.85 to 205.9 that contains one or more quantitative trait loci (QTL) for fasting insulin and a measure of insulin resistance, the quantitative insulin sensitivity check index. This region also encompasses loci identified for fasting glucose and Insulin_AUC (area under the curve). A separate Ͻ3 Mb QTL was identified for body weight. Using a novel penalized regression method we then estimated effects of alternative haplotype pairings under each locus. These studies highlight the utility of HS rats for fine-mapping genetic loci involved in the underlying causes of T2D. obesity; Type 2 diabetes; glucose tolerance; metabolism TYPE 2 DIABETES (T2D) IS A disease of relative insulin deficiency resulting from a combination of insulin resistance and decreased beta-cell function (50,57). This complex disorder is caused by a combination of both environmental and genetic factors. Although diet and exercise are the major environmental factors contributing to T2D (25), the genetic factors contributing to this disease are only beginning to be understood. Over the past several years, over 40 genes have been identified for T2D in human genome-wide association studies (GWAS) (see Refs. 38,62,78). Even when the effects of these genes are combined, however, they explain only 10% of the heritable variance (78), indicating that many genetic factors remain unidentified and highlighting our limited understanding of this disorder.We have previously used heterogeneous stock (HS) rats to fine-map a locus for glucose tolerance to 2.44 megabases (Mb) (64). The HS rat colony at the Medical College of Wisconsin (MCW) comprises outbred animals derived by the National Institutes of Health (NIH) in 1984 from a set of eight genetically and phenotypically diverse inbred founder strains: ACI/N, BN/N, BUF/N, F344/N, M520/N, MR/N, WKY/N, WN/N (23). HS populations are powerful tools for genetic studies because they provide a basis for high resolution mapping of quantitative trait loci (QTL) in a relatively short time period (64,72). Although none of the inbred founder strains of the HS rat colony ...

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Section: Discussionsupporting

confidence: 54%

Fine-mapping diabetes-related traits, including insulin resistance, in heterogeneous stock rats

Woods

Holl

Oreper³

et al. 2012

Physiological Genomics

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“…This is before other morbidities compound the diagnosis and may be due to attrition of beta cells occur over time [43]. It is of interest in these studies a fasting glucose value of 86 mg/dL was found as a cut-point of being potentially abnormal (Table 1) [44]. Obesity was the most consistent predictor of the MetS from adulthood, preceding the onset of high insulin levels [45].…”

Section: Predictors Of Prediabetes and Diabetesmentioning

confidence: 98%

“…Waist circumference ≥90th percentile and waist-to-hip ratio >0.5 are used as an index of central obesity for children between 10 and 16 ages. We recommend that fasting glucose ≥86 mg/dL [44], triglyceride ≥100 mg/dL, HDL-C < 45 mg/dL, and blood pressure ≥115 mmHg systolic or ≥75 mmHg diastolic can be considered as abnormal values for children (Table 1). Similarly, for adolescents over 16 years of age, criteria can be modified as FPG ≥ 100 mg/dL or known T2DM, triglyceride ≥100 mg/dL or specific treatment for high triglyceride, HDL-C < 45 mg/dL for males and <50 mg/ dL for females, or specific treatment for low HDL-C and systolic blood pressure ≥115 mmHg or diastolic blood pressure ≥75 mmHg or treatment of previously diagnosed hypertension.…”

Section: Existing Definitions For Metabolic Syndrome In Youthmentioning

confidence: 99%

Metabolic Syndrome: Bridging the Gap from Childhood to Adulthood

Ağırbaşlı

Tanrikulu

Berenson

2016

Cardiovascular Therapeutics

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SUMMARYChildhood and adolescence are particularly vulnerable periods of life to the effects of cardiometabolic risk and later development of atherosclerosis, hypertension, and diabetes mellitus. Developing countries with limited resources suffer most heavily from the consequences of cardiometabolic risk in children and its future implications to the global health burden. A better understanding of mechanisms leading to cardiometabolic risk in early life may lead to more effective prevention and intervention strategies to reduce metabolic stress in children and later disease. Longitudinal "tracking" studies of cardiometabolic risk in children provide a tremendous global resource to direct prevention strategies for cardiovascular disease. In this review, we will summarize the pathophysiology, existing definitions for cardiometabolic risk components in children. Screening and identifying children and adolescents of high cardiometabolic risk and encouraging them and their families through healthy lifestyle changes should be implemented to as a global public health strategy.

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“…The children with high fasting blood glucose have 49% lower glucose deposition index (504). More importantly, children with elevated fasting blood glucose were 3.4 and 2.1 times more likely to develop prediabetes and diabetes, respectively, as adults (378). …”

Section: Primary Prevention Of Physical Inactivity: Childhood Devmentioning

confidence: 99%

Lack of Exercise Is a Major Cause of Chronic Diseases

Booth

Roberts

Laye

2012

Comprehensive Physiology

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1,400

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Chronic diseases are major killers in the modern era. Physical inactivity is a primary cause of most chronic diseases. The initial third of the article considers: activity and prevention definitions; historical evidence showing physical inactivity is detrimental to health and normal organ functional capacities; cause versus treatment; physical activity and inactivity mechanisms differ; gene‐environment interaction (including aerobic training adaptations, personalized medicine, and co‐twin physical activity); and specificity of adaptations to type of training. Next, physical activity/exercise is examined as primary prevention against 35 chronic conditions [accelerated biological aging/premature death, low cardiorespiratory fitness (V o 2 max), sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, nonalcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, pre‐eclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The article ends with consideration of deterioration of risk factors in longer‐term sedentary groups; clinical consequences of inactive childhood/adolescence; and public policy. In summary, the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life. Taken together, conclusive evidence exists that physical inactivity is one important cause of most chronic diseases. In addition, physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life. © 2012 American Physiological Society. Compr Physiol 2:1143‐1211, 2012.

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Fasting Plasma Glucose Levels Within the Normoglycemic Range in Childhood as a Predictor of Prediabetes and Type 2 Diabetes in Adulthood

Abstract: To determine whether childhood elevated fasting plasma glucose (FPG) levels within the normoglycemic range predict diabetes in adulthood.

Cited by 78 publications

References 24 publications

Fine-mapping diabetes-related traits, including insulin resistance, in heterogeneous stock rats

Fine-mapping diabetes-related traits, including insulin resistance, in heterogeneous stock rats

Metabolic Syndrome: Bridging the Gap from Childhood to Adulthood

Lack of Exercise Is a Major Cause of Chronic Diseases

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