Carbohydrate metabolism in primary growth hormone resistance (Laron syndrome) before and during insulin-like growth factor-I treatment

Laron, Zvi; Avitzur, Yaron; Klinger, B.

doi:10.1016/0026-0495(95)90231-7

Cited by 68 publications

(73 citation statements)

References 21 publications

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“…In adults, a reduction in waist circumference (implying lower abdominal fat) with increasing birth weight is reported by some (17,18) but not others (8). Differences in the relation between birth weight and adolescent size may be related to a number of factors, including age, ethnicity, maternal glucose tolerance during pregnancy (19,20), changing body composition in adolescence, childhood exposures to diet and physical activity, and hormonal influences such as IGF-1 (21). The pattern of the association of birth weight to insulin sensitivity (M LBM ) in this study suggests greater insulin sensitivity with greater birth weight.…”

Section: Research Design and Methods -This Study Was Approved By The mentioning

confidence: 99%

Relation of Birth Weight to Fasting Insulin, Insulin Resistance, and Body Size in Adolescence

et al. 2003

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OBJECTIVE -A relationship between birth weight and the insulin resistance syndrome has been reported in adults but has not been defined in adolescents.RESEARCH DESIGN AND METHODS -Data were analyzed in 296 children (132 girls and 164 boys) mean age 15.0 Ϯ 1.2 years who had euglycemic insulin clamp studies (intravenous administration of 1 mU ⅐ kg -1 ⅐ min -1 of insulin balanced by a variable infusion of 20% glucose to maintain blood glucose at 100 mg/dl). Insulin sensitivity (M LBM ) was determined by glucose uptake per kg lean body mass (LBM), and parents reported birth weight.RESULTS -Birth weight ranged from 1,021 to 4,848 g (mean Ϯ SD 3,433 Ϯ 551), with 4.0% Ͻ2,500 g. Fat mass and BMI had U-shaped relations with birth weight after adjustment for race, age, sex, and blood pressure. Lean mass index (lean mass/height squared) was stable across birth weight quartiles. Fasting insulin decreased nonsignificantly across birth weight quartiles but became significant after adjustment for adolescent weight (P ϭ 0.008). Although M LBM was highest in the highest birth weight quartile, the pattern was not significant. Triglycerides tended to increase with birth weight, whereas LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) tended to decrease. Blood pressure was unrelated to birth weight.CONCLUSIONS -In this cohort, fat mass was greater in adolescents with low and high birth weight; fasting insulin was lower with higher birth weight after adjustment for adolescent weight. Insulin sensitivity increased nonsignificantly with birth weight. Diabetes Care 26:187-192, 2003L ow (1-5) and high (6) birth weight are both associated with an increased risk for type 2 diabetes and cardiovascular disease in adults. The relationship of birth weight to these diseases is thought to represent the influence of fetal nutrition on the prenatal programming of processes that effect long-term growth and metabolism (7,8). Studies in children and adolescents from different cultures suggest that an association between birth weight and the insulin resistance syndrome also can be identified early in life (9 -11).Previous studies in children have used fasting and postload glucose and insulin to relate birth weight to estimates of ␤-cell insulin production and insulin resistance (9 -11). However, serum and plasma insulin and glucose levels represent an integrated response to secretion, metabolism, and clearance of insulin and glucose, and it is generally agreed that the hyperinsulinemic-euglycemic clamp is a more accurate measure of insulin resistance (12). In the present study, the relationship of birth weight to factors associated with the insulin resistance syndrome was examined in adolescents who had hyperinsulinemic-euglycemic clamps performed as part of a longitudinal study on cardiovascular risk. RESEARCH DESIGN AND METHODS -This study was approved by the Institutional Review Board:Human Subjects Committee of the University of Minnesota. Written consent was obtained from all children and their parents/guardians.The children participating in ...

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Section: Research Design and Methods -This Study Was Approved By The mentioning

confidence: 99%

Relation of Birth Weight to Fasting Insulin, Insulin Resistance, and Body Size in Adolescence

et al. 2003

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“…25,26 In addition to vascular endothelial growth factor disturbances, other factors such as insulin-like growth factor-1 deficiency, could also be responsible for both, glucose instability and ROP. Insulin-like growth factor-1 deficiency is associated with glucose intolerance and frank diabetes which improves with replacement treatment 27 and relative insulin-like growth factor-1 deficiency, a common disturbance in VLBW infants, may also have a role in ROP development. 28,29 Severity of ROP is also greater in infants developing more frequent episodes of hypoxemia which is another common event during the early life of ELBW infants.…”

Section: Abnormal Glucose Levels In Elbw Infantsmentioning

confidence: 99%

Contribution of early glycemic status in the development of severe retinopathy of prematurity in a cohort of ELBW infants

et al. 2011

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Objective: The objective of this study is to investigate the relationship between glycemic status and severe retinopathy of prematurity (ROP).Study Design: This is a retrospective cohort study of 114 infants <1000 g admitted to a level IV neonatal intensive care unit within 48 h of life. A cumulative, time-weighted glucose level (TWGL) derived from plotting glucose values over time was included in logistic regression analysis to identify predictors for severe ROP.Result: Infants had 26.6 ± 2 weeks gestational age and had a birth weight of 782±136 g. TWGL during first 10 and 30 days of life were greater in the severe ROP group (P<0.01). Unlike single events of glucose levels X150 mg dl À1 , 10 days TWGL X100 mg dl À1 (odds ratio (OR) 5.2, P<0.02) and 30 days TWGL X118 mg dl À1 (OR 5.7, P<0.02) were predictors for severe ROP (univariate). Multivariate regression confirmed 30 days TWGL X118 mg dl À1 (OR 9.4 to 10) and gram-positive sepsis (OR 4.1 to 5) as predictors for severe ROP (P<0.05). Conclusion:High overall glycemic status is associated with the development of severe ROP.

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“…One exception is the group of individuals with GH receptor mutations who develop insulin resistance as adults. Administration of IGF-1 to these patients, who are unresponsive to GH, results in improvement in insulin sensitivity (15,16). This difficulty in distinguishing between the effects of GH suppression and the direct effects of IGF-1 has been addressed in the studies of Yakar et al (2).…”

Section: Food Intake and Gh Regulate Insulin-like Peptide Secretionmentioning

confidence: 99%

“…This is a wonderful example of knowledge gained by applying the Western scientific method to an Eastern herbal remedy. It will be very exciting if a pure compound emerges from the tea leaves as a pharmacological therapy for neonatal jaundice that is complementary or alternative to the current Western practice of phototherapy (16 IGF-1 and growth hormone (GH) interact with insulin to modulate its control of carbohydrate metabolism. A new study (see the related article beginning on page 96) shows that blocking the effect of GH in the presence of low serum IGF-1 concentrations enhances insulin sensitivity.…”

mentioning

confidence: 99%

The relative roles of growth hormone and IGF-1 in controlling insulin sensitivity

Clemmons

2004

J. Clin. Invest.

162

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Carbohydrate metabolism in primary growth hormone resistance (Laron syndrome) before and during insulin-like growth factor-I treatment

Cited by 68 publications

References 21 publications

Relation of Birth Weight to Fasting Insulin, Insulin Resistance, and Body Size in Adolescence

Relation of Birth Weight to Fasting Insulin, Insulin Resistance, and Body Size in Adolescence

Contribution of early glycemic status in the development of severe retinopathy of prematurity in a cohort of ELBW infants

The relative roles of growth hormone and IGF-1 in controlling insulin sensitivity

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