scholarly journals Insulin Resistance and Lipid Disorders in Pre-Pubertal Children Born Small for Gestational Age

2011 ◽  
Vol 70 ◽  
pp. 371-371
Author(s):  
A Kapitsinou ◽  
C Tsendidis ◽  
D Kyriakou ◽  
A Foteinou ◽  
A Drakatos ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Lipid Disorders

scholarly journals Premature small for gestational age infants fed an exclusive human milk-based diet achieve catch-up growth without metabolic consequences at 2 years of age

2018 ◽  
Vol 104 (3) ◽  
pp. F242-F247 ◽  
Author(s):  
Chonnikant Visuthranukul ◽  
Steven A Abrams ◽  
Keli M Hawthorne ◽  
Joseph L Hagan ◽  
Amy B Hair
Keyword(s):  
Insulin Resistance ◽  
Body Composition ◽  
Birth Weight ◽  
Human Milk ◽  
Premature Infants ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Insulin Level ◽  
Metabolic Outcomes ◽  
Catch Up

ObjectiveTo compare postdischarge growth, adiposity and metabolic outcomes of appropriate for gestational age (AGA) versus small for gestational age (SGA) premature infants fed an exclusive human milk (HM)-based diet in the neonatal intensive care unit.DesignPremature infants (birth weight ≤1250 g) fed an exclusive HM-based diet were examined at 12–15 months corrected gestational age (CGA) (visit 1) for anthropometrics, serum glucose and non-fasting insulin, and at 18–22 months CGA (visit 2) for body composition by dual-energy X-ray absorptiometry.ResultsOf 51 children, 33 were AGA and 18 were SGA at birth. The SGA group had weight gain (g/day) equal to AGA group during the follow-up period. SGA had a significantly greater body mass index (BMI) z-score gain from visit 1 to visit 2 (0.25±1.10 vs −0.21±0.84, p=0.02) reflecting catch-up growth. There were no significant differences in total fat mass (FM) and trunk FM between groups. SGA had significantly lower insulin level (5.0±3.7 vs 17.3±15.1 µU/mL, p=0.02) and homeostatic model of assessment-insulin resistance (1.1±0.9 vs 4.3±4.1, p=0.02). Although regional trunk FM correlated with insulin levels in SGA (r=0.893, p=0.04), they had lower insulin level compared with AGA and no difference in adiposity.ConclusionsSGA premature infants who received an exclusive HM-based diet exhibited greater catch-up growth without increased adiposity or elevated insulin resistance compared with AGA at 2 years of age. An exclusive HM-based diet may improve long-term body composition and metabolic outcomes of premature infants with ≤1250 g birth weight, specifically SGA.

scholarly journals Differential DNA methylation profile in infants born small-for-gestational-age: association with markers of adiposity and insulin resistance from birth to age 24 months

2020 ◽  
Vol 8 (1) ◽  
pp. e001402
Author(s):  
Marta Diaz ◽  
Edurne Garde ◽  
Abel Lopez-Bermejo ◽  
Francis de Zegher ◽  
Lourdes Ibañez
Keyword(s):  
Insulin Resistance ◽  
Dna Methylation ◽  
Body Composition ◽  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Diabetes Risk ◽  
Metabolic Dysfunction ◽  
A Genome ◽  
Methylation Profiling

IntroductionPrenatal growth restraint followed by rapid postnatal weight gain increases lifelong diabetes risk. Epigenetic dysregulation in critical windows could exert long-term effects on metabolism and confer such risk.Research design and methodsWe conducted a genome-wide DNA methylation profiling in peripheral blood from infants born appropriate-for-gestational-age (AGA, n=30) or small-for-gestational-age (SGA, n=21, with postnatal catch-up) at age 12 months, to identify new genes that may predispose to metabolic dysfunction. Candidate genes were validated by bisulfite pyrosequencing in the entire cohort. All infants were followed since birth; cord blood methylation profiling was previously reported. Endocrine-metabolic variables and body composition (dual-energy X-ray absorptiometry) were assessed at birth and at 12 and 24 months.ResultsGPR120 (cg14582356, cg01272400, cg23654127, cg03629447), NKX6.1 (cg22598426, cg07688460, cg17444738, cg12076463, cg10457539), CPT1A (cg14073497, cg00941258, cg12778395) and IGFBP 4 (cg15471812) genes were hypermethylated (GPR120, NKX6.1 were also hypermethylated in cord blood), whereas CHGA (cg13332653, cg15480367, cg05700406), FABP5 (cg00696973, cg10563714, cg16128701), CTRP1 (cg19231170, cg19472078, cg0164309, cg07162665, cg17758081, cg18996910, cg06709009), GAS6 (N/A), ONECUT1 (cg14217069, cg02061705, cg26158897, cg06657050, cg15446043) and SLC2A8 (cg20758474, cg19021975, cg11312566, cg12281690, cg04016166, cg03804985) genes were hypomethylated in SGA infants. These genes were related to β-cell development and function, inflammation, and glucose and lipid metabolism and associated with body mass index, body composition, and markers of insulin resistance at 12 and 24 months.ConclusionIn conclusion, at 12 months, abnormal methylation of GPR120 and NKX6.1 persists and new epigenetic marks further involved in adipogenesis and energy homeostasis arise in SGA infants. These abnormalities may contribute to metabolic dysfunction and diabetes risk later in life.

scholarly journals The Somatotropic Axis in Short Children Born Small for Gestational Age: Relation to Insulin Resistance

2002 ◽  
Vol 51 (1) ◽  
pp. 76-80 ◽  
Author(s):  
Katie A Woods ◽  
Maria Van Helvoirt ◽  
Ken K L Ong ◽  
Angelica Mohn ◽  
Jonathan Levy ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Somatotropic Axis ◽  
Short Children ◽  
Age Relation

scholarly journals Small for Gestational Age and Magnesium in Cord Blood Platelets: Intrauterine Magnesium Deficiency May Induce Metabolic Syndrome in Later Life

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Junji Takaya ◽  
Kazunari Kaneko
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Magnesium Deficiency ◽  
Blood Platelets ◽  
Later Life ◽  
Intracellular Magnesium ◽  
Increased Risk

Magnesium deficiency in pregnancy frequently occurs because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problems, but also consequences that might last in offspring throughout life. Many epidemiological studies have disclosed that small for gestational age (SGA) is associated with an increased risk of insulin resistance in adult life. We reported that intracellular magnesium of cord blood platelets is lower in SGA groups than that in appropriate for gestational age groups, suggesting that intrauterine magnesium deficiency may result in SGA. Taken together, intrauterine magnesium deficiency in the fetus may lead to or at least program insulin resistance after birth. In this review, we propose that intrauterine magnesium deficiency may induce metabolic syndrome in later life. We discuss the potential contribution of aberrant magnesium regulation to SGA and to the pathogenesis of metabolic syndrome.

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