Distribution of Adipose Tissue in the Newborn

Harrington, Tracey; Thomas, E. Louise; Frost, Gary; Modi, Neena; Bell, Jimmy D.

doi:10.1203/01.pdr.0000111202.29433.2d

Cited by 106 publications

(87 citation statements)

References 27 publications

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“…in subcutaneous abdominal adipose tissue but not in other depots (37). Subcutaneous trunk fat is an important fat compartment in utero (38), which may explain the transient increase in circulating FFA following GC exposure. However, although small-for-GA neonates have less subcutaneous fat than appropriate-for-GA neonates (38), we did not find that the FFA response to GC interacted with BW z score ( Table 3).…”

Section: Discussionmentioning

confidence: 95%

Transient Catabolic State with Reduced IGF-I after Antenatal Glucocorticoids

et al. 2007

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Glucocorticoid (GC) administration before preterm birth reduces neonatal morbidity but may restrain growth. Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1-1358 h before birth) and 49 newborns that did not. We found that recent GC exposure (Յ48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. The AA surge was greater in newborns with a birth weight z score Ͻ0 than in those with a z score Ͼ0. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. These changes may explain the growth-inhibitory effects of repeated antenatal GC administration. Future research should clarify the role of IGF-I in the protein-catabolic response to GC. (Pediatr Res 62: 295-300, 2007)

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Section: Discussionmentioning

confidence: 95%

Transient Catabolic State with Reduced IGF-I after Antenatal Glucocorticoids

et al. 2007

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“…We used no additional selection criteria, and recruited in keeping with the availability of the MRI scanner. We excluded mothers with preexisting diabetes and small-for-gestational-age infants because we have previously shown them to have altered AT distribution (13). We undertook assessments at the following two time points: within 2 weeks of birth and at 8-12 weeks after birth.…”

Section: Methodsmentioning

confidence: 99%

Development of Early Adiposity in Infants of Mothers With Gestational Diabetes Mellitus

Logan

Jeffries

et al. 2016

Diabetes Care

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OBJECTIVEInfants born to mothers with gestational diabetes mellitus (GDM) are at greater risk of later adverse metabolic health. We examined plausible candidate mediators, adipose tissue (AT) quantity and distribution and intrahepatocellular lipid (IHCL) content, comparing infants of mothers with GDM and without GDM (control group) over the first 3 postnatal months. RESEARCH DESIGN AND METHODSWe conducted a prospective longitudinal study using MRI and spectroscopy to quantify whole-body and regional AT volumes, and IHCL content, within 2 weeks and 8-12 weeks after birth. We adjusted for infant size and sex and maternal prepregnancy BMI. Values are reported as the mean difference (95% CI). RESULTSWe recruited 86 infants (GDM group 42 infants; control group 44 infants). Mothers with GDM had good pregnancy glycemic control. Infants were predominantly breast-fed up to the time of the second assessment (GDM group 71%; control group 74%). Total AT volumes were similar in the GDM group compared with the control group at a median age of 11 days (228 cm 3 [95% CI 2121, 65], P = 0.55), but were greater in the GDM group at a median age of 10 weeks (247 cm 3 [56, 439], P = 0.01). After adjustment for size, the GDM group had significantly greater total AT volume at 10 weeks than control group infants (16.0% [6.0, 27.1], P = 0.002). AT distribution and IHCL content were not significantly different at either time point. CONCLUSIONSAdiposity in GDM infants is amplified in early infancy, despite good maternal glycemic control and predominant breast-feeding, suggesting a potential causal pathway to later adverse metabolic health. Reduction in postnatal adiposity may be a therapeutic target to reduce later health risks.Diabetes in pregnancy is increasing and currently affects up to 5% of women in the U.K.(1) and up to 9.2% in the U.S. (2). Approximately 87.5% of cases are gestational diabetes mellitus (GDM), 7.5% are type 1 diabetes, and 5% are type 2 diabetes (1). The offspring of mothers with diabetes have greater risks of adverse metabolic sequelae in childhood and later life that appear to be additional to genetic predisposition (3-5).The underlying mechanisms are unclear, but increased infant adiposity is a plausible mediator because adiposity in childhood and adult life are associated with type 2 diabetes and cardiovascular disease (6). The Hyperglycemia and Adverse

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“…Compared with other mammals, humans have a high amount of white fat at birth, and it has been argued that this fat is an important energetic buffer for brain development against the risk of malnutrition following weaning. 23 Indeed, recent studies show that, in children born smaller, visceral fat is maintained despite fetal nutrient supply limitations, 24,25 suggesting the importance of non-thermogenic metabolic capacity in infancy across our evolution.…”

Section: Life Historymentioning

confidence: 99%

“…These show that although smaller babies have reduced subcutaneous fat with the reduction proportionate to birth size, visceral fat is preserved so that the smaller babies have relative visceral adiposity. 24,25 Given the labile function of visceral fat, 35 this provides a plausible route to later metabolic compromise.…”

Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 99%

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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Although variation in individual lifestyle and genotype are important factors in explaining individual variation in the risk of developing obesity in an obesogenic environment, there is growing evidence that developmentally plastic processes also contribute. These effects are mediated at least in part through epigenetic processes. These developmental pathways do not directly cause obesity but rather alter the risk of an individual developing obesity later in life. At least two classes of developmental pathway are involved. The mismatch pathway involves the evolved adaptive responses of the developing organism to anticipated future adverse environments, which have maladaptive consequences if the environment is mismatched to that predicted. This pathway can be cued by prenatal undernutrition or stresses that lead the organism to forecast an adverse future environment and change its developmental trajectory accordingly. As a result, individuals develop with central and peripheral changes that increase their sensitivity to an obesogenic environment. It provides a model for how obesity emerges in populations in rapid transition, but also operates in developed countries. There is growing experimental evidence that this pathway can be manipulated by, for example, postnatal leptin exposure. Secondly, maternal diabetes, maternal obesity and infant overfeeding are associated with a greater risk of later obesity. Early life offers a potential point for preventative intervention.

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Distribution of Adipose Tissue in the Newborn

Cited by 106 publications

References 27 publications

Transient Catabolic State with Reduced IGF-I after Antenatal Glucocorticoids

Transient Catabolic State with Reduced IGF-I after Antenatal Glucocorticoids

Development of Early Adiposity in Infants of Mothers With Gestational Diabetes Mellitus

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

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