Adipose Tissue Thymidine Kinase Activity in Man

Baum, David; Beck, Rebecca Q.; Hammer, Lawrence D.; Brasel, Jo Anne; Greenwood, M. R. C.

doi:10.1203/00006450-198602000-00004

Cited by 17 publications

(9 citation statements)

References 14 publications

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“…This may reflect a chance finding, or different maternal characteristics in the two cohorts, such as the greater maternal adiposity and maternal folate supplementation in the SWS cohort (22,40,41). Alternatively, adipocyte proliferation is high during the first year of life, but then remains low until a second proliferate phase from 9-14 years (42). Thus the processes which determine adiposity at 9 years might differ from those at 6 years.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Gene Promoter Methylation at Birth Is Associated With Child’s Later Adiposity

et al. 2011

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OBJECTIVEFixed genomic variation explains only a small proportion of the risk of adiposity. In animal models, maternal diet alters offspring body composition, accompanied by epigenetic changes in metabolic control genes. Little is known about whether such processes operate in humans.RESEARCH DESIGN AND METHODSUsing Sequenom MassARRAY we measured the methylation status of 68 CpGs 5′ from five candidate genes in umbilical cord tissue DNA from healthy neonates. Methylation varied greatly at particular CpGs: for 31 CpGs with median methylation ≥5% and a 5–95% range ≥10%, we related methylation status to maternal pregnancy diet and to child’s adiposity at age 9 years. Replication was sought in a second independent cohort.RESULTSIn cohort 1, retinoid X receptor-α (RXRA) chr9:136355885+ and endothelial nitric oxide synthase (eNOS) chr7:150315553+ methylation had independent associations with sex-adjusted childhood fat mass (exponentiated regression coefficient [β] 17% per SD change in methylation [95% CI 4–31], P = 0.009, n = 64, and β = 20% [9–32], P < 0.001, n = 66, respectively) and %fat mass (β = 10% [1–19], P = 0.023, n = 64 and β =12% [4–20], P = 0.002, n = 66, respectively). Regression analyses including sex and neonatal epigenetic marks explained >25% of the variance in childhood adiposity. Higher methylation of RXRA chr9:136355885+, but not of eNOS chr7:150315553+, was associated with lower maternal carbohydrate intake in early pregnancy, previously linked with higher neonatal adiposity in this population. In cohort 2, cord eNOS chr7:150315553+ methylation showed no association with adiposity, but RXRA chr9:136355885+ methylation showed similar associations with fat mass and %fat mass (β = 6% [2–10] and β = 4% [1–7], respectively, both P = 0.002, n = 239).CONCLUSIONSOur findings suggest a substantial component of metabolic disease risk has a prenatal developmental basis. Perinatal epigenetic analysis may have utility in identifying individual vulnerability to later obesity and metabolic disease.

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Section: Discussionmentioning

confidence: 99%

Epigenetic Gene Promoter Methylation at Birth Is Associated With Child’s Later Adiposity

et al. 2011

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“…Several studies favour the view that, during the first year of life, body fat accumulates through an increase of mean adipocyte size (hypertrophy), a characteristic feature of body fat increase (9,10). Other studies have also shown a sudden proliferation of (presumably) precursor cells in the subcutaneous adipose tissue of infants during the first year of life (11,12). As the number of adipocytes increases with the early onset of childhood obesity (13), it is reasonable to assume that the capacity of precursor cells to divide and to undergo possible self‐renewal is highest during the first year of life regardless of their differentiation into adipocytes taking place at that time or later in life.…”

Section: White Adipose Tissue Development In Early Lifementioning

confidence: 99%

Fatty acid composition of fats is an early determinant of childhood obesity: a short review and an opinion

Ailhaud

Guesnet²

2004

Obesity Reviews

169

125

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The importance of dietary fat in human obesity remains a controversial issue as the prevalence of overweight and obesity has increased despite no dramatic change in the amount of ingested fats over the past few decades. However, qualitative changes (i.e. the fatty acid composition of fats) have been largely disregarded. In this review, we summarize experimental evidence which supports polyunsaturated fatty acids of the omega6 series as being potent promoters of both adipogenesis in vitro and adipose tissue development in vivo during the gestation/lactation period. This conclusion is also supported by epidemiological data from infant studies as well as by the assessment of the fatty acid composition of mature breast milk and formula milk. It is proposed that unnoticed changes in fatty acid composition of ingested fats over the last decades have been important determinants in the increasing prevalence of childhood overweight and obesity.

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“…The enlargement of adipose tissue during its first rapid growth in the first year of life seems to be mainly due to an increase in the volume of already existing fat cells [7][8][9], More recent studies provide evi dence that the proliferation of adipocyte precursor cells may also be stimulated during this period [10,11]. From the end of the first year of life fat cell size in normalweight individuals seems to remain almost stable [7], The further growth of the adipose organ is probably due to an augmentation of fat cell number, especially evident dur ing its second period of rapid growth before and during puberty [7],…”

Section: Development Of Adipose Tissue In Normal Childrenmentioning

confidence: 99%

Body Fat in GH-Deficient Children and the Effect of Treatment

Wabitsch¹,

Heinze²

1993

Horm Res

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Children with isolated GH deficiency have enlarged fat depots due to increased fat cell volume. The fat cell number is however decreased compared with appropriate controls. Treatment of patients with GH results in a relative loss of body fat and shifts both fat cell number and fat cell volume towards normal. These findings of adipose tissue cellularity in GH-deficient children before and after treatment can be explained by results from in vitro studies indicating that GH exerts a variety of effects on the metabolism of mature fat cells and on the proliferation and differentiation of cultured preadipocytes. Therefore, GH is one of the factors that determines adipose tissue development during childhood.

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Adipose Tissue Thymidine Kinase Activity in Man

Cited by 17 publications

References 14 publications

Epigenetic Gene Promoter Methylation at Birth Is Associated With Child’s Later Adiposity

Epigenetic Gene Promoter Methylation at Birth Is Associated With Child’s Later Adiposity

Fatty acid composition of fats is an early determinant of childhood obesity: a short review and an opinion

Body Fat in GH-Deficient Children and the Effect of Treatment

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