Small for Gestational Age: Short Stature and Beyond

Saenger, Paul; Czernichow, P; Hughes, Ieuan A.; Reiter, Edward O.

doi:10.1210/er.2006-0039

Cited by 444 publications

(418 citation statements)

References 379 publications

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“…The thrifty phenotype hypothesis [38] suggests that the fetus adapts to an adverse intrauterine environment by diverting limited nutrients to favor the survival and development of vital organs, such as the brain, at the expense of growth. Important metabolic pathways would be permanently programmed during fetal life, leading to metabolic disturbances in adulthood [31,39]. There is evidence suggesting that the degree of weight gain Finally, elevated plasma FFAs inhibit the insulin signal transduction system [24,113,114].…”

Section: Adipocytokines In Children Born Small For Gestational Agementioning

confidence: 99%

Adipose Tissue: A Metabolic Regulator. Potential Implications for the Metabolic Outcome of Subjects Born Small for Gestational Age (SGA)

2007

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■ AbstractAdipose tissue is involved in the regulation of glucose and lipid metabolism, energy balance, inflammation and immune response. Abdominal obesity plays a key role in the development of insulin resistance because of the high lipolytic rate of visceral adipose tissue and its secretion of adipocytokines. Low birth weight subjects are prone to central redistribution of adipose tissue and are at high risk of developing metabolic syndrome, type 2 diabetes and cardiovascular disease. Intrauterine adipogenesis may play a key role in the fetal origin of the pathogenesis of metabolic syndrome, type 2 diabetes and cardiovascular disease. Therefore, knowledge of the behavior of visceral adipose tissue-derived stem cells could provide a greater understanding of the metabolic risk related to intrauterine growth retardation, with potential clinical implications for the prevention of long-term metabolic alterations.Keywords: diabetes · SGA · adipose tissue · glucose metabolism · lipids · insulin resistance · low birth weight Adipose tissue and insulin resistancePathophysiology of visceral adipose tissue: the role of free fatty acids dipocytes are highly specialized cells that maintain whole body energy homeostasis by regulating glucose and lipid metabolism. For a long time, adipocytes have been considered to be an energy depot that stores and mobilizes triglycerides [1]. Recently, adipocytes have also been recognized as an endocrine tissue because of the discovery of several adipocyte-derived molecules, including lipid metabolites and adipocytokines [2].Adipose tissue contains functionally distinct cellular subtypes, the white adipocyte, devoted to energy storage, and the brown adipocyte, which dissipates energy through thermogenesis. In the rat, brown adipose tissue is the major site of heat production. Brown fat also plays a major role in heat production in the neonates of many mammalian species. Its quantitative contribution to energy metabolism at maturity in large mammals, including humans, is uncertain. The storage of triglycerides and fatty acids in white adipose tissue occurs through the ability of insulin to stimulate significantly both glucose uptake and lipogenesis. Defects in fuel partitioning into adipocytes either because of increased adipose mass or increased circulating free fatty acids, results in dyslipidemia, obesity, insulin resistance and type 2 diabetes [3].The association between type 2 diabetes and obesity is well established. Several studies have docu-

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Section: Adipocytokines In Children Born Small For Gestational Agementioning

confidence: 99%

Adipose Tissue: A Metabolic Regulator. Potential Implications for the Metabolic Outcome of Subjects Born Small for Gestational Age (SGA)

2007

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“…Although this association is clearly established in adults (5), results in children are still conflicting (6). Some authors have suggested that IR, as a consequence of intrauterine growth retardation would be detectable as early as birth (7,8).…”

Section: Introductionmentioning

confidence: 99%

Retinol-binding protein 4 in neonates born small for gestational age

Giacomozzi

Ghirri

Lapolla

et al. 2010

J Endocrinol Invest

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ABSTRACT. Background: Retinol-binding protein 4 (RBP4) is an adipocyte-derived 'signal' that may contribute to the pathogenesis of insulin resistance and Type 2 diabetes. The relationship of RBP4 with insulin resistance and metabolic risk in human beings has been the subject of several studies. Subjects born small for gestational age (SGA) are at risk of insulin resistance and Type 2 diabetes. Though RBP4 could represent an early marker of insulin resistance, to date, none have determined RBP4 in SGA children. Aim: Our aim was to measure RBP4 concentrations in cord blood of SGA newborns compared with those in children born with a birth weight appropriate for gestational age (AGA) and to determine whether serum RBP4 levels at birth correlate with insulin sensitivity markers. Subjects and methods: Sixty-four newborns, 17 born SGA (mean gestational age: 36.4±2.1 weeks), and 47 born AGA (mean gestational age: 37.0±3.6 weeks) were studied. The main outcome measures included anthropometry, lipid profile, insulin, homeostasis model assessment, quantitative insulin-sensitivity check index, adiponectin, and RBP4. Results: RBP4 concentrations were significantly reduced in SGA newborns (p<0.002). No relationship was found between RBP4 and insulin sensitivity parameters. Stepwise regression analysis revealed that birth weight was the major predictor of RBP4 serum concentrations (p<0.001). Conclusion: RBP4 is reduced in SGA newborns, birth weight representing the major determinant of RBP4 concentrations, and is not related to insulin sensitivity. No significant difference in adiponectin levels and insulin sensitivity markers was found between SGA and AGA neonates. INTRODUCTIONRetinol-binding protein 4 (RBP4) is an adipocyte-derived 'signal' that may contribute to the pathogenesis of insulin resistance (IR) and Type 2 diabetes. RBP4 could play a role in obesity-induced IR, since chronic elevation of RBP4 in mice increases hepatic glucose production, down-regulates insulin signaling in muscle, and causes systemic IR (1). Furthermore, lowering elevated serum RBP4 levels in obese mice with a synthetic retinoid improves insulin sensitivity and normalizes glucose tolerance (1). In humans, the link between RBP4 and IR is less clear. In adulthood, serum RBP4 levels have been shown to correlate with the magnitude of IR in subjects with obesity, impaired glucose tolerance, and Type 2 diabetes (2). Moreover, elevated serum RBP4 was associated with components of the metabolic syndrome, including increased body mass index, waist-tohip ratio, serum triglyceride levels, and systolic blood pressure and decreased HDL cholesterol levels (2). In childhood, a relationship between serum RBP4 and obesity and components of the metabolic syndrome has been described in pre-pubertal and early pubertal children (3).Increased risk of developing IR and Type 2 diabetes in adulthood is associated with low birth weight (4). Although this association is clearly established in adults (5), results in children are still conflicting (6). Some authors have sugg...

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“…Although there were important differences in risk factors for diabetes between the two settings, estimates suggest that effect sizes of BMI on HOMA%S were the same in Limache and Ribeirao Preto. Although most studies have shown an effect of BW on HOMA%S, this observation is not unanimous [27]. Gupta et al found higher insulin resistance among Indian low BW children [28] whereas in the UK no association was observed in children [10,11].…”

Section: Interpretation Of the Findingsmentioning

confidence: 98%