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Ortiz Espejo M.,Hospital Universitario Reina Sofia | Gil Campos M.,Hospital Universitario Reina Sofia | Munoz Villanueva M.C.,Instituto Maimonides Of Investigacion Biomedica Imibic | Perez Navero J.L.,Hospital Universitario Reina Sofia
Anales de Pediatria | Year: 2012

Introduction: Extrauterine growth restriction (EUGR) is associated with severe nutritional deficit during the first weeks of life, which, as intrauterine growth restriction, may lead to metabolic anomalies in later stages of life. Patients and methods: A group of 38 prepuberty children with a history of EUGR were selected, along with a control group of 123 children with similar age and gender. Perinatal stage was assessed in the EUGR group. Anthropometric parameters, blood pressure, serum biochemical markers of carbohydrate metabolism, and lipid profile were measured in both groups. Results: The EUGR group had height and body mass index values significantly lower than in the control group (P<.001) and higher systolic and diastolic blood pressure (P<.001). The majority (70%) of EUGR children were below the 50th percentile for weight and height, and 55% were below the 25th percentile for body mass index (P<.001), as well as 46% and 37% above the 95% percentile for systolic and diastolic blood pressure, respectively (P<.001). The EUGR group had higher glucose levels (P<.001) and lower high density lipoprotein cholesterol (HDLc) (P<.001) than the control group, although without clinical relevance. Conclusions: Children with a history of EUGR have anthropometric, blood pressure and metabolic alterations in the prepuberty stage. It would be desirable to control the nutrition they receive in the perinatal period, and follow them up in childhood as alterations may occur in the future.

Pulido M.R.,University of Cordoba, Spain | Pulido M.R.,Research Center Biomedica En Red Fisiopatologia Of La Obesidad | Pulido M.R.,Instituto Maimonides Of Investigacion Biomedica Imibic | Diaz-Ruiz A.,University of Cordoba, Spain | And 23 more authors.
PLoS ONE | Year: 2011

Lipid droplets (LDs) are organelles that coordinate lipid storage and mobilization, both processes being especially important in cells specialized in managing fat, the adipocytes. Proteomic analyses of LDs have consistently identified the small GTPase Rab18 as a component of the LD coat. However, the specific contribution of Rab18 to adipocyte function remains to be elucidated. Herein, we have analyzed Rab18 expression, intracellular localization and function in relation to the metabolic status of adipocytes. We show that Rab18 production increases during adipogenic differentiation of 3T3-L1 cells. In addition, our data show that insulin induces, via phosphatidylinositol 3-kinase (PI3K), the recruitment of Rab18 to the surface of LDs. Furthermore, Rab18 overexpression increased basal lipogenesis and Rab18 silencing impaired the lipogenic response to insulin, thereby suggesting that this GTPase promotes fat accumulation in adipocytes. On the other hand, studies of the β-adrenergic receptor agonist isoproterenol confirmed and extended previous evidence for the participation of Rab18 in lipolysis. Together, our data support the view that Rab18 is a common mediator of lipolysis and lipogenesis and suggests that the endoplasmic reticulum (ER) is the link that enables Rab18 action on these two processes. Finally, we describe, for the first time, the presence of Rab18 in human adipose tissue, wherein the expression of this GTPase exhibits sex- and depot-specific differences and is correlated to obesity. Taken together, these findings indicate that Rab18 is involved in insulin-mediated lipogenesis, as well as in β-adrenergic-induced lipolysis, likely facilitating interaction of LDs with ER membranes and the exchange of lipids between these compartments. A role for Rab18 in the regulation of adipocyte biology under both normal and pathological conditions is proposed. © 2011 Pulido et al.

Garcia-Galiano D.,University of Cordoba, Spain | Garcia-Galiano D.,CIBER ISCIII | Garcia-Galiano D.,Instituto Maimonides Of Investigacion Biomedica Imibic | Tena-Sempere M.,University of Cordoba, Spain | And 2 more authors.
Current Pharmaceutical Design | Year: 2013

Nesfatin-1, derived from the precursor NEFA/nucleobindin2 (NUCB2), was initially identified as a feeding-suppressing neuropeptide, acting at central (mainly, hypothalamic) levels in a leptin-independent manner. However, recent experimental evidence strongly suggests that, rather than being a simple anorectic hypothalamic signal, nesfatin-1 operates at different tissues as an integral regulator of energy homeostasis and closely related neuroendocrine functions. On the latter, growing, albeit as yet fragmentary, evidence has pointed out recently that NUCB2/ nesfatin-1 is involved in the regulation of different aspects of reproductive maturation and function, by acting probably at different levels of the hypothalamic-pituitary-gonadal (HPG) axis. As documented by rodent studies, the reproductive facet of nesfatin-1 likely includes (i) a permissive role in (female) pubertal maturation, (ii) stimulatory effects on the gonadotropic axis, whose magnitude, in terms of LH responses, varies depending on the maturational stage and probably the sex and species, and (iii) direct expression and actions in the gonads. These features, together with the proven expression of NUCB2/nesfatin-1 in tissues with essential roles in the metabolic control of reproduction, such as the hypothalamus, adipose and pancreas, support a putative role of nesfatin-1 as neurohormonal signal linking body metabolic status, puberty and fertility. Curiously enough, although its reproductive dimension seems to be conserved in non-mammalian vertebrates, recent studies in goldfish have surfaced predominant inhibitory actions of nesfatin-1 at different levels of the HPG axis in fish. These findings illustrate our as yet limited understanding of this aspect of nesfatin-1 physiology, whose relevance in the joint control of metabolism and reproduction in health and disease warrants further investigation. © 2013 Bentham Science Publishers.

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