Number of colony-forming unit-Hill colonies among children and teenagers with obesity, dyslipidemia and breastfeeding history.

BACKGROUND AND AIMS: The number of colony-forming unit (CFU)-Hill colonies has been proposed as a biomarker of vascular function and cardiovascular risk in adults but information about its role in children is scarce. This study evaluates the associations between obesity, cardiovascular risk factors and breastfeeding history with the numbers of CFU-Hill colonies in a sample of young people. METHODS AND RESULTS: We selected 49 children and teenagers between ages 10 and 17 (65.3% boys) from Mexican Health Care system. Physical activity and Anthropometric measures data were registered. CFU-Hill colonies were cultured from mononuclear cells obtained from venous blood. We detected inverse associations between the formation of CFU-Hill colonies and body mass index (BMI; ß = -1.53; 95% confidence interval [CI], -1.92, -1.13), triglycerides (ß = -0.26; 95%CI = -0.34, -0.18), total cholesterol (ß = -0.13; 95%CI = -0.17, -0.08), Low Density Lipoprotein (LDL) (ß = -0.20; 95%CI = -0.31, -0.09) and glucose (ß = -0.37; 95%CI = -0.55, -0.18) using multivariate models. Breastfeeding duration showed a 1.46-colony increase for each month of breastfeeding (95%CI = 0.73, 2.18). CONCLUSIONS: CFU-Hill colony-forming capacity in children and teenagers was inversely associated with obesity, dyslipidemia and high blood levels of glucose. In contrast a longer breastfeeding duration was directly associated with an increased number of CFU-Hill colonies. However these results must be confirmed with further studies. Our findings support the importance of promoting breastfeeding and monitoring nutritional and metabolic status at an early age to prevent chronic disease development.

Fatty acids and neurodevelopment.

Knowledge of the importance of docosahexaenoic acid (DHA), arachidonic acid (AA), and long-chain polyunsaturated fatty acids (LCPUFAs) in neurodevelopment was originally obtained from animal studies. These fatty acids are rapidly accreted in brain during the first postnatal year in animal and human infants, and they are found in high concentrations in breast milk. Reports of enhanced intellectual development in breast-fed children, and reports linking LCPUFA deficiency with neurodevelopmental disorders have stressed the physiological importance of DHA in visual and neural systems. In addition to high concentrations of fatty acids in breast milk, they are also present in fish and algae oil and have recently been added to infant formulas. Esterified poplyunsaturated fatty acids act in cellular membranes, in signal transduction, in neurotransmission, and in the formation of lipid rafts. Nonesterified polyunsaturated fatty acids can modulate gene expression and ion channel activities, thus becoming neuroprotective agents. The conversion of linoleic acid and alpha-linolenic acid into ARA and DHA have led to randomized clinical trials that have studied whether infant formulas supplemented with DHA or both DHA and ARA would enhance visual and cognitive development. This review gives an overview of fatty acids and neurodevelopment, focusing on the findings from these studies.

Dexamethasone rapidly regulates TRH mRNA levels in hypothalamic cell cultures: interaction with the cAMP pathway.

The biosynthesis of thyrotropin-releasing hormone (TRH) in the hypothalamic paraventricular nucleus (PVN) is subject to neural and hormonal regulations. To identify some of the potential effectors of this modulation, we incubated hypothalamic dispersed cells with dexamethasone for short periods of time (1-3 h) and studied the interaction of this hormone with protein kinase C (PKC) and PKA signaling pathways. TRH mRNA relative changes were determined by the RT-PCR technique. One hour incubation with 10(-10)-10(-4) M dexamethasone produced a concentration-dependent biphasic effect: an inhibition was observed on TRH mRNA levels at 10(-10) M, an increase above control at 10(-8)-10(-6) M and a reduction at higher concentrations (10(-5)- 10(-4) M). The stimulatory effect of 10(-8) M dexamethasone on TRH mRNA was essentially independent of new protein synthesis, as evidenced by cycloheximide pretreatment. Changes in TRH mRNA levels were reflected by enhanced TRH cell content. Incubation with a cAMP analogue (8-bromo-cAMP, 8Br-cAMP) or with a PKC activator (12-O-tetradecanoylphorbol-13-acetate, TPA) increased TRH mRNA levels after 1 and 2 h, respectively. An increase in TRH mRNA expression was observed by in situ hybridization of dexamethasone or 8Br-cAMP-treated cells. The interaction of dexamethasone, PKA and PKC signaling pathways was studied by combined treatment. The stimulatory effect of 10(-7) M TPA on TRH mRNA levels was additive to that of dexamethasone; in contrast, coincubation with 10(-3) M 8-Br-cAMP and dexamethasone diminished the stimulatory effect of both drugs. An inhibition was observed when the cAMP analogue was coincubated with TPA or TPA and dexamethasone. These results demonstrate that dexamethasone can rapidly regulate TRH biosynthesis and suggest a cross talk between cAMP, glucocorticoid receptors and PKC transducing pathways.