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At least 451 records · Page 25Linked to original sources
PubMed2003

Hypothalamic neuropeptide Y/Y1 receptor pathway activated by a reduction in circulating leptin, but not by an increase in circulating ghrelin, contributes to hyperphagia associated with triiodothyronine-induced thyrotoxicosis.

Food intake is regulated by hypothalamic neuropeptides which respond to peripheral signals. Plasma ghrelin and leptin levels reflect peripheral energy balance and regulate hypothalamic neuropeptides such as neuropeptide Y (NPY), pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), melanin-concentrating hormone (MCH), and orexins. Thyroid hormone stimulates food intake in humans and rodents. However, the mechanisms responsible for this stimulation have not been fully elucidated. To investigate the hyperphagic response to triiodothyronine (T(3))-induced thyrotoxicosis, adult male rats were studied 7 days after daily intraperitoneal injections of T(3) or vehicle. T(3)-treated rats were markedly hyperphagic. During this hyperphagia, plasma leptin levels were markedly decreased. However, the expression of the ghrelin gene in the stomach and the plasma ghrelin concentrations did not differ between the 2 groups. Hypothalamic NPY mRNA levels were significantly increased and associated with a marked decreased in both hypothalamic POMC and CART mRNA levels in the T(3)-treated rats. Hypothalamic MCH and orexin mRNA levels did not differ between the 2 groups. In addition, hyperphagia was partially reversed by intracerebroventricular administration of the NPY Y1 receptor antagonist BIBO3304. Therefore, the decreased plasma leptin levels could contribute to hyperphagia in T(3)-induced thyrotoxicosis. However, plasma ghrelin levels did not contribute to this hyperphagia.

Animals↗
PubMedDate not supplied

Culture of cells from maternal circulation, in conditions favoring fetal endothelial cell expansion, does not facilitate the preferential expansion of circulating fetal cells.

OBJECTIVES: To establish optimal culture conditions for fetal endothelial cells, and determine whether these can be used for preferential expansion of fetal cells from maternal blood. METHODS: Human adult microvascular and umbilical vein endothelial cells were cultured in the presence of colony-stimulating factor-1 (CSF-1), placental growth factor (PlGF), and transforming growth factor-beta1 (TGF-beta1). The effect of each cytokine was assessed. We expanded peripheral blood mononuclear cells (PBMCs) from 18 pregnant women using the conditions most favorable to fetal cells; in specimens from women carrying male fetuses (n = 9), cell origin was determined by PCR (SRY locus). RESULTS: The optimal concentrations of CSF-1, PlGF and TGF-beta1 were 10, 100, and 5 ng/ml, respectively. PBMCs from maternal blood expanded in the presence or absence of the cytokines; PCR analysis showed no Y sequences in cultured maternal samples. CONCLUSION: Optimal concentrations of CSF-1, PlGF and TGF-beta1 for preferential expansion of fetal endothelial cells were determined in model cultures. However, when these conditions were applied to maternal blood samples, no fetal cells could be detected based on PCR for SRY in women carrying male fetuses.

Adolescent↗