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Objective: The objective of this study was to examine the changes in adipose tissue lipolytic capacity and insulin signaling in response to shortened sleep duration (SSD) in postmenopausal women. Methods: Adipose tissue from a randomized crossover study of nine healthy postmenopausal women (mean [SD], age: 59 [4] years; BMI: 28.0 [2.6] kg/m2) exposed to four nights of habitual and SSD (60% of habitual sleep) while following a eucaloric diet was examined ex vivo. Tissue lipolytic capacity was determined by measurement of secreted glycerol. Cellular insulin signaling was determined by measuring insulin‐mediated changes in Akt phosphorylation. RNA sequencing examined global transcriptional changes. Results: With SSD, basal glycerol secretion was reduced, and isoproterenol‐stimulated lipolysis was attenuated. Insulin concentration‐dependent increases in phosphorylated Akt observed in samples after habitual sleep were abrogated after SSD. However, insulin‐mediated suppression of lipolysis remained unaltered with changes in sleep duration. Increased transcription of genes involved in adipogenesis and fatty acid metabolism was observed after SSD. Conclusions: SSD blunts adrenergic stimulation of lipolysis without altering insulin‐mediated suppression of lipolysis in postmenopausal women. These changes in adipose tissue may potentiate fat gain independent of caloric intake. Therefore, interventions promoting sleep may be considered to mitigate abdominal adiposity in postmenopausal women. [ABSTRACT FROM AUTHOR]

Background: Impairments in cell migration during vertebrate gastrulation lead to structural birth defects, such as heart defects and neural tube defects. These defects are more frequent in progeny from diabetic pregnancies, and we have recently provided evidence that maternal diabetes leads to impaired migration of embryonic mesodermal cells in a mouse model of diabetic pregnancy. Methods: We here report the isolation of primary cell lines from normal and diabetes‐exposed embryos of the nonobese diabetic mouse strain, and characterization of their energy metabolism and expression of nutrient transporter genes by quantitative real‐time PCR. Results: Expression levels of several genes in the glucose transporter and fatty acid transporter gene families were altered in diabetes‐exposed cells. Notably, primary cells from embryos with prior in vivo exposure to maternal diabetes exhibited reduced capacity for cell migration in vitro. Conclusions: Primary cells isolated from diabetes‐exposed embryos retained a "memory" of their in vivo exposure, manifesting in cell migration impairment. Thus, we have successfully established an in vitro experimental model for the mesoderm migration defects observed in diabetes‐exposed mouse embryos. [ABSTRACT FROM AUTHOR]

Small molecules will need to be identified and/or developed that target protein classes limiting reprogramming efficiency. A specific class of proteins includes epigenetic regulators that silence, or minimize expression, of pluripotency genes in differentiated cells. To better understand the role of specific epigenetic modulators in reprogramming, we have used shRNA delivered by lentivirus to assess the significance of individual epi-proteins in reprogramming pluripotent gene expression.

Objective: The aim of this study was the detection and location of long form leptin receptor (OB-Rb) in different area of hypothalamus and pituitary in the pig during early pregnancy., Settings and Design: Expression of OB-Rb was examined by RT-PCR in the different area of hypothalamus: medial basal hypothalamus (MBH), preoptic area (POA), stalk median eminence (SME), as well as pituitary: the anterior (AP) and posterior (NP) lobe collected from gilts at days 14-16 (n=4) and 30-32 (n=4) of pregnancy., Results: The results showed that OB-Rb mRNA was expressed in the hypothalamus (MBH, POA and SME), pituitary (AP, NP) and adipose tissue in the pig during early pregnancy (at days 14-16 and 30-32)., Conclusion: These findings support the idea that leptin might play a role in the regulation of the hypothalamic-pituitary axis activity, and consequently in the control of pregnancy during critical period of embryo implantation in the pig.