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, activated p53 induces expression of growth-arrest genes, such as CDKN1A/p21 , to facilitate DNA damage repair. When encountering prolonged or catastrophic DNA damage, p53 triggers programmed cell death (apoptosis), primarily by transactivating genes that
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, Ehnvall et al . 2004 , Corbett et al . 2006 ). Recent animal studies have indicated that maternal malnutrition-induced impairment of fetal programing of the HPA axis function is associated with adult-onset dysregulation of the axis ( Chadio et al
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the pathogenicity of exonic HRPT2 mutations. While predictive programs may be useful in giving a preliminary indication of the effect of sequence variants on splicing, functional assays are required to determine the true effects, if any, on splicing
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Cell and Developmental Biology, Departments of
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MafA versus MafB, which allow Insulin activation, although not a more general endocrine differentiation program in this chick assay system. Figure 1 MafA, but not MafB, induces insulin expression in chick gut endoderm. Double immunofluorescence
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similar to decidua where there is close interaction between stromal and non-stromal cells (such as the thymus), glucocorticoids are known to play a key role in modulating programmed cell death ( Wyllie 1980 , Wyllie & Morris 1982 ). Therefore, to assess
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Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute
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Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute
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Nogueira-Neto JF Lisboa PC 2009 Temporal evaluation of body composition, glucose homeostasis and lipid profile of male rats programmed by maternal protein restriction during lactation . Hormone and Metabolic Research 41 866 – 873 . Fraga
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Department of Social and Administrative Sciences, MCPHS University, Boston, Massachusetts, USA
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School of Physical Education and Sport of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil
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The main aim of this investigation was to verify the effects of overtraining (OT) on the insulin and inflammatory signaling pathways in mice skeletal muscles. Rodents were divided into control (CT), overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up), and overtrained by running without inclination (OTR) groups. Rotarod, incremental load, exhaustive, and grip force tests were used to evaluate performance. Thirty-six hours after the grip force test, the extensor digitorum longus (EDL) and soleus were extracted for subsequent protein analyses. The three OT protocols led to similar responses of all performance evaluation tests. The phosphorylation of insulin receptor beta (pIRβ; Tyr), protein kinase B (pAkt; Ser473), and the protein levels of plasma membrane glucose transporter-4 (GLUT4) were lower in the EDL and soleus after the OTR/down protocol and in the soleus after the OTR/up and OTR protocols. While the pIRβ was lower after the OTR/up and OTR protocols, the pAkt was higher after the OTR/up in the EDL. The phosphorylation of IκB kinase alpha and beta (pIKKα/β; Ser180/181), stress-activated protein kinases/Jun amino-terminal kinases (pSAPK-JNK; Thr183/Tyr185), factor nuclear kappa B (pNFκB p65; Ser536), and insulin receptor substrate 1 (pIRS1; Ser307) were higher after the OTR/down protocol, but were not altered after the two other OT protocols. In summary, these data suggest that OT may lead to skeletal muscle insulin signaling pathway impairment, regardless of the predominance of eccentric contractions, although the insulin signal pathway impairment induced in OTR/up and OTR appeared to be muscle fiber-type specific.
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deficiencies ( Alatzoglou & Dattani 2009 , Kelberman et al . 2009 ). Since TSH is not elevated in CCH, this entity will evade diagnosis in TSH-based, primary CH screening programs, and patients are at risk of neurodevelopmental delay if severe CCH remains
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of Type 2 Diabetes (T4DM) study’. T4DM sought to determine whether treatment with testosterone, on the background of a lifestyle program, would prevent the progression of prediabetes to T2D or reverse newly diagnosed T2D in men aged 50 and over with
Department of Poultry Science, University of Arkansas, Fayetteville, Arkansas, USA
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Institute of Basic Medical Sciences, Faculty of Medicine, The Norwegian Transgenic Centre (NTS), University of Oslo, Oslo, Norway
Faculty of Biosciences and Aquaculture (FBA), Nord University, Steinkjer, Norway
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Secretory function of the pancreatic α-cell, in contrast to the pancreatic β-cell, does not appear to be a target of nutritional programming in late foetal life in sheep. Implications of gender differences in glucagon secretory patterns remain to be
