Barker hypothesis

FIGURE 17.3. A Modified Barker Hypothesis the susceptibility exposure paradigm used as a model to assess the effects of prenatal exposure to polycyclic aromatic hydrocarhons. Adapted with permission Ifom Neurotoxicology and Brown et al. (2007). 

Epigenetics has been included in several toxicological hypotheses. According to the Barker hypothesis a toxic event in early life can be the reason for the development of late-onset disease [125], As epigenetic mechanisms can act as molecular memories of previous stress, they are very likely to contribute to such disease mechanisms. Thus, it is important to understand by which mechanisms chemicals and drugs may interfere with epigenetic mechanisms. 

The idea is fetal programming. Fetal programming and its variants—such as the Barker hypothesis, the fetal or developmental origins hypothesis, the developmental origins of disease hypotheses, and some others—all refer to the same phenomenon An interaction of the environment with the fetus whose effects may not show up until years later and may or may not be transgenerational. Apart from this common thread, however, there are some significant differences in the emphasis of each hypothesis. 

The Barker hypothesis states that fetal environment, particularly maternal nutrition, can alter the physiology of the fetus such that it develops diseases in later life. This is also known as programming. Low birth weight is associated with a greater risk of CHD and diabetes mellitus. Individuals are particularly at risk if moving from an area of poor nutrition (experienced in the womb) to good nutrition (experienced as an adult). This is called catch-up growth. 

Barker, F. 1979. Trondhjemite definition, environrment and hypothesis of origin, in Trondhjemites, Dacites and related rocks. F. Barker (ed.). Elsevier Scientific Publishing Co., 1-12. 

Fall C, Hindmarsh P, Dennison E, Kellingray S, Barker D, Cooper C (1998) Programming of growth hormone secretion and bone mineral density in elderly men A hypothesis. J Clin Endocrinol Metab, 83 135-139. 

In the our previous pniblished works were presented results obtained by the same way on the ternary solid solutions Hgi-xCdxTe and Hgi-xZnxTe (Cebulski, et al.,2008 Polit et al., 2010 Sheregii et al.,2009 Sheregii et al., 2011). It was shown in these works that observed subtle structure of the two phonon sub-bands in case of ternary alloys can be successfully explained on base of the five structural cells model of H.W.Verleur and AS. Barker (V-B model) (Verleur Barker, 1966) thought the additional phonon lines were observed. Last one required the new hypothesis - the two wells potential model for Hg-atoms in lattice (Polit et al., 2010) - for explanation the experimental spectra. The V-B model will be presented in next sub-chapter. In this sub-chapter are exposed the FlK-sprectra concerning ternary alloys in order to illustrate the fact of multi-mode behaviour - main statement of the random version of the V-B model which is necessary to interpret of the exprerimental FIR-sprectra. 

It is noteworthy that when Barker first proposed this scheme of fatty acid oxidation, there was only inferential evidence for a role of CoA in butyrate oxidation in C. kluyveri, and there was no evidence of any kind to implicate CoA in the oxidation of fatty acids by animal enzyme systems. In fact it was not until one year later that a soluble system capable of oxidizing fatty acids in the presence of added CoA was prepared from animal tissues. It is therefore a tribute to Barker s imagination and conceptual analysis that within a few years after his report, his hypothesis was shown to be correct in every significant detail, not only in C. kluyveri but in higher animals as well.J... 

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