Agriculture Reference
In-Depth Information
individuals after a test meal with the rise after a glucose feeding.
Resistant starches
(RSs) have been defined as “the sum of starch and products of starch degradation
not absorbed in the small intestine of healthy individuals.” An in vitro analysis of
rates of digestion of foods to glucose has been developed, and it is reported that
rapidly available glucose (RAG) correlates with the GI (Englyst et al.). The nature
of slowly available glucose (SAG) in the assay has been investigated with various
starches; granular, supramolecular, and molecular structures of botanical starch
species all determine the ratio of RAG to SAG (Zhang et al. 2006a, 2006b, Ao
et al. 2007a, 2007b). Increasing the number of branches and reducing the length
of chains increases SAG (Ao, 2007a, 2007b). In vitro mucosal α-glucogenesis of
mice is slowed by experimental molecular adjustments of starch structure that are
only partially restored by amylase activity (Quezada-Calvillo et al., 2007a, 2007b).
Further investigations are needed to clarify the starch chemistry and enzyme molec-
ular mechanisms behind resistant food starches because of suspected roles of starch
digestion in glucose disorders such as type 2 diabetes and obesity.
summARy
The study of genomics leads to the conclusion that the human shares a com-
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mon ancestry with other life-forms.
The genomic roots of some human genes for secreted and membrane-bound
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digestive proteins were present in archael organisms about 3.5 bya. Others
appeared when bacteria diverged from archaea about 2.5 bya. Others only
appeared when eukarya appeared about 1 bya.
By the time of divergence of the human from rodent genomes at 0.06 bya,
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the loci of digestive genes in chromosomal neighborhoods became fixed.
The enzymes expressed by genes most essential for digestion and assimila-
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tion of negative energy often have redundancies at genome and activity lev-
els for the important digestive enzymes, such as γ-glutamyl transpeptidase,
which ensure normal phenotypes in the face of individual coding muta-
tions. Where no genomic redundancy exists, as with dipeptidyl peptidase
IV, mutated genes can result in clinical disorders.
Some may express reservations about the religious implications of the
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genomic roots of our nutritional heritage. In the words of Francis Collins,
director of the National Institutes of Health (NIH) Genome Project, “The
God of the bible is also the God of the genome” (Collins, 2006, p. 211; also
see Chapters 3 and 4).
The online GenBank of the NIH Genome Project presently contains over 65
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billion nucleotide bases from more than 61 m illion individual sequences. Over
240,000 named species are represented, and only about 16% of the sequences
are of human origin. The number of complete sequences of genomes of food
plants and animals is rapidly expanding (Benson et al., 2008).
Agriculture production was critical in the past 10 to 12 thousand years as
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food crops were developed to provide negative entropy through phenotype
selection. This process supported the growth of civilizations (see Chapters
1, 19-22).
