Trehalose Becomes Hot Ingredient to Drive Cosmeceutical and Neutraceutical Market - Has anti-aging functionality
Comments by J. C. Spencer
Trehalose continues to be in the news as an additive for foods and cosmetics. Research is verifying that trehalose has a unique functionality for significant cell protection. A common response to overcoming cell stresses is the increased storage of trehalose and glycogen. Structure of glucose molecules, their bonds, and the angle of their bonds trigger specific positive function including benefits for diabetics and a number of neurodegenerative diseases including Huntington’s, Alzheimer’s, and Parkinson’s.
Glycogen is the storage form of glucose in animals and humans which is analogous to the starch in plants. Glycogen is synthesized and stored mainly in the liver and the muscles. Structurally, glycogen is very similar to amylopectin with alpha acetal linkages, however, it has even more branching and more glucose units are present than in amylopectin. Various samples of glycogen have been measured at 1,700-600,000 units of glucose. The structure of glycogen consists of long polymer chains of glucose units connected by an alpha acetal linkage. Trehalose is a non-reducing disaccharide consisting of two glucose molecules bonded by an [alpha], [alpha] - 1, 1 glycosidic link which is stable at low pH conditions.
One of the most interesting recent discoveries is the possible role of trehalose and telomeres. Telomeres are the DNA-protein complexes at the ends of eukaryotic chromosomes. Telomeres are essential for maintaining genomic stability. In the human body the telomeres keep getting shorter with age and when they reach a certain length, the cells cannot divide.
In my book Expand Your Mind - Improve Your Brain in Chapter 16 Rogue electrons: the enemy within, I say, “Damage to the DNA shortens the telomere. The telomere is a structure containing a repeated DNA sequence found at both ends of every chromosome in the human body. It was discovered in the 1990s that as a cell divides, the telomere keeps getting shorter. When the telomere becomes a certain length, it sends a signal for the cell to no longer divide.
“A cell that cannot divide is called a senescent cell. A senescent cell is very much alive, but it simply cannot divide. This cell contributes to wrinkles, an aging look, and a tired feeling. When cells begin to malfunction, the immune system is compromised, soon resulting in chaos.”
Below are two articles dealing with trehalose and the telomeres. The first is a report out of Las Vegas today and the second is the abstract of a science paper explaining the effect of trehalose on the telomeres.
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LAS VEGAS 10/27/2008 - From cell-targeted compounds to powerful antioxidants, innovative ingredients are driving growth in the cosmeceutical market, according to several speakers at SupplySide West 2008.
Rebecca James Gadberry, YG Laboratories, discussed some cutting-edge options in the market. Scientists are turning to extremeophiles - members of the oldest domain of life - that thrive in extreme conditions of temperature, pH and more; these organisms have unique biochemistry and molecules that may be able to support humans in an increasingly more extreme world. Among the innovations are Trehalose, an antioxidant sugar, and Thermus Ferment, a heat-activated indirect antioxidant that can upregulate natural enzymatic activity. Additional new developments include products that can stabilize DNA, such as telomeres, and options that enhance mitochondrial lifespan and health, protecting against photoaging and endogenous oxidative stress.
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The genome-wide expression response to telomerase deletion in Saccharomycescerevisiae
Abstract
Loss of the protective function of telomeres has previously been hypothesized to cause a DNA damage response. Here, we report a genome-wide expression response, the telomerase deletion response (TDR), that occurs when telomeres can no longer be maintained by telomerase. The TDR shares features with other DNA damage responses and the environmental stress response. Unexpectedly, another feature of the TDR is the up-regulation of energy production genes, accompanied by a proliferation of mitochondria. Finally, a discrete set of genes, the “telomerase deletion signature”, is uniquely up-regulated in the TDR but not under other conditions of stress and DNA damage that have been reported. The telomerase deletion signature genes define new candidates for involvement in cellular responses to altered telomere structure or function.
Telomeres, the DNA-protein complexes at the ends of eukaryotic chromosomes, are essential for maintaining genomic stability. They prevent chromosome end-to-end fusions and protect chromosomal DNA ends against uncontrolled nucleolytic degradation. Thus, it has been suggested that a defining feature of telomeres is to prevent chromosome ends from being treated as double-strand breaks. Loss of telomere function elicits some responses in common with double-strand breaks (1, 2), but it has not been tested directly whether checkpoints and cellular responses exist that are specific for damage at the telomere.
Telomere length is replenished over multiple cell generations by addition onto chromosome ends of tandem repeats of simple-sequence telomeric DNA by the ribonucleoprotein reverse transcriptase telomerase. Positive regulators of telomerase action include DNA damage checkpoint and repair genes (3). In the yeast Saccharomyces cerevisiae, deleting telomerase causes progressive telomere shortening and eventual cell-cycle arrest in G2/M, resulting in senescence of most of the cell population (4- 6). It is unknown whether this arrest is caused by a DNA damage checkpoint that is activated directly as a result of short telomeres being recognized as double-strand breaks, or whether it is an indirect consequence of chromosomal fusions at nonfunctional telomeres and subsequent breakage of the resulting dicentric chromosomes.
From the senescing yeast cells, a subpopulation of survivor cells that replicate telomeres by recombination emerges (4). Known requirements for the generation and growth of survivor cells include the double-strand break repair/recombination proteins Rad52p, Rad51p, Rad50p, Rad59p, and Sgs1p (4, 6-10). However, very little is known about how recombination pathways are activated for telomere maintenance or what additional adaptive changes may be required for survivors to arise and proliferate.
We examined genome-wide changes in mRNA transcript levels after deleting TLC1, the telomerase RNA component, in S. cerevisiae. Here we show that such cells exhibit a previously uncharacterized gene expression profile, which we have termed the telomerase deletion response (TDR). Telomere shortening evoked genome-wide responses that had both similarities to, and significant differences from, responses caused by other types of DNA damage. Aspects of the environmental stress response (ESR; ref. 11) were activated once telomeres became sufficiently short. A subset of the ESR was sustained in survivors. Oxidative phosphorylation genes became up-regulated and mitochondria proliferated specifically in senescent cells. Comparisons of the genome-wide response to telomerase deletion with a variety of DNA damage and stress conditions identified a small group of genes that is uniquely up-regulated in the TDR, defining a “telomerase deletion signature” response. Together, these changes suggest that adaptive strategies exist for life without telomerase
Shivani Nautiyal, Joseph L. DeRisi, and Elizabeth H. Blackburn*
+Author Affiliations
Department of Biochemistry, University of California, Box 0448, San Francisco, CA 94143.
Edited by Carol A. Gross, University of California, San Francisco, CA, and approved May 13, 2002
http://www.pnas.org/content/99/14/9316.abstract
Anti-aging | 
g/ml), ADP (20 
