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Trehalose helping diabetes, triglycerides, kidney diseases, and neurodegenerative diseases?
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Can trehalose play a role in helping diabetes, triglycerides, kidney diseases, and neurodegenerative diseases? We are seeking the answer.
Comments by J. C. Spencer:

We are in the early stages of our Sugar Pilot Surveys and what we are discovering is encouraging. Obviously more research is needed. Some diabetics are monitoring their own blood sugar levels and reporting to us they appear more normal as long as they are eating trehalose. When they stop using trehalose, the sugar load escalates. We are receiving wide spread reports of essential tremors diminishing or ceasing while using trehalose. One family gave us an antidotal report of the husband with tremors of the mouth that made eating very difficult. The wife placed a quarter teaspoon of trehalose under his tongue and the tremors stopped almost immediately.

The following abstract of a science paper references trehalose, macronutrient storage, insulin-like receptors, diabetes, triglycerides, and neurodegenerative diseases. To say the least, for all of these to be referenced in one paper is rather astounding. I do not pretend to fully understand what all this means. But, I openingly contend that it is interesting.

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A Caenorhabditis elegans model of insulin resistance: altered macronutrient storage and dauer formation in an OGT-1 knockout.
Hanover JA, Forsythe ME, Hennessey PT, Brodigan TM, Love DC, Ashwell G, Krause M.

Laboratories of Cell Biochemistry and Biology and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. jah@helix.nih.gov

O-linked N-acetylglucosamine (O-GlcNAc) is an evolutionarily conserved modification of nuclear pore proteins, signaling kinases, and transcription factors. The O-GlcNAc transferase (OGT) catalyzing O-GlcNAc addition is essential in mammals and mediates the last step in a nutrient-sensing "hexosamine-signaling pathway." This pathway may be deregulated in diabetes and neurodegenerative disease. To examine the function of O-GlcNAc in a genetically amenable organism, we describe a putative null allele of OGT in Caenorhabditis elegans that is viable and fertile. We demonstrate that, whereas nuclear pore proteins of the homozygous deletion strain are devoid of O-GlcNAc, nuclear transport of transcription factors appears normal. However, the OGT mutant exhibits striking metabolic changes manifested in a approximately 3-fold elevation in trehalose levels and glycogen stores with a concomitant approximately 3-fold decrease in triglycerides levels. In nematodes, a highly conserved insulin-like signaling cascade regulates macronutrient storage, longevity, and dauer formation. The OGT knockout suppresses dauer larvae formation induced by a temperature-sensitive allele of the insulin-like receptor gene daf-2. Our findings demonstrate that OGT modulates macronutrient storage and dauer formation in C. elegans, providing a unique genetic model for examining the role of O-GlcNAc in cellular signaling and insulin resistance.

Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11266-71. Epub 2005 Jul 28.
http://www.ncbi.nlm.nih.gov/sites/entrez