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Subject:
From:
Gary Jackson <[log in to unmask]>
Reply To:
Paleolithic Eating Support List <[log in to unmask]>
Date:
Wed, 20 Aug 1997 12:30:19 -0700
Content-Type:
text/plain
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 The team scanned a
> database of human gene sequences and found just one closely related
to
> daf-2: the insulin receptor gene, which helps dispose of dietary
sugar in
> the blood.
> Corbie
>
I had this reference stored and I think it ties in with your article.
It certainly could be yet another reason to keep low carb and keep
a tight control on blood glucose. Yet another reason why I think
too much attention is placed on diabetes, the end stage, and not on
the lack blood sugar control that leads up to it long before it
becomes diabetes.

Gary

Title
     Genetic influences on glucose neurotoxicity, aging, and diabetes:
a possible role for glucose hysteresis.
Author
     Mobbs CV
Address
     Fishberg Center for Neurobiology, Mt. Sinai School of Medicine,
New York, NY 10129.
Source
     Genetica, 1993, 91:1-3, 239-53
Abstract
     Glucose may drive some age-correlated impairments and may mediate
some effects of dietary restriction on
     senescence. The hypothesis that cumulative deleterious effects of
glucose may impair hypothalamic neurons
     during aging, leading to hyperinsulinemia and other
age-correlated pathologies, is examined in the context of
     genetic influences. Susceptibility to toxic effects of
gold-thio-glucose (GTG) is correlated with longevity
     across several mouse strains. GTG and chronic hyperglycemia
induce specific impairments in the
     ventromedial hypothalamus similar to impairments which occur
during aging. GTG and a high-calorie diet
     both induce chronic hyperinsulinemia, leading initially to
hypoglycemia, followed by the development of
     insulin resistance and hyperglycemia. Aging in humans and rodents
appears to entail a similar pattern of
     hyperinsulinemia followed by insulin resistance. In humans,
genetic susceptibility to high-calorie diet-induced
     impairments in glucose metabolism is extremely common in many
indigenous populations, possibly due to
     the selection of the 'thrifty genotype'. It is suggested that the
'thrifty genotype' may entail enhanced sensitivity
     to the neurotoxic effects of glucose, and may represent an
example of antagonistic pleiotropy in human
     evolution. These data are consistent with the hypothesis that
genetic susceptibility of hypothalamic neurons
     to the cumulative toxic effects of glucose (glucose neurohumoral
hysteresis) may correlate with genetic
     influences on longevity.
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