Individuals who have selective impairment of insulinstimulated
glucose disposal at the level of skeletal muscle
develop compensatory hyperinsulinemia following
CHO-containing meals. Several lines of evidence suggest
that other insulin-stimulated pathways are, however,
normally responsive to the hormone, becoming therefore
overstimulated following carbohydrate intake. Such conditions
occur, for example at renal tubular level, where
day-long insulin-mediated sodium retention was enhanced
in insulin-resistant, hyperinsulinemic humans,
despite identical dietary intake of both sodium and carbohydrate
. In addition, greater insulin-mediated inhibition
of protein catabolism was also demonstrated in
insulin-resistant as compared to control subjects .
We suggest that this overall increase of other insulin
signalling pathways is a pro-aging factor, probably of
greater relevance than hyperglycemia. The degree of
hyperglycemia, seen in glucose-tolerant individuals with
selective muscle resistance to insulin-stimulated glucose
1304 F. C. FACCHINI et al.
metabolism, is, in fact, only of mild (;20&ndash;50%) entity
until diabetes ensues.
This hypothesis, although speculative, is supported by
studies in invertebrate and mammalian models where it
was determined that whether overall insulin signalling is
reduced by mutations, like in C. elegans, or by lowered
plasma glucose and insulin levels, as it occurs in the
calorie-restricted rodent, a similar outcome becomes apparent:
extension of lifespan and, at any given age after
maturity, decreased prevalence of ARD.
- 提姆Lv 71 decade agoFavorite Answer
本文是假設胰島素耐性導致的高胰島素症，才是造成老化的重要因子。Source(s): HYPERINSULINEMIA: THE MISSING LINK AMONG OXIDATIVE STRESS AND AGE-RELATED DISEASES?