X-Message-Number: 12507
Date: Tue, 5 Oct 1999 19:29:25 -0700 (PDT)
From: Doug Skrecky <>
Subject: glucose accelerates vascular aging

Authors
  Yamada S.  Ohkubo C.
Institution
  Department of Physiological Hygiene, National Institute of Public Health,
  Tokyo, Japan.
Title
  The influence of frequent and excessive intake of glucose on
  microvascular aging in healthy mice.
Source
  Microcirculation.  6(1):55-62, 1999 Mar.
Abstract
  OBJECTIVE: The purpose of this study was to verify the following working
  hypothesis. Even in healthy individuals with normoglycemic adaptability,
  microvascular aging caused by the accumulation of advanced
  glycosylation end products (AGEs) in vascular walls would occur, when the
  blood glucose level is maintained intermittently high due to
  frequent and excessive sugar intake for a prolonged period. METHODS: Male
  BALB/c mice were divided into four groups: the S group raised with
  glucose-enriched feed and the C group with ordinary feed, as
  well as the SG group with the glucose-enriched feed and
  special drinking water supplemented with 0.25% aminoguanidine (AG), and the
  CG group with ordinary feed and this special drinking water. After 6 months,
  a mouse dorsal skinfold chamber was mounted on the skin of the back for the
  intravital-microscopic observations of microvasculature. RESULTS: Blood
  glucose levels were within normal ranges in all four animal
  groups, indicating their saccharometabolism to be normal. An autofluorescent
  AGE-positive ratio in the S group was 71.4%, and that in the C group was
  33.3%. Mean caliber of arterial microvessels was smallest in the S group. The
  SG and CG group showed the caliber larger than the groups without AG.
  Vascular lesion indices were significantly larger in the S group than those
  of the groups with AG. The indices were particularly small in the SG group. A
  decrease of amplitudes in thicker vessels and an increase of vasomotor
  frequencies in thinner ones were demonstrated in the S group. The features of
  vasomotion differed in the groups with and without AG. CONCLUSIONS:
  Microvascular aging was clearly noticed in the S group. It
  has been concluded that vasomotor inhibition was generated in addition to
  hypertrophy and fragility in arterial microvessels of the group. It is
  further concluded that AG protects blood vessels from hypertrophy and
  fragility, but it downregulates vasomotion.

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