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.