Yamada S. Ohkubo C.
Department of Physiological Hygiene, National Institute of Public Health, Tokyo, Japan.
The influence of frequent and excessive intake of glucose on microvascular aging in healthy mice.
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.