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Improved metabolic control in patients with non‐insulin‐dependent diabetes mellitus is associated with a slower accumulation of glycation products in collagen *
Author(s) -
SALMELA P. I.,
OIKARINEN A. I.,
UKKOLA O.,
KARJALAINEN A.,
LINNALUOTO M.,
PUUKKA R.,
RYHÄNEN L.
Publication year - 1995
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1995.tb01735.x
Subject(s) - glycation , fructosamine , medicine , endocrinology , diabetes mellitus , metabolic control analysis , insulin , advanced glycation end product , glycosylation , chemistry , biochemistry
. Twenty‐one patients with non‐insulin‐dependent diabetes in poor metabolic control were subjected to intensified therapy, in most cases with insulin, to investigate whether it is possible to slow down the accumulation of advanced glycosylation end products of collagen by improving glycaemic control. Fasting and mean daily blood glucose, serum fructo‐samine and glycohaemoglobin levels, as well as glycation of collagen were measured before and after 1.5 years of intensified therapy. All these parameters except for fructosamine correlated significantly with fasting blood glucose and glycohaemoglobin when measured before the insulin therapy was started, when the patients had had poor but stable metabolic control for a long period of time. After 1.5 years of intensified therapy the level of glycation of collagen did not significantly correlate with the fasting blood glucose or glycohaemoglobin levels, suggesting that the non‐enzymatic glycosylation of collagen reflects a longer period of metabolic control of diabetes than the glycohaemoglobin level. Intensified treatment improved previously poor metabolic control in patients with non‐insulin‐dependent diabetes, and this improvement was reflected in a decrease in fasting and mean daily blood glucose levels, serum fructosamine and glycohaemoglobin concentrations, and in the level of early products of glycation of collagen. The average content of advanced glycosylation end products of collagen, assayed in terms of collagen‐linked fluorescence did not decrease. However, they accumulated more slowly in the patient tercile with the greatest decrease in the level of fasting blood glucose than in the tercile with the smallest decrease, and even a decrease in fluorescence was observed in the patients with the greatest improvement in the metabolic control. Our findings suggest that the improvement of metabolic control in non‐insulin‐dependent diabetes is reflected in a slower accumulation of advanced glycosylation end products in collagen. If the slower accumulation of advanced glycosylation end products in collagen is translated into a slower development of the long‐term complications of diabetes remains to be studied.

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