TY - JOUR
T1 -
Insulin edema in diabetes mellitus associated with the 3243 mitochondrial tRNA
Leu(UUR)
mutation; Case reports
AU - Suzuki, Yoshihiko
AU - Kadowaki, Hiroko
AU - Taniyama, Matsuo
AU - Kadowaki, Takashi
AU - Katagiri, Hideki
AU - Oka, Yoshitomo
AU - Atsumi, Yoshihito
AU - Hosokawa, Kazuhiro
AU - Tanaka, Yasushi
AU - Asahina, Takayuki
AU - Momiyama, Yukihiko
AU - Matsuoka, Kempei
PY - 1995/1/1
Y1 - 1995/1/1
N2 -
We encountered a patient with diabetes mellitus due to the 3243 mitochondrial tRNA mutation(DM-Mt3243), who developed insulin edema and hepatic dysfunction after starting insulin. Such a rare phenomenon was unlikely to be a fortuitous coincidence in mitochondrial diabetes, as none in 197 non-mutant NIDDM patients had same episode. Moreover, similar leg edema was noticed in another DM-Mt3243 patient, and other two DM-Mt3243 patients had leg edema which responded to coenzyme Q10. These observations suggest further a role of mitochondrial function on leg edema. The mechanism of his insulin edema may involve vasomotor changes induced by the rapidly glycemic control, because our case of insulin edema had a prominent increase of strong succinate dehydrogenase reactive vessels. Alternatively, myocardial dysfunction might have produced leg edema and hepatic dysfunction, because he had subclinical myocardial dysfunction, judged by imaging with β-methyl-p-(
123
I)- iodophenyl-pentadecanoic acid. The third explanation is that a rapid improvement of glycemic control might have induced hepatic reoxygenation and the production of reactive oxygen species in the liver that contributed to cell damage. Thus, although we cannot draw definite conclusion, our experiences here suggest that mitochondrial dysfunction is important in the etiology of insulin edema.
AB -
We encountered a patient with diabetes mellitus due to the 3243 mitochondrial tRNA mutation(DM-Mt3243), who developed insulin edema and hepatic dysfunction after starting insulin. Such a rare phenomenon was unlikely to be a fortuitous coincidence in mitochondrial diabetes, as none in 197 non-mutant NIDDM patients had same episode. Moreover, similar leg edema was noticed in another DM-Mt3243 patient, and other two DM-Mt3243 patients had leg edema which responded to coenzyme Q10. These observations suggest further a role of mitochondrial function on leg edema. The mechanism of his insulin edema may involve vasomotor changes induced by the rapidly glycemic control, because our case of insulin edema had a prominent increase of strong succinate dehydrogenase reactive vessels. Alternatively, myocardial dysfunction might have produced leg edema and hepatic dysfunction, because he had subclinical myocardial dysfunction, judged by imaging with β-methyl-p-(
123
I)- iodophenyl-pentadecanoic acid. The third explanation is that a rapid improvement of glycemic control might have induced hepatic reoxygenation and the production of reactive oxygen species in the liver that contributed to cell damage. Thus, although we cannot draw definite conclusion, our experiences here suggest that mitochondrial dysfunction is important in the etiology of insulin edema.
KW - Diabetic neuropathy
KW - Hepatic dysfunction
KW - Insulin edema
KW - Mitochondrial diabetes due to tRNA mutation at position 3243
KW - Post-treatment neuropathy
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UR - http://www.scopus.com/inward/citedby.url?scp=0028784192&partnerID=8YFLogxK
U2 - 10.1016/0168-8227(95)01113-7
DO - 10.1016/0168-8227(95)01113-7
M3 - Article
C2 - 8591701
AN - SCOPUS:0028784192
VL - 29
SP - 137
EP - 142
JO - Diabetes Research and Clinical Practice
JF - Diabetes Research and Clinical Practice
SN - 0168-8227
IS - 2
ER -