title: [Changes in diameter size and F-actin expression in the myocytes of patients with diabetes and streptozotocin-induced diabetes model rats].
abstract: Diabetes mellitus may be an independent risk factor for disturbance of cardiac function, but the detailed mechanism remains unclear. In the present study, histological examinations were carried out on 25 hearts from diabetes model rats as well as myocardial biopsy materials from patients with diabetes (n = 25). The mean diameter of the cardiac myocytes in humans was 12.2 +/- 0.5 microns in the control group of patients without diabetes mellitus or hypertension (n = 6), 13.7 +/- 0.8 microns in the hypertension group (n = 3), 9.0 +/- 1.7 microns in the diabetes group (n = 8), and 11.9 +/- 2.0 microns in the diabetes with hypertension group (n = 8). The cardiac myocytes of diabetic patients appeared to be atrophic. Comparison of the size of myocytes in the control rats vs streptozotocin-induced diabetes model rats (n = 7, each) was 5.4 +/- 0.2 vs 5.2 +/- 0.3 microns at 2 weeks; 5.9 +/- 0.1 vs 4.9 +/- 0.9 microns at 12 weeks, and 5.7 +/- 0.1 vs 4.0 +/- 0.2 microns at 24 weeks, respectively, and gradually decreased in streptozotocin rats with aging. Immuno-histochemistry with phaloidin was used to assess F-actin in the cardiac myocytes. The relative cross-sectional area of F-actin in the cardiac myocytes of streptozotocin rats was compared to that in non-streptozotocin rat myocytes. F-actin fluorescence in streptozotocin rats was 89.9 +/- 3.9% at 2 weeks, 77.9 +/- 6.4% at 12 weeks, and 56.8 +/- 5.7% at 24 weeks, indicating a decrease in F-actin. These results suggest that the smaller myocytes observed in patients with diabetes and streptozotocin rats are related to the decrease in F-actin in myocytes.
authors.affiliation: First Department of Internal Medicine, Fukushima Medical University.
authors.forename: M
authors.initials: M
authors.lastname: Kawaguchi
authors.forename: T
authors.initials: T
authors.lastname: Asakura
authors.forename: F
authors.initials: F
authors.lastname: Saito
authors.forename: O
authors.initials: O
authors.lastname: Nemoto
authors.forename: K
authors.initials: K
authors.lastname: Maehara
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: N
authors.initials: N
authors.lastname: Sugai
authors.forename: Y
authors.initials: Y
authors.lastname: Maruyama
mesh_terms: D000199:Actins / Q000032:analysis*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001284:Atrophy; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000473:pathology*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin
chemical_list: D000199:Actins; D013311:Streptozocin