title: Morphometric analysis of muscle fibre types in rat locomotor and postural skeletal muscles in different stages of chronic kidney disease.
abstract: Muscle weakness and progressive loss of skeletal muscle mass are serious complications of chronic kidney disease (CKD). The pathogenesis of this condition is still poorly understood. The study investigated fibre type distribution and diameter in functionally different skeletal muscles: locomotor, gastrocnemius muscle (MG) and postural, longissimus thoracis muscle (ML) together with an evaluation of metabolic disturbances and nutritional parameters of rats with different stages of CKD. Wistar rats were randomized to a sham operation - CON, uninephrectomy - CKD1/2 or subtotal nephrectomy - CKD5/6. After 4 weeks, serum concentration haemoglobin (Hb), haptoglobin (Hp), MCP-1, advanced glycation end products (AGEs), and homocysteine (Hcy) were measured. Muscle specimens were stained for myofibrillary ATPase and NADH-diaphoreses activity according to Ziegan's method. There was a significant increase in the percentage of IID/X with a concomitant decrease of IIB fibres in ML in CKD1/2 vs. CON and CKD5/6. IIB fibre diameters in ML were smaller (53.4±7.3 vs. 58.1±8.1 and 59.8±11.2; p=0.08) for CKD5/6 vs. CKD1/2 and CON, respectively. There were significant differences for CKD5/6 and CKD1/2 vs. CON in: Hb (11.4±3.1; 13.7±0.7 and 14.1±1 g/dl), Hp (1.6±0.6; 1.6±0.6 and 0.7±0.4 mg/ml), AGEs (5.1±0.6; 4.3±1.2 and 4.6±0.9 AU), Hcy (7.2±1.2; 5.1±0.5 and 4.9±0.5 M), MCP-1 (609±255; 489±265 and 292±113 pg/ml), respectively. We concluded that early stages of CKD could induce the process of compensatory fast to slow fibre transformation, while in more advanced CKD this process may be blocked and atrophy of fast-twitch fibres may occur, predominantly in non-locomotor muscles. These disturbances can be secondary to CKD-related metabolic burden and inflammation.
authors.affiliation: Department of Nephrology, Hypertension and Internal Diseases of Ludwig Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Bydgoszcz, Poland. flis3@wp.pl.
authors.forename: M
authors.initials: M
authors.lastname: Flisinski
authors.forename: A
authors.initials: A
authors.lastname: Brymora
authors.forename: G
authors.initials: G
authors.lastname: Elminowska-Wenda
authors.forename: J
authors.initials: J
authors.lastname: Bogucka
authors.forename: K
authors.initials: K
authors.lastname: Walasik
authors.forename: A
authors.initials: A
authors.lastname: Stefanska
authors.forename: P
authors.initials: P
authors.lastname: Strozecki
authors.forename: J
authors.initials: J
authors.lastname: Manitius
mesh_terms: D000818:Animals; D018932:Chemokine CCL2 / Q000097:blood; D017127:Glycation End Products, Advanced / Q000097:blood; D006242:Haptoglobins / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D006710:Homocysteine / Q000097:blood; D008124:Locomotion; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000473:pathology*; D011187:Posture; D017208:Rats, Wistar; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000473:pathology*
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D017127:Glycation End Products, Advanced; D006242:Haptoglobins; D006454:Hemoglobins; C529146:Hp protein, rat; D006710:Homocysteine