Both hypothyroidism and hyperthyroidism increase plasma irisin levels in rats

BackgroundA recently discovered hormone, irisin is accepted to be significantly involved in the regulation of body weight. Thyroid functions may be, directly or indirectly, associated with irisin.AimThe aim of the present study is to determine the effect of experimental thyroid dysfunction on irisin levels in rats.MethodsThe study registered 40 adult male Sprague-Dawley rats, which were allocated to groups as follows: 1. Control; 2. Hypothyroidism induced by injection of 10 mg/kg/day intraperitoneal propylthiouracil (PTU) for 3 weeks; 3. Hypothyroidism (PTU 2 weeks) + L-thyroxin (1.5 mg/kg/day for 1 week); 4. Hyperthyroidism induced in rats by 3-week thyroxin (0.3 mg/kg/day); 5. Hyperthyroidism + PTU. At the end of the study, blood samples were collected to quantify free triiodothyronine (FT3), free triiodothyronine (FT4) and irisin levels.ResultsFT3and FT4levels were reduced in hypothyroidism and were significantly elevated in hyperthyroidism (p < 0.001). Irisin values, on the other hand, were found to be elevated in both hypothyroidism and hyperthyroidism groups (p < 0.001).ConclusionThe results of the study suggest that irisin values increase in thyroid dysfunction, hypo- and hyperthyroidism, and that when hypothyroidism is corrected by thyroxin administration and hyperthyroidism by PTU injection, plasma irisin values go back to normal.

The effect of thyroid dysfunction on nesfatin-1 and adiponectin levels in rats

BackgroundChanges in thyroid hormone concentrations may affect adiponectin concentrations through various mechanisms. A molecule released primarily from the fat cells adiposities; adiponectin has important effects on the regulation of body weight.AimThe present study aimed to explore the effects of experimental thyroid dysfunction and its treatment on nesfatin-1 and adiponectin levels in rats.MethodsThe study included 40 adult male Sprague-Dawley rats which were grouped as follows: (1) control; (2) hypothyroidism [hypothyroidism was induced by intraperitoneal injection of 10 mg/kg/day propylthiouracil (PTU) for 3 weeks]; (3) hypothyroidism + thyroxine group [after hypothyroidism was induced by 2-week PTU injection, they were treated with high-dose L-thyroxine (1.5 mg/kg/day) for 1 week]; (4) hyperthyroidism [hyperthyroidism was induced by 3-weeks’ thyroxine injection (0.3 mg/kg/day)]; (5) hyperthyroidism + PTU (after hyperthyroidism was induced by 2-weeks’ thyroxine injection, the animals were given 10 mg/kg/day PTU for 1 week). Blood samples taken at the end of the study were analyzed to measure nesfatin-1 and adiponectin levels.ResultsIt was found that nesfatin-1 levels increased in hypothyroidism, while adiponectin levels decreased (p < 0.001). In experimental hyperthyroidism, on the other hand, both nesfatin-1 and adiponectin levels were found significantly elevated (p < 0.001).ConclusionThe results of the study indicate that nesfatin-1 and adiponectin levels were modified considerably in hypo- and hyperthyroidism, whereas with the restoration of the thyroid function, modified hormone levels went back to normal.

Features of inflammation course in rats with experimental hyper- and hypothyroidism

Aim. To mark out the features of inflammatory reactions alterations in rats with experimental thyroid gland dysfunction. Methods. Experimental hypothyroidism was modeled by daily thiamazole intake in 50 Wistar rats. Hyperthyroidism was modeled with daily lyothyronine intake in 50 Wistar rats. An inflammation was modeled by artificial gum injury. 10 intact rats were examined as a control group. Results. Experimental hypothyroidism was accompanied by leukocyte biocidity decrease both in blood and periodontium, decreased lysosomal enzymes activity and antioxidant activity, and accumulation of lipid peroxidation products. Periodontal suppurations at experimental inflammation were 1.5 more frequent in rats with hypothyroidism compared to controls due to decreased leukocyte biocidity and antioxidant activity. Experimental hyperthyroidism was associated with increased biocidity and decreased functional reserves in phagocytes both in blood and periodontium, as well as antioxidant activity decrease and lipid peroxidation intensification. Changes of tumor necrosis factor alpha blood concentration both in hypothyroidism and hyperthyroidism corresponded with changes of phagocyte biocidity. The rate of periodontal suppuration in rats with hyperthyroidism was twice lower on the day 7 compared to controls due to high leukocyte and macrophage biocidity. Conclusion. Experimental hypothyroidism was accompanied by intensifying of lipid peroxidation and decreased tissue reparation ability; experimental hyperthyroidism was associated with increased biocidity and decreased functional reserves in phagocytes, and less evident decrease of compensatory abilities of antioxidant system lipid peroxidation intensification compared to hypothyroidism.

Salt sensitivity in experimental thyroid disorders in rats

This study assessed salt sensitivity, analyzing the effects of an increased saline intake on hemodynamic, morphological, and oxidative stress and renal variables in experimental thyroid disorders. Six groups of male Wistar rats were used: control, hypothyroid, hyperthyroid, and the same groups treated with salt (8% via food intake). Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 6 wk. Finally, BP and HR were recorded directly, and morphological, metabolic, plasma, and renal variables were measured. High-salt intake increased BP in thyroxine-treated rats but not in control or hypothyroid rats. High-salt intake increased cardiac mass in all groups, with a greater increase in hyperthyroid rats. Urinary isoprostanes and H2O2 were higher in hyperthyroid rats and were augmented by high-salt intake in all groups, especially in hyperthyroid rats. High-salt intake reduced plasma thyroid hormone levels in hyperthyroid rats. Proteinuria was increased in hyperthyroid rats and aggravated by high-salt intake. Urinary levels of aminopeptidases (glutamyl-, alanyl-, aspartyl-, and cystinylaminopeptidase) were increased in hyperthyroid rats. All aminopeptidases were increased by salt intake in hyperthyroid rats but not in hypothyroid rats. In summary, hyperthyroid rats have enhanced salt sensitivity, and high-salt intake produces increased BP, cardiac hypertrophy, oxidative stress, and signs of renal injury. In contrast, hypothyroid rats are resistant to salt-induced BP elevation and renal injury signs. Urinary aminopeptidases are suitable biomarkers of renal injury.