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Selected Publication:
Ragginer, C.
Impact of nitric oxide on thyroidal dysfunctions and related metabolic disorders
[ Dissertation ] Medical University of Graz; 2013. pp. 65
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- Authors Med Uni Graz:
- Ragginer Christine
- Advisor:
- Gruber Hans-Jürgen
- Renner Wilfried
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- Abstract:
- Objective: Nitric oxide pathway might play a crucial role in the pathophysiology of thyroid dysfunctions. This study aimed to investigate the impact of nitric oxide (NO) on hypothyroid (HYPO) and hyperthyroid (HYPER) Sprague Dawley rats and its associations with metabolic dysfunctions under controlled diet. Furthermore, the effects of the nitric oxide donor sodiumnitroprusside (SNP) on thyroid dysfunctions were also assessed. Methods: Sprague Dawley rats (n=107) were subdivided into normal diet and high-fat diet (HFD) groups and grouped into controls, HYPO, HYPER and SNP treated groups. Hypothyroidism was induced through propylthiouracil, whereas hyperthyroidism by triiodothyronine (T3). After 12 weeks of T3 treatment, serum nitrogen oxides (NOX), endogenous asymmetric dimethylarginine (ADMA), metabolic parameters like glucose, insulin, oxidized low density lipoproteins (oxLDL) and serum triglycerides (TG), C-reactive protein (CRP), body weight and food intake were analysed. Results: HYPO rats showed decreased serum T3 levels, HYPER rats increased T3 compared to controls. Diet had no impact on T3. Thyroid dysfunctions were accompanied by changes in calorie intake and body weight. Serum NOX was significantly reduced in normal diet HYPO rats. SNP administration compensated the decrease and markedly increased T3. NO synthase inhibitor ADMA levels were significantly higher in the HFD control group than in the normal diet controls. ADMA was declined in both HYPO groups and increased in normal diet HYPER rats. Regarding the glucose- and insulin metabolism we found significantly increased glucose levels in HFD HYPOs whereas serum insulin was significantly decreased in HYPOs regardless of diet. Hyperthyroidism did not affect the glucose- and insulin metabolism. Next, measurement of TG and oxLDL showed that both parameters were increased in HYPER rats, treatment with SNP partially reversed this effect. In HYPOs, regardless of diet, serum TG levels were similar to controls and oxLDL was significantly decreased. SNP treatment of normal diet HYPOs reversed this decrease. Moreover, regression analyses revealed a highly significant association of oxLDL and NOX in the normal diet controls. Conclusions: An association of thyroid dysfunctions with reduced bioavailability of NO and alterations of ADMA levels could be established. Treatment with the NO donor SNP resulted in an increase of serum T3 levels. Moreover, NO is associated with metabolic risk factors like oxLDL. The present results demonstrate that the NO pathway is implicated in thyroid dysfunctions, which may be of clinical relevance.