Rats made hypothyroid by administration of radioactive iodine and age-matched controls were individually caged and offered a choice between either water or varying concentraions of sweet (sucrose), bitter (quinine sulfate), salty (NaCl) or sour HCl solutions to drink ad libitum for 48 h periods. Comparative measurements were made of the volume of test solution consumed to that of total volume consumed and were expressed as taste preferences. Throughout a wide range of concentrations, taste preferences for sucrose were significantly lower (P less than 0.001) and those for quinine sulfate and NaCl significantly higher (P less than 0.001) in hypothyroid animals than in controls. Taste preferences for HCl were generally similar in both groups. Daily intraperitoneal injections of thyroxine, 10 mug/100 g body wt. to hypothyroid rats for 18-24 days eliminated completely the difference between hypothyroid and control rats in taste preference for quinine sulfate. These studies show that significant and reversible changes in taste preferences occur in rats rendered hypothyroid with radioactive iodine.
We have previously reported that in old rats, reversal of age‐related vascular dysfunction by exercise training correlates with an increase in circulating adiponectin and its signaling within coronary vascular smooth muscle. In the current study, we investigated the effect of deletion of adiponectin on exercise training‐induced vascular adiponectin. C57BL/6 wild‐type (WT) or homozygous adiponectin knockout (AdipoKO) mice were obtained at 10–12 wks of age and underwent treadmill exercise training (EX) (12 m/min, 5° incline, 1 hr/day, 5 days/wk for 8 wks) or remained sedentary (SED) in cages. Arterioles isolated from cardiac and soleus muscle were assessed for contractile and vasodilatory function, and capillarity of the soleus muscle was evaluated. Exercise training increased flow‐induced dilation significantly in coronary arterioles of WT mice (P<0.01 EX vs. SED), but decreased flow‐induced dilation in coronary arterioles from AdipoKO mice. ACh‐induced dilation was reduced in coronary arterioles from AdipoKO mice as compared to those from WT mice (P<0.05 AdipoKO vs. WT). Exercise training reduced ACh‐induced dilation in arterioles from WT mice, but increased ACh‐induced dilation in arterioles from AdipoKO mice. Baseline capillarity increased in the soleus muscle of AdipoKO mice as compared to WT mice, but an exercise training‐induced increase in capillarity, detected in WT mice, was absent in AdipoKO mice. Contractile responsiveness to phenylephrine was increased in arterioles from the soleus muscle of both WT and AdipoKO mice (P<0.01 EX vs. SED in both WT and AdipoKO). These data indicate that adiponectin is a critical contributor to exercise training‐induced vascular adaptations; however, locally produced adiponectin may be more critical than circulating adiponectin in mediating these adaptations.Support or Funding InformationFlorida State University College of MedicineThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Circulating adiponectin levels have been shown to correlate with microvascular coronary function, suggesting a cardioprotective effect. Our previous work has shown that adiponectin deficiency decreases coronary smooth muscle contractile function and physiological cardiac hypertrophy that is not reversed with exercise training. However, it is unknown if adiponectin deficiency adversely affects endothelial‐dependent coronary vasodilation, leading to cardiac abnormalities. We tested the hypotheses that adiponectin is necessary for acetylcholine (ACh) and flow‐induced vasodilation in coronary arterioles. It was also hypothesized that exercise training would improve cardiac function in exercise trained wild‐type, but not adiponectin knock‐out (AdipoKO) mice.MethodsC57BL/6 wild‐type (WT) or homozygous AdipoKO mice were obtained at 10 weeks of age and underwent treadmill exercise (12 m/min, 5° incline, 1 hour/day, 5 days/week for 8 weeks) or remained sedentary in cages. At the end of the training/sedentary period, coronary resistance arterioles (intraluminal diameter <150 mm) were isolated, cannulated, and placed under an inverted microscope equipped with a video camera and caliper to record luminal diameter. Vasodilatory responses to ACh (1e‐9 to 1e–4M) and changes in flow (Pressure differences = 2–60 cm H2O) were then assessed. Pre/post cardiac function was measured with a high‐resolution imaging system (Vevo 2100), with M‐mode, and was used to assess ejection fraction, fractional shortening, and left ventricular (LV) mass. Pulsed‐wave Doppler was used to calculate isovolumic relaxation (IVRT)/contraction (IVCT) time.Resultsexercise‐trained WT mice demonstrated physiological cardiac hypertrophy, indicated by a significant increase in LV mass (P<0.05). Exercise‐trained WT mice also had a significantly greater ejection fraction and fractional shortening (both; p<0.05). In contrast, cardiac hypertrophy was absent in exercise‐trained AdipoKO mice and a significant decrease in ejection fraction and fractional shortening was found (both; p>0.05). Further, both sedentary groups were shown to have significant declines in fractional shortening and ejection fraction (p<0.05). Exercise‐training maintained both IVRT/IVCT in the WT mice; however, a significant (p<0.05) lengthening of the IVRT/IVCT was shown in exercise‐trained AdipoKO and WT sedentary mice (p<0.05). The sedentary AdipoKO was shown to have an increase in IVRT only (p<0.05). Sedentary WT mice had significantly greater mean vasodilation to ACh compared to sedentary AdipoKO (p<0.01). Exercise‐training led to increased flow‐induced dilation in the WT (p<0.05), but not the AdipoKO mice (p>0.05).Conclusionthese results indicate that adiponectin is necessary for improvements in cardiac function during exercise training in young adult mice. Additionally, adiponectin may help with preserved cardiac function and that flow‐induced coronary arteriolar vasodilation may have contributed to this response.Support or Funding InformationFSU Research FundsThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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