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Exogenous thyroxine (T4) attenuates glucose intolerance and insulin resistance in obese Otsuka Long‐Evans Tokushima Fatty rats (688.12)
Author(s) -
VazquezAnaya Guillermo,
Martinez Bridget,
Nakano Daisuke,
Nishiyama Akira,
Ortiz Rudy
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.688.12
Subject(s) - medicine , endocrinology , insulin resistance , blood pressure , carbohydrate metabolism , insulin
Thyroid hormones (TH) regulate metabolism and their levels are altered with the development of metabolic syndrome (MetS), which is associated with insulin resistance (IR) and hypertension. TH analogues and derivates may be effective treatments for glucose intolerance and IR, but their effects on the hypertension associated with MetS are not well described. To assess the effects of thyroxine (T4) on glucose regulation and systolic blood pressure (SBP), an oral glucose tolerance test (oGTT) was performed and arterial pressure monitored on four groups of rats (n=7‐8): 1) lean control strain, LETO, 2) obese OLETF, 3) LETO + T4 (8.0µg/100g BW/d x 5wks), and 4) OLETF + T4. While a strain effect on SBP was detected, T4 did not alter the pressure. T4 attenuated glucose intolerance in OLETF rats by 15 %, and improved insulin clearance by 33%. IR index (IRI) decreased 34% in treated OLETF compared to untreated OLETF. TH profiles were measured to assess the status of the hypothalamus‐pituitary‐thyroid axis. Total T4 (60 ± 11 vs. 30 ± 7 nmol/L) and total triiodothryonine (T3)(1.5± 0.2 vs. 0.67 ±0.13 nmol/L) were higher in OLETF compared to LETO. The results suggest that despite a hyperthyroid state in OLETF rats, improvements in glucose intolerance and IR with exogenous T4 were not sufficient to ameliorate the hypertension associated with the development of MetS. Furthermore, the data suggest that the associated hypertension in this model is not a consequence of metabolic derangement, but likely other factors independent of glucoregulation. Grant Funding Source : National Institute of Health (NIH)