ArticleJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology2014
Early diabetes treatment does not prevent sympathetic dysinnervation in the streptozotocin diabetic rat heart.
Article in Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 12 citations in OpenAlex.
- Acute effects of empagliflozin on open-loop baroreflex function and urine output in streptozotocin-induced type 1 diabetic rats.The journal of physiological sciences : JPS · 2024Article
- [Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2021Article
- Renal and cerebral RAS interaction contributes to diabetic kidney disease.American journal of translational research · 2019Article
- Heart Rate Variability as Early Biomarker for the Evaluation of Diabetes Mellitus Progress.Journal of diabetes research · 2016Article
- Trying to prevent diabetic cardiovascular autonomic neuropathy: more questions than answers.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2014Article
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4 authors at 1 institution in 1 country.
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Abstract
backgroundPositron emission tomography (PET) studies have demonstrated reduced sympathetic neuronal integrity in high-fat diet fed streptozotocin insulin-resistant diabetic rats in parallel with abnormal early-to-atrial transmitral velocity. We hypothesized that administration of anti-glycemic drugs early after diabetes induction would prevent sympathetic neuronal dysfunction. METHODS AND
resultsMale Sprague-Dawley rats fed high-fat diet were administered streptozotocin (45 mg·kg(-1), ip, n = 23) to induce diabetes or vehicle alone (n = 6). Diabetic rats were randomized to receive insulin (4 U·day(-1)), metformin (650 mg·kg(-1)·day(-1)), rosiglitazone (4 mg·kg(-1)·day(-1)), or no treatment 1 week after streptozotocin. Small animal PET imaging using the norepinephrine analog [(11)C]meta-hydroxyephedrine (HED) at baseline and 8 weeks of diabetes determined sympathetic neuronal integrity. Echocardiography assessed cardiac function. Plasma norepinephrine levels were determined in parallel. Ex vivo immunoblotting was performed at the end of the experiment to compare the relative expression of various proteins involved in metabolic and noradrenergic signaling. Insulin restored blood glucose and lipid levels to normal. Despite improved plasma lipid levels, neither metformin nor rosiglitazone reduced blood glucose. At 8 weeks, untreated and treated diabetics displayed a 39%-42% reduction in myocardial HED standardized uptake values (P < .05). In all diabetic groups, plasma norepinephrine was elevated (2.3- to 3.3-fold, P < .05) and norepinephrine reuptake transporter expression reduced (28%-35%, P < .05) compared to non-diabetics. Doppler echocardiography revealed delayed development of prolonged mitral valve deceleration and elevated early-to-atrial filling velocity ratio among treated diabetic rats.
conclusionEarly glycemic treatment of insulin-resistant diabetic rats did not prevent deterioration of sympathetic neuronal integrity though ventricular filling abnormalities were delayed.
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