Sanya Roysommuti

Taurine supplementation is recommended during perinatal life to provide sufficient taurine for fetuses and newborns. Furthermore, perinatal taurine supplementation affects cardiovascular and metabolic functions in adult life. In adults, taurine supplementation is reported to improve exercise training. The present study explored the effects of perinatal taurine supplementation followed by dynamic exercise training on cardiovascular and metabolic functions in adult male rats. Pregnant Wistar rats were maintained on water containing or lacking 3% taurine from conception to weaning. After weaning, male offspring were fed normal rat chow and water throughout the study. At 4 weeks of age, the taurine-treated and taurine-untreated rats were subjected to either a swimming exercise protocol (10–30 min a day, 5 day a week) for 12 weeks (Ex and TEx) or remained sedentary (C and T). At 16 weeks of age, kidney weight, mean arterial pressure, baroreflex sensitivity, plasma leptin, plasma triglyceride, blood urea nitrogen, plasma creatinine, and SGOT were not significantly different among the four groups. Compared to the control, perinatal taurine supplementation alone did not significantly affect any of the measured cardiovascular and metabolic parameters. Exercise training significantly decreased bodyweight, heart rate, and visceral adipocyte size, irrespective of perinatal taurine supplementation, but increased SGPT and heart weight when compared to the control. However, the effect of exercise on SGPT, but not heart weight, was abolished by perinatal taurine supplementation. These data indicate that perinatal taurine supplementation not only preserves the beneficial effects of dynamic exercise training on cardiovascular and metabolic functions but also prevents exercise-induced organ damage in adult male rats. Keywords Arterial pressure Baroreflex Exercise Metabolism Perinatal taurine Rat

Taurine plays an important role in neural growth and function from early to adult life, particularly in learning and memory via BDNF action. This study tested the hypothesis that BDNF differentially potentiates entorhinal-hippocampal synaptic transmission in vivo in adult rats. In anesthetized male Sprague-Dawley rats, a stainless steel recording electrode with an attached microinjector was placed into CA1 and the dentate gyrus to record fEPSP, and a paired stainless steel electrode was inserted into entorhinal cortex for continuous paired-pulse stimulation of that brain region. In the dentate gyrus, microinjection of BDNF resulted in a gradual increase in the peak slope of the fEPSP. Following the infusion, the peak fEPSP began to rise in about 8 min, reached a maximum of 120 ± 2% (from baseline) by about 20 min, and remained near peak elevation (~115%) for more than 30 min. In contrast, the same dose of BDNF when injected into CA1 had no consistent effect on fEPSP slopes in the CA1. Further, an equimolar cytochrome C (horse heart) infusion had no significant effect on fEPSP slopes in either the dentate gyrus or CA1. The potentiation effect of BDNF in the dentate gyrus is consistent with a significant increase in power spectral density of dentate gyrus field potentials at 70–200 Hz, but not at frequencies below 70 Hz. In addition, the CA1 power spectral density was not affected by BDNF (compared to cytochrome C). These data indicate that in vivo BDNF potentiates entorhinal-hippocampal synaptic transmission in dentate gyrus, but not in CA1. Keywords BDNF Dentate gyrus Entorhinal cortex Field potential Hippocampus Power spectral density

Maternal dyslipidemia induces metabolic and cardiovascular disorders in adult offspring. This study tests the hypothesis that perinatal taurine supplementation prevents the adverse effects of maternal dyslipidemia on growth and cardiovascular function in adult rat offspring. Female Wistar rats were fed normal rat chow and water with (Dyslipidemia) or without dyslipidemia induction (Control) by intraperitoneal Triton WR-1339 injection, three times a week for 4 weeks. The female Control and Dyslipidemia rats were supplemented with (Control+T, Dyslipidemia+T) or without 3% taurine in water from conception to weaning. After weaning, male and female offspring were fed normal rat chow and water throughout the experiment. At 16 weeks of age, body weights significantly increased in male but not female Dyslipidemia compared to other groups, while visceral fat content significantly increased in both male and female Dyslipidemia groups. Further, both sexes displayed similar high fasting blood sugar and normal plasma leptin levels among the groups. While plasma total cholesterol and triglycerides significantly increased only in female Dyslipidemia, low-density lipoprotein cholesterol increased in both male and female Dyslipidemia groups. Mean arterial pressures and heart rates significantly increased, while baroreflex sensitivity decreased in male and female Dyslipidemia compared to all other groups. High-density lipoprotein cholesterol did not significantly different among male or female groups. These changes of the male and female Dyslipidemia group were ameliorated by perinatal taurine supplementation. The present study indicates that perinatal taurine supplementation prevents the adverse effects of maternal dyslipidemia on growth and cardiovascular function in both male and female, adult offspring.

Perinatal taurine depletion and high sugar intake from weaning onward worsen cardiac damage and arterial pressure control after ischemia/reperfusion (IR) in adult male and female rats, which can be ameliorated by high taurine diets or inhibition of renin-angiotensin system. This study tests if taurine supplementation ameliorates cardiac damage and arterial pressure control in adult female rats via alterations of both cardiac and systemic renin-angiotensin system. Female Sprague-Dawley rats were fed normal rat chow and drank water alone (control, C) or water containing 3% beta-alanine (taurine depletion, TD) from conception to weaning, and female offspring were subjected to high sugar intake (normal rat chow and 5% glucose in water; CG and TDG) or the normal rat diet (CW and TDW). At 7 weeks of age, half of the rats in each group received 3% taurine in water (CW+T, CG+T, TDW+T, and TDG+T). One week later, rats were subjected to IR or Sham procedures followed by renal nerve recording, plasma and cardiac angiotensin II measurements. Cardiac angiotensin II levels significantly elevated in CG, TDW, and TDG. Further, plasma angiotensin II concentrations were significantly elevated only in the TDG, in consistent with a significant increase in renal nerve activity to juxtaglomerular cells, but not renal vessels and tubules. These abnormalities were ameliorated by short-term taurine supplementation. Thus, in adult female rats that are perinatally depleted of taurine followed by high sugar intake after weaning, taurine supplementation decreases the adverse effects of cardiac IR via inhibition of both cardiac and systemic renin-angiotensin system overactivity.

Previous studies indicate that perinatal compromise of taurine causes cardiovascular disorders in adults via the influence of taurine on renin-angiotensin system (RAS). This study tested whether perinatal inhibition of the RAS would itself alter the adult cardiovascular system in a similar way. Female Sprague-Dawley rats were fed normal rat chow and given water alone (Control) or water containing captopril (400 mg/l) from conception until weaning. Then, the male offspring drank water or water containing captopril until 5 weeks of age followed by normal rat chow and water alone until 7 weeks of age. Thereafter, they drank water alone (Control, Captopril) or 1% NaCl solution (Control+1%, Captopril+1%). At 9 weeks of age, all animals were implanted with femoral arterial and venous catheters. Forty-eight hours later, blood chemistry, glucose tolerance, and hemodynamic parameters were determined in freely moving conscious rats. Then, the same experiments were repeated 2 days after captopril treatment. Body weights, kidney and heart to body weight ratios, fasting and non-fasting blood sugar, glucose tolerance, and heart rates were not significantly different among groups. Further, plasma sodium, mean arterial pressure, and sympathetic activity significantly increased whereas baroreflex sensitivity decreased in Captopril+1% compared to other groups. These changes were normalized by acute captopril treatment and the arterial pressure differences also by acute ganglionic and central adrenergic blockade. The present study suggests that inhibition of the RAS in the early life induces RAS overactivity, leading to salt-sensitive hypertension via sympathetic nervous system overactivity and depressed baroreflex sensitivity in adult male rats.

This study tests the hypothesis that perinatal taurine imbalance impairs renal function in adult female rats via alterations in estrogen activity. Female Sprague-Dawley rats were fed normal rat chow and water containing 3% beta-alanine (TD), 3% taurine (TS) or water alone (C) from conception until weaning. Then, female offspring received normal rat chow and water with (CG, TDG, TSG) or without (CW, TDW, TSW) 5% glucose. At 7–8 weeks of age, renal function at rest and after acute saline load was tested in conscious, restrained female rats treated with non-selective estrogen receptor blocker tamoxifen for a week. Compared to control, TD or TS did not affect mean arterial pressure (MAP). Tamoxifen significantly increased resting MAP only in TDG compared to TDW groups. Although renal blood flow did not significantly differ among the groups, renal vascular resistance increased in TSG compared to CW, CG, and TSW groups. Glomerular filtration rate and water and sodium excretion were not significantly different among the groups. Compared to CW, saline load significantly depressed fractional water excretion in CG, TDW, TDG, and TSW, and fractional sodium excretion in CG, TDW, TDG, TSW, and the TSG groups. Potassium excretion was not significantly different among the corresponding groups. Fractional potassium excretion significantly increased in TDW compared to CG and in TSG compared to CG and TSW groups. These differences were abolished by tamoxifen treatment. These data indicate that in adult female rats, perinatal taurine imbalance, particularly followed by high sugar intake, alters renal function via an estrogenic mechanism.

This study tests the hypothesis that perinatal taurine supplementation followed by a high sugar diet since weaning impairs renal function via renin-angiotensin system (RAS) overactivity in adult female rats. Female Sprague-Dawley rats were fed normal rat chow and given water alone or water containing 3% taurine from conception until weaning. After weaning, the female rats received normal rat chow and water with (CG, TSG) or without (CW, TSW) 5% glucose throughout the experiment. At 7–8 weeks of age, renal function at rest and after an acute saline load was tested in conscious female rats after a week of captopril treatment. Body, heart, and kidney weights were not significantly different among the eight groups. Mean arterial pressures and heart rates were also not different among the groups. While effective renal blood flow did not significantly differ among the eight groups, TSG displayed higher renal vascular resistance compared to CW, CG, and TSW groups. Glomerular filtration rate, filtration fraction, and water and sodium excretion did not significantly differ among the groups. Compared to CW, the saline load significantly depressed fractional water excretion in CG and TSW and fractional sodium excretion in CG, TSW, and TSG groups. Captopril treatment abolished these differences but significantly decreased potassium excretion in CG, TSW, and TSG compared to CW and abolished the increased fractional potassium excretion in TSG compared to CG and TSW groups. These data strongly suggest that in adult female rats, perinatal taurine supplementation, particularly followed by high sugar intake, alters renal function via altered RAS activity.

Perinatal taurine depletion followed by high sugar intake after weaning adversely affects myocardial and arterial pressure function following a myocardial ischemia and reperfusion (IR) insult in adult female rats. This study tests the hypothesis that taurine supplementation ameliorates this adverse effect. Female Sprague-Dawley rats were fed normal rat chow and drank water containing β-alanine from conception until weaning (taurine depletion, TD). After weaning, female offspring were fed normal rat chow and drank either water containing 5% glucose (TDG) or water alone (TDW). At 6–7 weeks of age, half the rats in each group were supplemented with taurine and 1 week later subjected to cardiac IR. Body weight, heart weight, plasma electrolytes, plasma creatinine, blood urea nitrogen, and hematocrit were not significantly different among the four groups. The mean arterial pressures significantly increased in all groups after IR, but values were not significantly different among the four groups. Heart rates were significantly increased after IR only in TDW group. Compared to TDW, TDG displayed increased plasma cardiac injury markers (creatinine kinase-MB, troponin T, and N-terminal prohormone brain natriuretic peptide), increased sympathetic activity, decreased parasympathetic activity, and decreased baroreflex sensitivity after IR. Taurine supplementation completely restored the baroreflex and autonomic dysfunction of TDG to TDW levels and partially decreased myocardial injury after cardiac IR. The present study indicates that in adult female rats, perinatal taurine depletion followed by high sugar intake after weaning exacerbates cardiac IR injury and arterial pressure dysregulation and these adverse effects can be partially prevented by taurine supplementation.

This study tests the hypothesis that perinatal taurine supplementation prevents diabetes mellitus and hypertension in adult offspring of maternal diabetic rats. Female Wistar rats were fed normal rat chow and tap water with (Diabetes group) or without diabetic induction by intraperitoneal streptozotocin injection (Control group) before pregnancy. Then, they were supplemented with 3% taurine in water (Control+T and Diabetes+T groups) or water alone from conception to weaning. After weaning, both male and female offspring were fed normal rat chow and tap water throughout the study. Blood chemistry and cardiovascular parameters were studied in 16-week old rats. Body, heart, and kidney weights were not significantly different among the eight groups. Further, lipid profiles except triglyceride were not significantly different among male and female groups, while male Diabetes displayed increased fasting blood glucose, decreased plasma insulin, and increased plasma triglyceride compared to other groups. Compared to Control, mean arterial pressures significantly increased and baroreflex control of heart rate decreased in both male and female Diabetes, while heart rates significantly decreased in male but increased in female Diabetes group. Although perinatal taurine supplementation did not affect any measured parameters in Control groups, it abolished the adverse effects of maternal diabetes on fasting blood glucose, plasma insulin, lipid profiles, mean arterial pressure, heart rate, and baroreflex sensitivity in adult male and female offspring. The present study indicates that maternal diabetes mellitus induces metabolic and cardiovascular defects more in male than female adult offspring, and these adverse effects can be prevented by perinatal taurine supplementation.