Glucoregulatory effect of butyrate is associated with elevated circulating VEGF and reduced cardiac lactate in high fructose fed rats.

Background: High fructose diet has been linked with impaired body metabolism and cardiovascular diseases. Sodium butyrate (NaB) was documented to improve glucoregulation and cardiometabolic problems associated with high fructose diet (HFrD) but the mechanisms behind it are unclear. As a result, the purpose of this study was to look into the effects of NaB on VEGF and cardiac lactate in HFrD-induced dysmetabolism. Methods: Twenty male Wistar rats of weight 130-140 g were assigned randomly after a week of acclimation into four groups: Control diet (CTR), High fructose drink (HFrD); 10 % (w/v), NaB (200 mg/kg bw), and HFrD + NaB (200 mg/kg bw). The animals were induced to be unconscious with 50 mg/kg of pentobarbital sodium intraperitoneally, blood samples were taken via cardiac puncture and cardiac tissue homogenates were obtained for Fasting Blood Sugar (FBS) and plasma insulin, cardiac glycogen, plasma and cardiac glycogen synthase, plasma and cardiac nitric oxide as well as vascular endothelial growth factor (VEGF). Result: HFrD resulted in statistical elevation body and cardiac weight, plasma glucose, plasma insulin, cardiac lactate, glycogen and decreased nitric oxide level (NO) when compared with the control group. Administration of NaB reduced cardiac weight, blood glucose, plasma insulin, cardiac lactate while nitric oxide and glycogen increased (P < 0.05). NaB increased plasma glycogen synthase in normal rats, plasma and cardiac circulating VEGF in HFrD administered rats (P < 0.05) while no change was produced in plasma and cardiac glycogen synthase level of HFrD treated rats. Conclusion: Sodium butyrate improves glucoregulation by reducing cardiac lactate and increasing circulating VEGF in HFrD-treated rats.

Sodium butyrate aggravates glucose dysregulation and dyslipidemia in high fat-fed Wistar rats.

Sodium butyrate (NaB), a short chain fatty acid (SCFA) has been shown to improve metabolic, glucose and lipid signaling. High fat diet elicits increased risk of cardiometabolic disease due to dysmetabolism, altered endothelial function and elevated oxidant activities. This study aims at evaluating the effect of NaB on high fat diet-fed female Wistar rats, and the possible role of vascular endothelial growth factor (VEGF). Twenty female Wistar rats with mean weight of 120 ± 5 g were divided randomly after one week of acclimatization into four groups: Control diet (CTR), High fat diet (HFD), NaB (200 mg/kg), and HFD + NaB. After six weeks of the experimental procedure, blood samples were collected by cardiac puncture. Data were analyzed and expressed in mean ± SEM and p-values <0.05 were accepted as significant. Data showed that HFD increased lactate dehydrogenase (LD) and free fatty acid (FFA), but not triglyceride (TG) and total cholesterol (TC). It also led to insulin resistance (elevated fasting blood glucose, insulin and homeostasis model assessment for insulin resistance). These effects of HFD were accompanied by increased lipid peroxidation (malondialdehyde and 4-hydroxynonenal). Sodium butyrate significantly decreased circulating nitric oxide (NO) and LD while increasing FFA, TG, insulin resistance, aggravated lipid peroxidation and increased VEGF in HFD rats (P < 0.05). We speculated therefore, that NaB aggravated glucose dysregulation and dyslipidemia, which is accompanied by increased VEGF.

ThE profile of anthRopometRy and psyChosocial issuEs on campus (TERRACE) study: A study protocol and preliminary results.

Background: Obesity among the youth is a major public health problem. Globally, the burden of obesity has been on the increase, particularly among young persons, with associated psychosocial issues. This study aimed to present the rationale and design of ThE profile of anthRopometRy And psyChosocial issuEs on campus (TERRACE) Study and as well report some preliminary findings obtained on the anthropometric and psychosocial profile of young persons in some tertiary institutions in Oyo State, Nigeria. Methods: This study first described the methodology of the main study (TERRACE Study) and also provided a report of the preliminary data. The TERRACE study adopted a cross-sectional design of eligible and consenting adults between 16-35 years of age. A three-stage multi-stage sampling technique was used to recruit the participants. Questionnaire, weighing scales, and other tools were used to collect data on socio-demographic, cardiovascular profile, sleep, anthropometric, and psychological variables. Descriptive and inferential statistics were used for data analysis, using SPSS version 23 software. Result: The preliminary data were obtained from 225 participants recruited from three tertiary institutions in Ibadan metropolis, with mean age of 21.5 ±â€¯3.8 years. The majority were females (77.3%) and self-employed, with an average income less than 10,000 naira monthly (less than $25/month at an exchange rate of 400 naira/dollar). The males had higher systolic blood pressure compared to females and constituted a higher proportion of current smokers compared to females (was significant (p < 0.0001 and 0.011 respectively). A fifth (20.4%) of the population were underweight, while overweight and obese people accounted for 12%. They were mostly depressed, (183(87.9%) were moderate to severe depression), more of the females compared to males were anxious. Conclusion: The preliminary results revealed a high burden of underweight, obesity and psychosocial issues among the young people in Ibadan, Nigeria. Further findings to be obtained from the TERRACE Study would enhance the development of an effective public intervention in addressing anthropometric- and psychosocial-related health problems as well as provide baseline data for further studies among this population.

Sildenafil augments fetal weight and placental adiponectin in gestational testosterone-induced glucose intolerant rats.

Testosterone induces intra-uterine growth restriction (IUGR) with maternal glucose dysregulation and oxidant release in various tissues. Adiponectin, which modulates the antioxidant nuclear factor erythroid 2-related factor 2 (Nrf2) signaling is expressed in the placenta and affects fetal growth. Sildenafil, a phosphodiesterase type 5 inhibitor (PDE5i), used mainly in erectile dysfunction has been widely studied as a plausible pharmacologic candidate in IUGR. Therefore, the present study sought to determine the effect of PDE5i on placental adiponectin/Nrf2 pathway in gestational testosterone-induced impaired glucose tolerance and fetal growth. Fifteen pregnant Wistar rats were allotted into three groups (n = 5/group) receiving vehicles (Ctr; distilled water and olive oil), testosterone propionate (Tes; 3.0 mg/kg; sc) or combination of testosterone propionate (3.0 mg/kg; sc) and sildenafil (50.0 mg/kg; po) from gestational day 14-19. On gestational day 20, plasma and placenta homogenates were obtained for biochemical analysis as well as fetal biometry. Pregnant rats exposed to testosterone had 4-fold increase in circulating testosterone compared with control (20.9 ± 2.8 vs 5.1 ± 1.7 ng/mL; p < 0.05) whereas placenta testosterone levels were similar in testosterone- and vehicle-treated rats. Exposure to gestational testosterone caused reduction in fetal and placental weights, placental Nrf2 and adiponectin. Moreover, impaired glucose tolerance, elevated plasma triglyceride-glucose (TyG) index, placental triglyceride, total cholesterol, lactate, malondialdehyde and alanine aminotransferase were observed in testosterone-exposed rats. Treatment with sildenafil improved glucose tolerance, plasma TyG index, fetal and placental weights and reversed placental adiponectin in testosterone-exposed pregnant rats without any effect on placental Nrf2. Therefore, in testosterone-exposed rats, sildenafil improves impaired glucose tolerance, poor fetal outcome which is accompanied by augmented placental adiponectin regardless of depressed Nrf2.

Sodium acetate ameliorated systemic and renal oxidative stress in high-fructose insulin-resistant pregnant Wistar rats.

Pregnancy is an insulin-resistant condition especially at near term predisposing maternal kidneys to hyperinsulinemia-induced oxidative stress. The impact of fructose on renal metabolic dysregulation and oxidative stress in pregnancy requires elucidation. Short-chain fatty acids (SCFAs) are known for protective roles in oxidative stress conditions. Therefore, the study aimed at investigating fructose-induced glucose dysregulation and renal oxidative stress in pregnant and non-pregnant rats and the possible preventive role of SCFA, acetate. Thirty female Wistar rats were grouped (n = 5/group). Three groups were made pregnant (P); the other three remained non-pregnant (NP). Both pregnant and non-pregnant rats received drinking water (control), 10% fructose (w/v) (NP+F or P+F), and 10% (w/v) fructose plus sodium acetate (200 mg/kg) (NP+F+A or P+F+A) for 3 weeks. Renal and plasma glutathione antioxidant index (GSH/GSSG), G6PDH, and adenosine were significantly lower in NP+F and P+F groups compared with control while renal and plasma adenosine deaminase (ADA), xanthine oxidase (XO), uric acid (UA), lactate dehydrogenase (LDH), and malonaldehyde (MDA) were significantly elevated in NP+F and P+F groups compared with controls. HOMA-IR showed marked impairment in both NP+F and P+F groups. The P+F group revealed greater suppression in plasma and renal G6PDH-dependent antioxidant index, adenosine, and aggravation of LDH, MDA compared with the NP+F group (p < 0.05). Sodium acetate reduces plasma and renal surrogate oxidative stress markers, improved G6PD-dependent antioxidant index, and HOMA-IR in NP+F and P+F groups. Pregnancy exacerbates fructose-induced insulin resistance and renal oxidative stress whereas acetate ameliorated fructose-induced redox and glucose dysregulation in pregnant and non-pregnant rats.

Uric acid is a key player in salt-induced endothelial dysfunction: the therapeutic role of Stigma maydis (corn silk) extract.

Hyperuricemia has been implicated in the pathogenesis and complications of cardiovascular diseases with associated elevated oxidant events. There is evidence that excessive salt intake results in cardiometabolic disturbances but the mechanism is elusive. Also, Stigma maydis (corn silk) is noted for its antioxidant properties among other beneficial roles. This study, therefore, aimed to establish the effect of high-salt diet (SD) on uric acid (UA) production and the role of S. maydis in salt-induced phenotypes. Four groups of randomly selected rats (n = 5) were fed with normal rat feed, corn silk extract (500 mg/kg), SD (8%) and corn silk extract plus high-salt feed. After 6 weeks of the experimental procedure, each animal was anesthetized by exposure to chloroform vapor and blood samples collected by cardiac puncture. Data were expressed in means ± SEM and p values <0.05 were accepted as significant. SD resulted in reduced plasma superoxide dismutase (SOD), nitric oxide (NO), and glutathione peroxidase (GPx) but not endothelial nitric oxide synthase. Also, plasma UA and vascular cell adhesion molecule-1 (VCAM-1) increased in the SD group compared with control. However, S. maydis extract in the SD-exposed group increased NO and GPx and not SOD. Also, S. maydis extract attenuated UA and VCAM-1. In conclusion, high-salt intake may initiate deleterious cardiovascular events through UA-dependent mechanism and S. maydis extract has therapeutic potential in high-salt-induced oxidative damage and/or UA-dependent endothelial pathologies.