ABSTRACT
Aims: To elucidate the effect of estrogen and folic acid on high fat (butter) induced lipid profile (total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), and triglyceride (TG)) and on tissue texture changes in mice. Designs: Randomized block design. Place and Duration of Study: Department of Physiology and Department of Pathology, Faculty of Veterinary Science, Bangladesh Agricultural University, Mymensingh-2202, Bangladesh between January 2012 and April2012. Methodology: 2 months old 50 male Swiss Albino mice (Mus musculus) were used for this study and divided into equal groups. Group A (control) was fed with normal rat pellet. Mice in the group B was fed with butter; group C was fed with butter and estrogen; group D was fed with butter and folic acid and group E was fed with butter, estrogen and folic acid. The atheroprotective effect of estrogen and folic acid was evaluated based on weight gain, biochemical parameters and histopathology. Results: The highest body weight gain was detected in group B (P<0.001). In biochemical study, group B showed the increase in total plasma cholesterol, especially low density lipoprotein (LDL), and triglyceride (TG) (P<0.001) compared to other treated groups. Group C, D and E showed a lower level of total plasma cholesterol (P<0.001) compared to group B. Among them group E showed the lowest total plasma cholesterol level (P<0.001). In histopathological study, the aorta of butter treated group showed sloughing of lining endothelium, increased aortic wall thickness and loss of integrity of tunica intima. It also revealed fatty changes in liver in animal models fed with butter, compared with those on a normal diet. Conclusions: 20% butter supplementation would be able to cause a rise in lipid profile and produce degenerative changes in aorta and liver and addition of estrogen or folic acid in butter supplemented diet counteracts the adverse effect.
ABSTRACT
Objective: Both plasma glucose and glycosylated hemoglobin are the recommended tools to diagnose diabetes by the International Expert Committee and World Health Organization (WHO). The aim of this study was to compare these two parameters in the diagnosis of diabetes in a selected group of Bangladeshi subjects. Materials and Methods: This cross-sectional study included 800 subjects attending the outdoor in a tertiary healthcare center during the period of September 2009 to September 2010. Fasting, postprandial (2 hours after glucose load) plasma glucose and HbA1c were measured. Diabetes is defined according to HbA1c and plasma glucose. Subjects were classified into three groups according to HbA1c values (HbA1c: =6.5%, HbA1c: 6.0-6.4% and HbA1c: < 6.0%) and also in the diabetics, prediabetics (IGT+IFG) and nondiabetics by plasma glucose. Results of the HbA1c classified subjects were compared with the plasma glucose classified subjects to see the inequity of classification. Results: Inequity of classification occurred for 11.87% of the total subjects with HbA1c =6.5% but impaired (8.25%) and nondiabetic (3.62%) by plasma glucose; for 10.13% of the subjects with HbA1c: 6.0-6.4% but diabetic (3.25%) and nondiabetic (6.88%) by plasma glucose, and for 8.5% of the total subjects with HbA1c <6.0% but diabetic (1.88%) and impaired (6.62%) by plasma glucose. Concordant classification occurred for 69.5% and inequity of classification occurred for 30.5% of the total study subjects. Conclusion: Inequity of classification of diabetes by HbA1c and plasma glucose is remarkable in the study population.
ABSTRACT
Background & objectives: A wealth of information concerning the essential role of renal sympathetic nerve activity (RSNA) in the regulation of renal function and mean arterial blood pressure homeostasis has been established. However, many important parameters with which RSNA interacts are yet to be explicitly characterized. Therefore, the present study aimed to investigate the impact of acute renal denervation (ARD) on sodium and water excretory responses to intravenous (iv) infusions of either norepinephrine (NE) or angiotensin II (Ang II) in anaesthetized spontaneously hypertensive rats (SHR). Methods: Anaesthetized SHR were acutely denervated and a continuous iv infusion of NE (200 ng/min/kg) or Ang II (50 ng/min/kg) was instigated for 1 h. Three 20-min urine clearances were subsequently collected to measure urine flow rate (UV) and absolute sodium excretion (UNaV). Results: Higher UV and UNaV (P<0.05) were observed in denervated control SHR as compared to innervated counterparts. The administration of NE or Ang II to innervated SHR produced lower UV and UNaV (P<0.05 vs. innervated control SHR). Lower diuresis/natriuresis response to ARD was observed in NE-treated SHR compared to denervated control SHR (P<0.05). Salt and water excretions in denervated NE-treated SHR, however, were significantly higher (P<0.05) relative to the excretion levels in control denervated SHR. Conversely, there was a higher (all P<0.05) diuresis/natriuresis response to ARD when Ang II was administered to SHR compared to denervated control or innervated Ang II-treated SHR. Interpretation & conclusions: NE retains its characteristic antidiuretic/antinatriuretic action following ARD in SHR. Typical action of Ang II on salt and water excretions necessitates the presence of an intact renal innervation. Ang II is likely to facilitate the release of NE from renal sympathetic nerve terminals through a presynaptic site of action. Moreover, there is a lack of an immediate enhancement in the renal sensitivity to the actions of NE and Ang II following ARD in a rat model of essential hypertension.