scholarly journals Influence of time of feeding on dam performance prepartum and postpartum and its impact on its kids

2021 ◽  
Vol 45 (1) ◽  
Author(s):  
Moyosore Joseph Adegbeye ◽  
Oluwatosin Bode Omotoso ◽  
Adebowale Noah Fajemisin ◽  
Samuel Olanrewaju Aro ◽  
Damilola Deborah Obadare ◽  
...  

Abstract Background This study was conducted to evaluate the impact of time of feeding on the performance of WAD goats during pregnancy, and to assess how the time of feeding of the dam affect the growth of their kids’ postpartum. Twelve (12) pregnant does were used in the pre-partum and in the postpartum, the same 12 lactating does and their 12 kids (1 kid per doe) were used. The dams were randomly distributed into three treatments and were fed once daily either in the morning, noon, or evening at 0600 h, 12:00 h and 18:00 h respectively under the natural light–dark cycle. Result Serum creatinine in noon-fed does was higher (P = 0.005) than in morning and evening-fed does. In addition, low density lipoprotein in morning-fed gravid does was the high (P = 0.007) compared to noon-fed does while the evening-fed does had the lowest. During postpartum, morning and noon-fed dams consumed more feed (forage, concentrate, and total daily feed intake) than evening-fed dams (P ≤ 0.006). Kid weight of morning-fed does was numerically higher than noon-fed does, which was higher than kids of evening-fed does. Conclusion This study shows that time of feeding did not affect the performance of pregnant WAD goats. However, it has the potential to influence the serum parameters of pregnant animals. It also showed that time of feeding influences maternal feed intake postpartum and can influence the growth of the kids.

2019 ◽  
Vol 10 (4) ◽  
pp. 3704-3710
Author(s):  
Helisha Ruth Obonyo ◽  
Senthemarai Selvi V

The current research was intended to comprehend hypoglycemic and anti-lipidaemic exercises of hydrated common bean (phaseolus Vulgaris L.) seed extracts on streptozotocin-induced diabetic albino rats. At a set portion fluctuate of 100, 200,300 mg/kg body weight of common bean extracts was orally directed as one portion for every day to polygenic disorder rats for a measure of thirty days. The impact of P.vulgaris L. on hypoglycemic, glycosylated hemoprotein (HbA1c) and blood serum lipid profile (Total cholesterin), Triglyceride (TG), very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), High-density lipoprotein (HDL)) in plasma were estimated in the regular and diabetic induced rat. The outcomes demonstrated that quick glucose,serum TC, TG, LDL, VLDL, levels were significantly (p<0.05) attenuate, while blood serum HDL, the level was extensively (p<0.05) upgraded inside the diabetic rats. The inconclusive amount of pace of 300 mg/kg is more reasonable than that of a hundred mg/kg. Our examination so shows that Phaseolus vulgaris L has a powerful adversary to diabetic and anti-lipidaemic impacts on streptozotocin-induced diabetic rats, and results were comparable to reference drug glibenclamide.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Jui-Ting Hsiung ◽  
Maria Marroquin ◽  
Kamyar Kalantar-Zadeh

Background: Studies suggests that in the general population, hyperlipidemia may confer higher risk of developing chronic kidney disease (CKD). But, there is conflicting data as to whether statins can protect renal function or slow renal degradation. We sought to examine the impact of statins on the association of low-density lipoprotein cholesterol (LDL) and risk of incident CKD. Methods: Our cohort included 1,439,756 US veterans without chronic kidney disease (CKD), but with LDL measured between 2004-2006, who were followed until 2014. Incident CKD was defined as over 3 estimated glomerular filtration rate (eGFR) measurements <60 mL/min/1.73m 2 at least 90 days apart. Patients with a statin prescription at the time of LDL measurement were identified. Cox models were used to estimate the associations between LDL with incident CKD. Model adjustments include demographics, comorbidities, smoking status, prescription of fibrate or niacin, body mass index, albumin, high-density lipoprotein cholesterol, and triglycerides. Results: The cohort included 5% females, 16% African Americans, 26% diabetics, and 30% statin-users, with a mean age of 60±13 years. The median [IQR] of LDL and eGFR were 109 [88,133] mg/dL and 83 [72,94] mL/min/1.73m 2 , respectively. A J-shaped association between LDL and incident CKD were observed in both those on statin and not on a statin after adjustment. Low LDL (<70 mg/dL) was associated with a higher risk of incident CKD compared to the reference (LDL 70-<100 mg/dL) regardless of statin use. High LDL ≥160 mg/dL was associated with the highest of risks of incident CKD (HR: 1.08, 95% CI: 1.04, 1.13, and HR: 1.10, 95% CI: 1.07, 1.12, for statin use and no statin use, respectively). Conclusion: Both high and low LDL were associated with higher incident CKD risk independent of statin use in this US veteran cohort. Further studies are needed to understand how to manage cardiovascular disease risk by lowering LDL while simultaneously reducing risk of CKD.


2020 ◽  
Vol 9 (23) ◽  
Author(s):  
Peter Willeit ◽  
Calvin Yeang ◽  
Patrick M. Moriarty ◽  
Lena Tschiderer ◽  
Stephen A. Varvel ◽  
...  

Background Conventional "low‐density lipoprotein cholesterol (LDL‐C)" assays measure cholesterol content in both low‐density lipoprotein and lipoprotein(a) particles. To clarify the consequences of this methodological limitation for clinical care, our study aimed to compare associations of “LDL‐C” and corrected LDL‐C with risk of cardiovascular disease and to assess the impact of this correction on the classification of patients into guideline‐recommended LDL‐C categories. Methods and Results Lipoprotein(a) cholesterol content was estimated as 30% of lipoprotein(a) mass and subtracted from “LDL‐C” to obtain corrected LDL‐C values (LDL‐C corr30 ). Hazard ratios for cardiovascular disease (defined as coronary heart disease, stroke, or coronary revascularization) were quantified by individual‐patient‐data meta‐analysis of 5 statin landmark trials from the Lipoprotein(a) Studies Collaboration (18 043 patients; 5390 events; 4.7 years median follow‐up). When comparing top versus bottom quartiles, the multivariable‐adjusted hazard ratio for cardiovascular disease was significant for “LDL‐C” (1.17; 95% CI, 1.05–1.31; P =0.005) but not for LDL‐C corr30 (1.07; 95% CI, 0.93–1.22; P =0.362). In a routine laboratory database involving 531 144 patients, reclassification of patients across guideline‐recommended LDL‐C categories when using LDL‐C corr30 was assessed. In “LDL‐C” categories of 70 to <100, 100 to <130, 130 to <190, and ≥190 mg/dL, significant proportions (95% CI) of participants were reassigned to lower LDL‐C categories when LDL‐C corr30 was used: 30.2% (30.0%–30.4%), 35.1% (34.9%–35.4%), 32.9% (32.6%–33.1%), and 41.1% (40.0%–42.2%), respectively. Conclusions “ LDL‐C” was associated with incident cardiovascular disease only when lipoprotein(a) cholesterol content was included in its measurement. Refinement in techniques to accurately measure LDL‐C, particularly in patients with elevated lipoprotein(a) levels, is warranted to assign risk to the responsible lipoproteins.


2011 ◽  
Vol 121 (9) ◽  
pp. 397-403 ◽  
Author(s):  
Martijn C.G.J. Brouwers ◽  
Marleen M.J. van Greevenbroek ◽  
Jason S. Troutt ◽  
Angela Bonner Freeman ◽  
Ake Lu ◽  
...  

The aim of the present study was to investigate the relationship between circulating PCSK9 (proprotein convertase subtilisin kexin type 9) and FCHL (familial combined hyperlipidaemia) and, when positive, to determine the strength of its heritability. Plasma PCSK9 levels were measured in FCHL patients (n=45), NL (normolipidaemic) relatives (n=139) and their spouses (n=72). In addition, 11 FCHL patients were treated with atorvastatin to study the response in PCSK9 levels. PCSK9 levels were higher in FCHL patients compared with NL relatives and spouses: 96.1 compared with 78.7 and 82.0 ng/ml (P=0.004 and P=0.002 respectively). PCSK9 was significantly associated with both TAG (triacylglycerol) and apolipoprotein B levels (P<0.001). The latter relationship was accounted for by LDL (low-density lipoprotein)–apolipoprotein B (r=0.31, P=0.02), not by VLDL (very-low-density lipoprotein)–apolipoprotein B (r=0.09, P=0.49) in a subgroup of subjects (n=59). Heritability calculations for PCSK9 using SOLAR and FCOR software yielded estimates of 67–84% respectively (P<0.0001). PCSK9 increased from 122 to 150 ng/ml in 11 FCHL patients treated with atorvastatin (40 mg) once daily for 8 weeks (P=0.018). In conclusion, plasma PCSK9 is a heritable trait associated with both FCHL diagnostic hallmarks. These results, combined with the significant rise in PCSK9 levels after statin therapy, warrant further studies in order to unravel the exact role of PCSK9 in the pathogenesis and treatment of this highly prevalent genetic dyslipidaemia.


2005 ◽  
Vol 73 (7) ◽  
pp. 4315-4322 ◽  
Author(s):  
Kambiz Yaraei ◽  
Lee Ann Campbell ◽  
Xiaodong Zhu ◽  
W. Conrad Liles ◽  
Cho-chou Kuo ◽  
...  

ABSTRACT Chlamydia pneumoniae is a common respiratory pathogen that is associated with an increased risk of cardiovascular disease. However, the mechanisms by which C. pneumoniae contributes to cardiovascular disease have not been determined yet. C. pneumoniae infection may accelerate the death of cells within atherosclerotic lesions and contribute to the formation of unstable lesions. To test this hypothesis, the impact of C. pneumoniae infection on the death of lipid-loaded mouse macrophages was investigated. It was observed that RAW 264.7 cells are highly susceptible to the toxic effects of oxidized low-density lipoprotein (LDL) and exhibit markers of cell death within 24 h of treatment with as little as 5 μg/ml oxidized LDL. Subsequent infection with either live C. pneumoniae or heat-killed or UV-inactivated C. pneumoniae at a low multiplicity of infection for 24 to 72 h stimulated both additional binding of annexin V and the uptake of propidium iodide. Thus, C. pneumoniae augments the effects of oxidized LDL on cell death independent of a sustained infection. However, unlike oxidized LDL, C. pneumoniae infection does not activate caspase 3 or induce formation of the mitochondrial transition pore or the fragmentation of DNA, all of which are classical markers of apoptosis. Furthermore, primary bone marrow macrophages isolated from mice deficient in Toll-like receptor 2 (TLR-2) but not TLR-4 are resistant to C. pneumoniae-induced death. These data suggest that C. pneumoniae kills cells by a caspase-independent pathway and that the process is potentially mediated by activation of TLR-2.


2009 ◽  
Vol 94 (3) ◽  
pp. 761-764 ◽  
Author(s):  
Manivannan Srinivasan ◽  
Brian A. Irving ◽  
Ketan Dhatariya ◽  
Katherine A. Klaus ◽  
Stacy J. Hartman ◽  
...  

Abstract Context: Levels of dehydroepiandrosterone (DHEA) and its sulfate form (DHEAS) are inversely associated with cardiovascular mortality in men but not women. Very little evidence is available on the impact of DHEA administration on lipoprotein profile in women. DHEAS levels are very low/undetectable in hypoadrenal women. Objective: The objective of the study was to determine the impact of DHEA replacement on lipoprotein profile in hypoadrenal women. Design and Setting: A double-blind, randomized, placebo-controlled, cross-over design study was conducted at the Mayo Clinic. Participants: Thirty-three hypoadrenal Caucasian women (mean ± sd; age 50.3 ± 15.2 yr, body mass index 26.6 ± 4.4 kg/m2) took part in the study. Intervention: Study participants were assigned to receive either a placebo or 50 mg/d of DHEA for 3 months each. Lipid levels and lipoprotein profile were analyzed using the Lipo Science Lipoprotein nuclear magnetic resonance system. Main Outcome Measures: Changes in various lipoprotein sizes and levels were measured. Results: The DHEA period had higher plasma DHEAS levels than during placebo (&lt;0.3 ± 0.0 vs. 3.5 ± 1.3 nmol/liter, P &lt; 0.001). DHEA replacement significantly reduced total cholesterol (20.0 vs. −22, P = 0.02) and high-density lipoprotein (HDL) levels (2.0 vs. −6.0, P = 0.006) and tends to reduce triglyceride and total low-density lipoprotein levels. Although, DHEA replacement had no effect on low-density lipoprotein particle size, it significantly reduced larger HDL particles and to modest extent small HDL particles. Conclusions: Our study findings showed that oral DHEA administration in hypoadrenal women results in an unfavorable lipoprotein profile. The results warrant long-term studies to determine the impact of DHEA replacement on cardiovascular risk.


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