This study determined the effects of dietary copper (Cu), molybdenum (Mo) and sulphur (S) on urinary Cu and zinc (Zn) excretion in cattle. Four Simmental and four Angus heifers were fed low (L) or high (H) levels (mg/kg DM) of Cu (5,40), Mo (1,10) and S (0.2,0.5%). Initially two of each breed was fed either LCu or HCu (2 mo). Then all eight animals were fed sequentially LCuHS (1.5 mo), HCuHS, HCuHMo and HCuHMoHS (2 mo each). Simmental had a higher urine flow, increased concentration and total excretion of urinary Cu and Zn compared to Angus, but only total Zn excretion was significantly higher. Urinary Cu excretion was greatest with the HCuHMoHS diet. Urinary Zn excretion significantly increased with HS but not HS in combination with HMo and/or HCu. This study, together with previously reported biliary excretion, allows a direct comparison of urinary and biliary Cu and Zn excretion responses to dietary Cu, Mo and S.
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http://dx.doi.org/10.1016/j.rvsc.2011.01.024 | DOI Listing |
Front Nutr
January 2025
Clinical Center of Reproductive Medicine, Lianyungang Maternal and Child Health Hospital, Lianyungang, China.
Background: Salt usage patterns have been associated with a risk of multiple diseases; however, their relationship with heavy metal exposure has not been extensively studied.
Methods: This study analyzed survey data from 11,574 NHANES participants. Weighted linear regression models were used to examine the relationship between the type of salt used by participants, the frequency of adding salt at the table, and the frequency of adding regular or seasoned salt to cooking or food preparation, and urinary concentrations of 10 heavy metals.
World J Cardiol
January 2025
Department of Cardiology, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan 030012, Shanxi Province, China.
This article discusses the study by Grubić Rotkvić on the mechanisms of action of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in patients with type 2 diabetes mellitus (T2DM) and heart failure (HF). T2DM and HF are highly comorbid, with a significantly increased prevalence of HF in patients with T2DM. SGLT2i exhibit potential in reducing hospitalization rates for HF and cardiovascular mortality through multiple mechanisms, including improving blood glucose control, promoting urinary sodium excretion, reducing sympathetic nervous system activity, lowering both preload and afterload on the heart, alleviating inflammation and oxidative stress, enhancing endothelial function, improving myocardial energy metabolism, and stabilizing cardiac ion homeostasis.
View Article and Find Full Text PDFWorld J Cardiol
January 2025
Chinese Academy Medical Sciences, Fuwai Yunnan Hospital, Kunming 650000, Yunnan Province, China.
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors represent a cutting-edge class of oral antidiabetic therapeutics that operate through selective inhibition of glucose reabsorption in proximal renal tubules, consequently augmenting urinary glucose excretion and attenuating blood glucose levels. Extensive clinical investigations have demonstrated their profound cardiovascular efficacy. Parallel basic science research has elucidated the mechanistic pathways through which diverse SGLT-2 inhibitors beneficially modulate pulmonary vascular cells and arterial remodeling.
View Article and Find Full Text PDFBMC Med
January 2025
Yueyang Centre for Disease Control and Prevention, Yueyang, Hunan Province, China.
Background: A 12-month cluster randomized controlled trial (RCT) demonstrated the effectiveness of an application-based education program in reducing the salt intake and systolic blood pressure (SBP) of schoolchildren's adult family members. This study aimed to assess whether the effect at 12 months persisted at 24 months.
Methods: Fifty-four schools were randomly assigned to either the intervention or control group.
Am J Kidney Dis
January 2025
Division of Nephrology and Hypertension, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Renal tubular acidoses (RTAs) are a subset of non-anion gap metabolic acidoses that result from complex disturbances in renal acid excretion. Net acid excretion is primarily accomplished through the reclamation of sodium bicarbonate and the buffering of secreted protons with ammonia or dibasic phosphate, all of which require a series of highly complex and coordinated processes along the renal tubule. Flaws in any of these components lead to the development of metabolic acidosis and/or a failure to compensate fully for other systemic acidoses.
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