Short communication: commercial diets for pigs in the United States contain more calcium than formulated.

Data from Europe indicate that commercial diets for pigs and poultry contain significantly more Ca than formulated. Therefore, a survey of commercial pig diets used in the United States was conducted to test the hypothesis that the analyzed concentrations of total Ca and total P in commercial pig diets in the United States are not greater than formulated values. A total of 103 diet samples from the commercial swine industry in the United States were collected between 2019 and 2021. Diet samples were provided by feed mills, feed companies, or swine farms located in major swine-producing states in the United States including NC, TN, IA, IN, KS, MN, NE, and IL. Diets were formulated for nursery pigs, growing-finishing pigs, or sows. Each company provided formulated values for total Ca and P in all samples. Samples were sent to the University of Illinois where they were ground and analyzed for Ca and P by inductively coupled plasma-optical emission spectrometry. The formulated values for Ca and P were regressed against analyzed values, and the intercept was considered the estimated under- or over-supply of each mineral. Results indicated that there was an average of 0.19 percentage units more Ca (model; P < 0.001) in the diets than formulated, whereas, for total P, the average oversupply was only 0.06 percentage units (model; P < 0.001). In conclusion, diets used in the U.S. swine industry contain more total Ca than formulated, whereas total P is close to formulated values, which indicates that greater importance is given to P than to Ca in formulation. However, the current data indicate that more attention should be given to the actual concentration of Ca in all Ca-containing feed ingredients to avoid Ca oversupply and its detrimental effect on P digestibility and growth performance of pigs fed diets that do not contain excess P.

Calcium is often oversupplied in pig diets because limestone, the main source of Ca in pig diets, is an inexpensive feed ingredient and is often used as a carrier in premixes or a diluent in feed ingredients. However, excess Ca may be detrimental to P digestibility and pig growth performance. It was recently reported that commercial pig and poultry diets sold in Europe contain significantly more Ca than formulated, but it is not known if the Ca concentrations in commercial pig diets in the United States also contain more Ca than formulated. Therefore, a survey of commercial diets from the United States was conducted to compare analyzed and formulated values for Ca. A total of 103 diets were collected from feed mills, feed companies, or swine integrators in the United States between 2019 and 2021. Samples were analyzed for total Ca and total P. Results from the regression model used to evaluate the data indicated that diets on average contained 0.19 percentage units more total Ca and 0.06 percentage units more total P than expected. Thus, more attention needs to be paid to the inclusion of Ca in pig diets to avoid Ca oversupply and the negative effects of Ca on pig growth performance.

Melatonin inhibits vascular smooth muscle cell proliferation and apoptosis through upregulation of Sestrin2.

Excessive vascular smooth muscle cell (VSMC) proliferation contributes to the development of atherosclerosis and restenosis. Furthermore, apoptosis of VSMCs accelerates plaque rupture in the atherosclerotic vessels. Therefore, a strategy that regulates both VSMC proliferation and apoptosis is essential for the development of novel pharmacological tools for the treatment of atherosclerosis. Despite mounting evidence supporting the benefits of melatonin in diverse metabolic diseases, the role of melatonin in VSMC growth remains largely unknown. The present study revealed that melatonin inhibited both proliferation and apoptosis of primary cultured rat VSMCs. Melatonin induced mitochondrial energetic stress in VSMCs and subsequent induction of Sestrin2 via C/EBPß. Melatonin-induced Sestrin2 suppressed mTORC1 activity in VSMCs, contributing to suppression of VSMC proliferation. Additionally, melatonin-induced upregulation of Sestrin2 blocked apoptosis by preventing excessive ROS generation. The results demonstrated that melatonin controlled VSMC proliferation and apoptosis via Sestrin2-mediated inhibition of mTORC1 and ROS scavenging. Therefore, melatonin should be considered as a lead compound for therapies aimed at preventing vessel lumen constriction during the course of atherosclerosis and restenosis.

Metabolic Regulation of Methionine Restriction in Diabetes.

Although the effects of dietary methionine restriction have been investigated in the physiology of aging and diseases related to oxidative stress, the relationship between methionine restriction (MR) and the development of metabolic disorders has not been explored extensively. This review summarizes studies of the possible involvement of dietary methionine restriction in improving insulin resistance, glucose homeostasis, oxidative stress, lipid metabolism, the pentose phosphate pathway (PPP), and inflammation, with an emphasis on the fibroblast growth factor 21 and protein phosphatase 2A signals and autophagy in diabetes. Diets deficient in methionine may be a useful nutritional strategy in patients with diabetes.

Tid1, a cochaperone of the heat shock 70 protein and the mammalian counterpart of the Drosophila tumor suppressor l(2)tid, is critical for early embryonic development and cell survival.

Tid1 is the mammalian counterpart of the Drosophila tumor suppressor Tid56 and is also a DnaJ protein containing a conserved J domain through which it interacts with the heat shock protein 70 (Hsp70) family of chaperone proteins. We generated a Tid1 conditional mutation in mice, and the subsequent global removal of the Tid1 protein was achieved by crossing these conditional knockout mice with general deletor mice. No Tid1(-/-) embryos were detected as early as embryonic day 7.5 (E7.5). Nonetheless, Tid1-deficient blastocysts were viable, hatched, formed an inner cell mass and trophectoderm, and implanted (E4.5), suggesting that the homozygous mutant embryos die between E4.5 and E7.5. To assess the function of Tid1 in embryonic cells, mouse embryonic fibroblasts with the homologous Tid1 floxed allele were produced. Tid1 removal in these cells led to massive cell death. The death of Tid1-deficient cells could be rescued by ectopic expression of wild-type Tid1 but not by expression of the Tid1 protein that had a mutated J domain and was thus incapable of binding to Hsp70. We propose that Tid1 is critical for early mammalian development, most likely for its function in sustaining embryonic-cell survival, which requires its association with Hsp70.