Dietary complex probiotic supplementation changed the composition of intestinal short-chain fatty acids and improved the average daily gain of weaned piglets.

Probiotics are a group of active microorganisms that form colonies within the body and alter the composition of the flora in a specific area to provide benefits to the host. In this study, a total of 96 Duroc × Landrace × Yorkshire weaned piglets with an initial body weight (BW) of 8.56 ± 0.53 kg were employed in a randomized complete block design for a 28-day experiment. Pigs were randomly divided into two treatment groups: the control group (CON) and the complex probiotic group (CON + 0.2% probiotics), respectively. The study found that through the 28-day experiment, the average daily gain (ADG) of the complex probiotic group was significantly higher than that of the CON (p < 0.05). However, compared with the CON, the feed conversion efficiency significantly decreased on days 0-14 (p < 0.05). The addition of dietary complex probiotic significantly increased the villus height (VH) of duodenum and ileum, acetate, propionate, butyrate, and total short-chain fatty acids (SCFAs) in feces, and decreased fecal methyl mercaptans, acetic acid, and CO2 (p < 0.05). It concluded that feeding weaned piglets 0.2% complex probiotic increased the VH of duodenum and ileum, as well as changed the content of SCFAs in feces. This ultimately led to an increase in ADG.

Multifunctional roles of zinc in Alzheimer's disease.

Zinc is the second abundant trace element in the human central nervous system (CNS). Zinc homeostasis is impaired in the elderly population and Alzheimer's disease (AD) patients. Due to the failures of ß-amyloid (Aß)- and microtubule-associated protein tau (MAP-tau, tau)-targeting drugs, many researchers consider AD as a multifactorial disease. Emerging evidence demonstrates that zinc is also widely associated with the development of AD. Zinc dyshomeostasis hypothesis of AD has been proposed. In this review, we summarize the role of zinc in Aß production, protein quality control, redox homeostasis, tau phosphorylation, and BDNF signaling. Due to the multifunctional roles of zinc, when zinc dyshomeostasis occurs, it may influence these different biological activities. Zinc dyshomeostasis could be a therapeutic target for AD treatment. However, there is no consensus on the zinc concentration alteration and the effect of zinc overload or zinc deficiency in AD patients, mouse models and cell lines. Given these significant differences across reported studies, it still needs a long time for clinical application in the treatment of AD.