Milk fat content is an important criterion for assessing milk quality and is one of the main target traits of dairy cattle breeding. Recent studies have shown the importance of melatonin in regulating lipid metabolism, but the potential effects of melatonin on milk fat synthesis in bovine mammary epithelial cells (BMECs) remain unclear. Here, we showed that melatonin supplementation at 10 μmol/L significantly downregulated the mRNA expression of lipid metabolism–related genes and resulted in lower lipid droplet formation and triglyceride accumulation. Moreover, melatonin significantly upregulated melatonin receptor subtype melatonin receptor 1a (MT1) gene expression, and the negative effects of melatonin on milk fat synthesis were reversed by treatment with the nonselective MT1/melatonin receptor subtype melatonin receptor 1b (MT2) antagonist. However, a selective MT2 antagonist did not modify the negative effects of melatonin on milk fat synthesis. In addition, KEGG analysis revealed that melatonin inhibition of milk fat synthesis may occur via the mTOR signaling pathway. Further analysis revealed that melatonin significantly suppressed the activation of the mTOR pathway by restricting the phosphorylation of mTOR, 4E‐BP1, and p70S6K, and the inhibition of melatonin on milk fat synthesis was reversed by mTOR activator MHY1485 in BMECs. Furthermore, in vivo experiments in Holstein dairy cows showed that exogenous melatonin significantly decreased milk fat concentration. Our data from in vitro and in vivo studies revealed that melatonin suppresses milk fat synthesis by inhibiting the mTOR signaling pathway via the MT1 receptor in BMECs. These findings lay a foundation to identify a new potential means for melatonin to modulate the fat content of raw milk in Holstein dairy cows.
Osteoarthritis (OA) is characterized by the degeneration and destruction of articular cartilage. Allicin, a dietary garlic active constituent, exerts anti-inflammatory effects on several diseases. However, its effects on OA have not been clearly elucidated. In this study, we explored the effects of allicin on OA in both in vitro and in vivo models. Allicin inhibited interleukin-1β (IL-1β) induced overproduction of nitric oxide, inducible nitric oxide synthase, prostaglandin E2, and cyclooxygenase-2, as well as pro-inflammatory cytokines tumor necrosis factor alpha and interleukin-6 in chondrocytes in a dose-dependent manner. Meanwhile, allicin reversed the overproduction of metalloproteinase-13 and a disintegrin and metalloproteinase with thrombospondin motifs-5 and the decrease of aggrecan and type II collagen. Furthermore, allicin dramatically suppressed IL-1β-stimulated PI3K/Akt/NF-κB activation in chondrocytes. In vivo, treatment with allicin prevented the destruction of cartilage and inhibited PI3K/Akt/NF-κB activation in the cartilage of mice OA models. Taken together, these results indicate that allicin may be a potential therapeutic agent for OA.
The relationship between weight change and risk of hip fracture is still controversial. We searched PubMed and Embase for studies on weight change and risk of hip fracture. Eight prospective studies were included. The weight loss studies included 85592 participants with 1374 hip fractures, and the weight gain studies included 80768 participants with 732 hip fractures. Weight loss is more likely a risk factor of hip fracture, with an adjusted RR (Relative Risk) (95% CI) of 1.84 (1.45, 2.33). In contrast, weight gain can decrease the risk of hip fracture, with an adjusted RR (95% CI) of 0.73 (0.61, 0.89). Dose-response meta-analysis shows that the risk of hip fracture is an ascending curve, with an increase of weight loss above the line of RR = 1; this trend is consistent with the results of forest plots that examine weight loss and hip fracture. For weight gain and risk of hip fracture, the descending curve below the line of RR = 1; this trend is consistent with the results of forest plots that examine weight gain and hip fracture. Our meta-analysis suggests that weight loss may be a risk factor for hip fracture and that weight gain may be a protective factor for hip fracture.
In this study, Modic Changes was more common in the lowest two levels, especially in L5/S1. Additionally, the sub-types (type I and type II) were also more likely to appear in L5/S1. It appeared that there existed a correlation between MC and biomechanics. And it seemed that local biomechanical stress might contributed to the distribution of MC and the conversion of type I to type II for the patients treated conservatively.
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