No abstract

Chronic cold stress can trigger biochemical and physiological changes in living organisms, which leads to a rapid loss of homeostasis. However, the biochemical responses of the organism to chronic cold stress are unclear. In this study, we systematically analysed the metabonomic changes under chronic cold stress by using a (1)H NMR-based metabonomics approach in conjunction with clinical biochemistry assessments. We found that chronic cold exposure caused significant elevation in the levels of lipoproteins (HDL, LDL), lactate, acetoacetate, creatine, creatinine, choline metabolites (GPC, PC and betaine), TMAO and taurine but reduction in the levels of VLDL, glutamine, glycine and glycerol in plasma. Increased levels in urinary TCA cycle intermediates (2-ocoglutarate and citrate), acetoacetate, taurine, TMAO, betaine and hippurate were also found in model rats, together with the reduction of creatinine and tryptophan levels. The results indicated that chronic cold stress caused widespread metabolic changes involved in lipid and energy metabolism, gluconeogenesis, the TCA cycle, and gut microbiota disorders, accompanied with hepatic and renal dysfunction. These findings provide a comprehensive insight into the biochemical consequences and metabolic responses to chronic cold stress in rats.

Acute alcoholic liver damage is a common illness and poses a potential health risk for humans presently.Salvianic acid (SA) has been found to be effective in liver protection. However, the mammalian systems responses to acute alcohol exposure and the underlying biochemical mechanism of SA treatment are not clear. In this study, we systematically analysed the acute alcohol-induced metabonomic changes and the therapeutic effect of SA by using a 1 H NMR-based metabonomics approach together with histopathological and clinical biochemistry assessments. The rats in the treatment and model groups were gavaged with 5 g kg À1 BW edible alcohol once every 12 h three times to establish the acute alcoholic liver damage model. SA-treated rats were gavaged with 20 mg kg À1 SA for five days before alcohol administration. The model rats presented acute alcoholic injury with centrilobular inflammation and necrosis. SA treatment not only alleviated the hepatic damage but also promoted the recovery of liver function. We found that acute alcohol exposure induced significant elevation of lactate, glycerol, acetate, creatine and ketone bodies but reduction of glycine and TMAO/betaine. SA reversed the metabolic changes in multiple metabolic pathways, including anaerobic glycolysis, fatty acid oxidation, lipolysis, oxidative stress, creatinine and methylation metabolism. These findings provide an overview of the biochemical consequences of acute alcohol intake and new insights into the SA effects on acute alcoholic liver injury, demonstrating metabonomics as a powerful approach for examining the molecular mechanisms of Traditional Chinese Medicine.