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Epigallocatechin gallate (EGCG) and L-theanine (LTA) are important bioactive components in tea that have shown promising effects on nutrient metabolism. However, whether EGCG alone or combined with LTA can regulate the glucose, lipid, and protein metabolism of healthy rats remains unclear. Therefore, we treated healthy rats with EGCG or the combination of EGCG and LTA (EGCG+LTA) to investigate the effects of EGCG on nutrient metabolism and the role of LTA in the metabolism-regulatory effects of EGCG. The results showed that compared with the control group, EGCG activated insulin and AMP-activated protein kinase (AMPK) signals, thus regulating glucose, lipid, and protein metabolism. Compared with EGCG, EGCG+LTA enhanced hepatic and muscle glycogen levels and suppressed phosphorylation of AMPK, glycogen synthase 2, mammalian target of rapamycin, and ribosomal protein S6 kinase. In addition, EGCG+LTA inhibited the expression of liver kinase B1, insulin receptor and insulin receptor substrate, and promoted the phosphorylation level of acetyl-CoA carboxylase. Furthermore, both EGCG and EGCG+LTA were harmless for young rats. In conclusion, EGCG activated AMPK and insulin pathways, thereby promoting glycolysis, glycogen, and protein synthesis and inhibiting fatty acid (FA) and cholesterol synthesis. However, LTA cooperated with EGCG to promote glycogen metabolism and suppressed the effect EGCG on FA and protein synthesis via AMPK signals.

Redox and inflammation imbalances are associated with increased levels of advanced glycation end products (AGEs), leading to the degeneration of body function. l-Theanine, derived from tea, reportedly inhibits AGE formation in vitro. We investigated the effects on AGE content, oxidative stress, and inflammatory factors in d-galactose-induced aging rats for prevention and treatment of age-related liver dysfunction. l-Theanine increased activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, thus enhancing total antioxidant capacity, and decreasing malondialdehyde and nitric oxide synthase levels in serum and liver. Levels of the pro-inflammatory factors, interleukin (IL)-1β, tumour necrosis factor-alpha, and IL-6 were decreased in serum and liver, whereas those of anti-inflammatory factors, IL-4 and IL-10, were increased in the serum. Further, l-theanine inhibited AGE production and decreased the levels of the liver function markers, alanine aminotransaminase and aspartate aminotransferase. It also significantly increased the mRNA expression levels of FoxO1 and downregulated NF-κB(p65) but suppressed the phosphorylation of both FOXO1 and NF-κB (p65). Moreover, l-theanine effectively attenuated d-galactose-induced oedema and vacuole formation, thus protecting the liver. Overall, l-theanine reversed the d-galactose-induced imbalance in oxidative stress and inflammatory responses, reduced AGEs content in aging rats, maintained homeostasis in the body, and ameliorated liver aging., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2019. Published by Elsevier Inc.)

l-Theanine is an important component found in tea and has positive effects on nutrient absorption and transport. However, whether l-theanine can regulate glucose, lipid, and protein metabolism remains unknown. This study aims to investigate the effects of l-theanine on glucose, lipid, and protein metabolism in male Sprague-Dawley rats and characterize the underlying mechanisms. Compared to the control group, l-theanine increased the contents of hepatic and muscle glycogen, serum total protein (TP), and albumin (Alb), lowered the serum low-density lipoprotein cholesterol (LDL-C) level, decreased the activity of acetyl-CoA carboxylase (ACC), and enhanced carnitine palmitoyl transferase-1 (CPT-1) activity in the liver. Additionally, l-theanine upregulated the mRNA expression of phosphofructokinase (PFKL), CPT-1, insulin receptor (INSR), insulin receptor substrate (IRS), and liver kinase B1 (LKB1) and downregulated the mRNA expression of phosphoenolpyruvate carboxykinase 1 (PCK1), glucose-6-phosphatase catalytic subunit (G6PC), fatty acid synthase (FAS), and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR). Moreover, l-theanine upregulated the expression of PFKL, glycogen synthase 2 (GYS2), ribosomal protein S6 (S6), INSR, IRS, and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) proteins; downregulated the expression of FAS, sterol regulatory element binding protein-1c (SREBP-1c), and HMGCR proteins; enhanced the phosphorylation of the mammal target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), protein kinase B (AKT), and AMP-activated protein kinase (AMPK); and decreased the phosphorylation of glycogen synthase kinase 3β (GSK-3β) and ACC1. Furthermore, 100 mg kg-1l-theanine was more effective at eliciting these effects than 200 and 400 mg kg-1l-theanine. In conclusion, l-theanine can regulate glucose, lipid, and protein metabolism via insulin and AMPK and their downstream signaling pathways.