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⁻¹ L-theanine was more effective at eliciting these effects than 200 and 400 mg kg⁻¹ L-theanine. In conclusion, L-theanine can regulate glucose, lipid, and protein metabolism via insulin and AMPK and their downstream signaling pathways.

The maintenance of homeostasis is essential for mitigating stress and delaying degenerative diseases such as Alzheimer’s disease (AD). AD is generally defined as the abnormal production of β‐amyloid (Aβ) and advanced glycation end products (AGEs). The effects of l‐theanine on Aβ and AGE generation were investigated in this study. Decreased AGEs and Aβ_1-42 levels were reflected by increased acetylcholine (ACh) concentration and acetylcholinesterase (AChE) activity inhibition compared to model rats. l‐Theanine also inhibited nuclear factor‐κB (p65) protein expression by activating sirtuin1 (SIRT1), reducing inflammatory factor expression, and downregulating the mRNA and protein expression of AGE receptors (RAGE). Superoxide dismutase 2 and catalase protein expressions were markedly upregulated by l‐theanine, whereas oxidative stress‐related injury was alleviated. The expression of peroxisome proliferator‐activated receptor‐γ coactivator 1α (PGC‐1α) was also found to be increased. H&E staining showed that the apoptosis of hippocampal neurons was mitigated by decreased Bax and cleaved‐caspase‐3 protein expression and the increase of Bcl‐2 protein expression. Moreover, l‐theanine increased the gene and protein expression of brain‐derived neurotrophic factor (BDNF). These findings suggest that the potential preventive effects of l‐theanine against AD may be attributed to its regulation of SIRT1 and BDNF proteins and its mitigation of AGEs/RAGE signaling pathways in the brain tissue of AD model rats.

Objective. This study is aimed at teasing out the correlation of plasma D‐dimer (D‐D) levels to age, metastasis, TNM stage (tumor‐node‐metastasis classification), and treatment in non‐small‐cell lung cancer (NSCLC) patients of different ages, to facilitate early diagnosis of hypercoagulable state, choose appropriate treatment, and use appropriate anticoagulants. Hence, thrombosis and complications caused by excessive anticoagulants can be prevented; thrombus or disseminated intravascular coagulation (DIC) and other complications in elderly patients with NSCLC can be reduced or avoided. By monitoring the level of plasma D‐D in patients with NSCLC, recurrence and metastasis can be predicted in the early stage and the TNM stage can be evaluated. Methods. A total of 670 patients with NSCLC were selected in Shanxi Bethune Hospital from March 2014 to October 2020 as the experimental group, and 950 healthy people were selected from the physical examination center of the same hospital as the control group. The data of patients with NSCLC diagnosed for the first time without any treatment were collected and grouped based on metastasis, TNM stage, treatment, and pathological type, and the correlation with plasma D‐D level was analyzed. Plasma D‐D levels were measured by immunoturbidimetry on an ACL TOP 700 Automatic Coagulation Analyzer. The patients were further divided into two groups according to different treatment methods, and the differences in plasma D‐D levels between patients receiving chemotherapy and those receiving targeted therapy in different treatment cycles were analyzed. The correlation between D‐D levels and age in healthy controls was analyzed. The difference in D‐D levels between NSCLC patients and healthy controls of the same age was analyzed. Results. All data of both the experimental group and the control group were normally distributed. The average age of the experimental group was 61.31 ± 6.23 (range: 36‐92) years. The average age of the control group was 61.14 ± 11.12 (range: 35‐85) years. There was no significant difference in gender between the experimental group and the control group (p > 0.05). The plasma D‐D level of NSCLC patients was significantly higher than that of the healthy controls (p < 0.05). No significant difference in plasma D‐D level was found between NSCLC patients of different genders, and the finding was similar between healthy controls of different genders (p > 0.05). Significant difference in the D‐D level was found between the groups of 30‐59 years and 60‐69 years (p < 0.05), between groups of 60‐69 years and 70‐79 years (p < 0.05), and between 70‐79 years and ≥80 years (p < 0.05). The plasma D‐D level of patients ≤ 79 years old increased with age, but it decreased in those over 80 years old. According to Pearson correlation analysis, there was a positive correlation between the D‐D level and the age of NSCLC patients under 79 years old (p < 0.05). The differences in D‐D levels between the four age groups were statistically significant (p < 0.05), showing an upward trend of the D‐D level in healthy controls with the increase of age. There were statistically significant differences in D‐D levels between NSCLC patients and healthy controls of the matching age group (p < 0.05), suggesting that NSCLC patients had significantly higher D‐D levels than healthy people of the same age group. The differences in D‐D levels between NSCLC patients without metastasis, NSCLC patients with metastasis, and healthy people were statistically significant (p < 0.05). The patients with metastasis had the highest D‐D level, and healthy people had the lowest D‐D level. The difference in plasma D‐D levels between patients of different TNM stages was statistically significant (p < 0.05). Patients with an advanced TNM stage tended to have higher D‐D levels. The TNM stage and D‐D level of NSCLC patients changed significantly before and after treatment. An earlier stage was related to a more obvious change in D‐D levels after treatment with a statistically significant difference (p < 0.05). A more advanced stage was associated with a smaller change in the D‐D level after treatment, with no statistically significant difference (p > 0.05). The plasma D‐D levels before and after four cycles of chemotherapy or targeted therapy were higher than those of the healthy control group, and the differences were statistically significant (p < 0.05). The D‐D level of patients after chemotherapy was significantly lower than that before chemotherapy (p < 0.05), but there was no significant difference before and after targeted therapy (p > 0.05). The D‐D level after the first cycle of chemotherapy was higher than that before chemotherapy. The level of D‐D after the third and fourth cycles was significantly lower than that before chemotherapy (p < 0.05). No significant difference was found between the D‐D level before treatment and that after four cycles of chemotherapy (p > 0.05). Conclusion. It is suggested that coagulation test indexes should be included to evaluate the treatment regimen for NSCLC patients. Most patients with NSCLC are in a hypercoagulable state, which is related to age, tumor invasion and metastasis, recurrence, and treatment. Regular monitoring of plasma D‐D levels can facilitate early diagnosis of a hypercoagulable state and timely and appropriate use of anticoagulants, to avoid or reduce complications such as venous thromboembolism in NSCLC patients and to prevent the risk of bleeding caused by excessive anticoagulants. Clinicians can choose the treatment with less harm and maximum benefit for NSCLC patients based on the plasma D‐D level. When in a hypercoagulable state, the body’s blood viscosity increases, making it more conducive to the growth and infiltration of tumor cells. Our study shows that the recurrence and metastasis of NSCLC are related to coagulation indexes, which provides a theoretical basis for the early diagnosis and treatment of recurrent and metastatic NSCLC.

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.