Effects and Mechanisms of Tea for the Prevention and Management of Diabetes Mellitus and Diabetic Complications: An Updated Review

Abstract

Diabetes mellitus has become a serious and growing public health concern. It has high morbidity and mortality because of its complications, such as diabetic nephropathy, diabetic cardiovascular complication, diabetic neuropathy, diabetic retinopathy, and diabetic hepatopathy. Epidemiological studies revealed that the consumption of tea was inversely associated with the risk of diabetes mellitus and its complications. Experimental studies demonstrated that tea had protective effects against diabetes mellitus and its complications via several possible mechanisms, including enhancing insulin action, ameliorating insulin resistance, activating insulin signaling pathway, protecting islet β-cells, scavenging free radicals, and decreasing inflammation. Moreover, clinical trials also confirmed that tea intervention is effective in patients with diabetes mellitus and its complications. Therefore, in order to highlight the importance of tea in the prevention and management of diabetes mellitus and its complications, this article summarizes and discusses the effects of tea against diabetes mellitus and its complications based on the findings from epidemiological, experimental, and clinical studies, with the special attention paid to the mechanisms of action.

Keywords: complication; diabetes mellitus; epigallocatechin-3-gallate; mechanisms; polyphenol; tea.

Figure 1

Chemical structures of main catechins in tea.

Figure 2

The molecular mechanisms of EGCG against diabetes mellitus and its complications. EGCG has shown effects against T2DM by improving IR, against diabetic cardiovascular disease by decreasing TG and [Ga²⁺], against diabetic nephropathy by decreasing ROS and against diabetic neuropathy by increasing Nrf2. The arrow means the direction of actions, and the black full lines indicate upregulation and red dotted lines refer to downregulation or inhibition. CRP, C-reactive protein; MAPK p38-NIK, NF-κB inducing kinase; LKB1, kelch-like ECH-associated protein-1; EEF2K, eukaryotic elongation factor-2 kinase; ARE, antioxidant-responsive element; GSK-3β, glycogen synthase kinase-3β; IR, insulin resistance; MnSOD, Mn superoxide dismutase; NA, noradrenalin; s6k1, ribosomal protein S6 kinase 1; AC, adenylate cyclase; HSL, hormone-sensitive lipase; TG, triglyceride; FA, fatty acid; GL, glycerinum; GSH, glutathione; GSSH, oxidized glutathione; mTOR, the target of rapamycin; EGCG, epigallocatechin gallate; IKK, IκB kinase; NF-κB, nuclear factor-κB; iNOS, inducible nitric oxide synthase; TNF-α, tumor necrosis factor-α; Nrf2, nuclear factor-erythrocyte-associated factor 2; PI3K, phosphatidylinositol 3-hydroxykinase; Akt, protein kinase B; AMPK, adenylic acid-activated protein kinase; T2DM, type 2 diabetes mellitus; GLUT, glucose transporter type; PKA, protein kinase A; ATP, adenosine triphosphate; cAMP, cyclic Adenosine monophosphate; COMT, catechol-O-methyltransferase, an enzyme responsible for the degradation of noradrenalin.

Figure 3

The association between tea and diabetes and its complications. Tea has effects on type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) by protecting pancreatic β-cells and ameliorating insulin resistance. Besides, due to the anti-inflammatory and antioxidant properties of tea, diabetic complications, including diabetic cardiovascular complication, diabetic nephropathy, diabetic neuropathy, and diabetic hepatic tissue injury, could be prevented and treated by tea and its bioactive components.