Other possible mechanism of black tea against obesity

Other possible mechanism of black tea against obesity and dyslipidemia also has been proposed. Both TF2a and TF2b are found to reduce micellar solubility of cholesterol in vitro[86,87]. Moreover, TF3 is more effective in inhibiting pancreatic lipase activity than that of EGCG by reducing triacylglycerol lgk974 and consequently suppressing postprandial hypertriacylglycerolemia [88]. These actions contributed to the prevention of black tea polyphenols against diet-induced obesity in animals [81]. In addition to the effects of reducing postprandial lipids absorption, drinking black tea also reduced postprandial blood glucose levels and enhanced insulin response in healthy human subjects [89]. Solutions of black tea increased insulin activity in rat adipocytes [90]. One of the potential mechanisms includes theaflavins mimicked the effects of insulin and insulin-like growth factor-1 (IGF-1) by initiating phosphorylation of Forkhead transcription factor O1a (FOXO1a) and repressing phosphoenolpyruvate carboxykinase (PEPCK) promoter activity. FOXO1a and PEPCK are both important components of the insulin-signaling pathway [91]. The phosphorylation of FOXO1a may be mediated by AMPK [92,93], which is the key metabolic regulatory enzyme activated by black tea polyphenols.
Potential use of black tea in neurodegenerative disorders Parkinson\'s disease (PD) and Alzheimer\'s disease (AD) are age-dependent neurodegenerative disorders [94]. Parkinson\'s disease is characterized by accumulation of α-synuclein protein of Lewy bodies and loss of dopaminergic neurons [95]. Consumption of black tea was associated with the reduced risk of Parkinson\'s disease in an epidemiology study. It was concluded that ingredients of black tea other than caffeine were responsible for the beverage\'s inverse association with Parkinson\'s disease [96]. In 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD, oral administration of black tea extract before or after 6-OHDA treatment reduced dopaminergic neuron damage and improved motor and neurochemical deficits [97]. In another neurotoxin 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced PD animal model, oral treatment of TF1 was effective in reduction of oxidative stress-induced neurodegeneration and apoptosis by suppressing Bax down-regulation and increasing Bcl-2. It also effectively reduced inflammatory mediators (IL-1β, IL-6, TNF-α, IL-10) and ameliorated dopamine transporters’ reduction and behavioral deficits [98–100]. Black tea may also be beneficial in the treatment of AD. In AD, it is believed that the neurodegeneration is caused by the cleavage product of amyloid precursor protein (APP) and the aggregation of amyloid β peptide (Aβ) in brain. Black tea extract inhibited Aβ42 peptides-induced lipid membrane destabilization that may protect membrane damage [101] (Table 7). In primary culture of rat hippocampal cell, black tea extract displayed neuroprotective effect by the inhibition of Aβ-induced cytotoxicity [102]. Black tea polyphenols including theaflavins and EGCG inhibited formation of toxic amyloid-β (Aβ) and α-synuclein (αS) fibrils in vitro by stimulating the assembly of Aβ and αS into nontoxic spherical aggregates that are independent of their antioxidant effects [103]. TF3 was less susceptible to oxidation and had an increased efficacy under oxidizing conditions than EGCG [103]. EGCG was effective in reducing the β-amyloid mediated cognitive impairment in Alzheimer transgenic mice [104]. It would be interesting to find out if TF3 is more potent in same animal model. In addition to the direct effects on Aβ aggregation, both TF2a and TF3 were found to inhibit PAI-1 activity, which has been implicated in the accumulation of Aβ plague in brain [105,106]. Results from all these in vitro studies look promising and further in vivo and clinical studies are needed to confirm the efficacy of black tea polyphenols in the treatment of PD and AD.