Academic literature on the topic 'Caffeine metabolism rate'

Abstract The metabolism of [8-14C ]adenine and [2-14C]caffeine was examined in leaf segments from flush shoots of tea cultivars with high and low caffeine content. The caffeine biosynthesis pathway from AMP via theobromine was operative in both high and low caffeine containing cultivars. There was a m ore rapid rate of caffeine biosynthesis from [8-14C ]adenine in the high caffeine cultivars while the rate of degradation of both adenine nucleotides and caffeine into CO2 was greatest in cultivars with a low endogenous caffeine content. Cell-free p reparations from tea shoots contained an N-methyltransferase, that is a keyenzyme in the caffeine biosynthesis pathway; more in-vitro activity was detected in preparations from high caffeine containing cultivars. The data obtained suggest that the high caffeine containing cultivars have a more rapid rate of caffeine biosynthesis and a slower rate of caffeine catabolism than cultivars with a low endogenous caffeine content

Purpose This work investigated if treatment with caffeine or 2,4-dinitrophenol (DNP) induce expression of peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1α) and increase both mitochondrial biosynthesis and metabolism in skeletal muscle. Methods Human rhabdomyosarcoma cells were treated with either ethanol control (0.1% final concentration) caffeine, or DNP at 250 or 500 μM for 16 or 24 hours. PGC-1α RNA levels were determined using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). PGC-1α protein and mitochondrial content was determined using flow cytometry and immunohistochemistry. Metabolism was determined by quantification of extracellular acidification rate and oxygen consumption rate. Results Treatment with either caffeine or DNP induced PGC-1α RNA and protein as well as mitochondrial content compared with control. Treatment with caffeine and DNP also significantly increased oxidative metabolism and total metabolic rate compared with control. Caffeine similarly increased metabolism and mitochondrial content compared with DNP. Conclusion This work identified that both caffeine and DNP significantly induce PGC-1α, and increase both metabolism and mitochondrial content in skeletal muscle.

The magnitude of coffee-induced thermogenesis and the influence of coffee ingestion on substrate oxidation were investigated in 10 lean and 10 obese women, over two 24-h periods in a respiratory chamber. On one occasion the subjects consumed caffeinated coffee and on the other occasion, decaffeinated coffee. The magnitude of thermogenesis was smaller in obese (4.9 +/- 2.0%) than in lean subjects (7.6 +/- 1.3%). The thermogeneic response to caffeine was prolonged during the night in lean women only. The coffee-induced stimulation of energy expenditure was mediated by a concomitant increase in lipid and carbohydrate oxidation. During the next day, in postabsorptive basal conditions, the thermogenic effect of coffee had vanished, but a significant increase in lipid oxidation was observed in both groups. The magnitude of this effect was, however, blunted in obese women (lipid oxidation increased by 29 and 10% in lean and obese women, respectively). Caffeine increased urinary epinephrine excretion. Whereas urinary caffeine excretion was similar in both groups, obese women excreted more theobromine, theophylline, and paraxanthine than lean women. Despite the high levels of urinary methylxanthine excretion, thermogenesis and lipid oxidation were less stimulated in obese than in lean subjects.

Examination of urine excretion of caffeine metabolites has been a simple but common way to determine the metabolism and effect of caffeine, but the relationship between urinary metabolites and urine flow rate is less discussed. To explore the association between urinary caffeine metabolite levels and urine flow rate, 1571 participants from the National Health and Nutrition Examination Survey (NHANES) 2011–2012 were enrolled in this study. We examined the association between urinary caffeine metabolites and urine flow rate with linear regression models. Separate models were constructed for males and females and for participants aged <60 and ≥60 years old. A positive association was found between concentrations of several urinary caffeine metabolites and urine flow rate. Three main metabolites, namely, paraxanthine, theobromine, and caffeine, showed significance across all subgroups. The number of caffeine metabolites that revealed flow-dependency was greater in males than in females and was also greater in the young than in the elderly. Nevertheless, the general weakness of NHANES data, a cross-sectional study, is that the collection is made at one single time point rather than a long-term study. In summary, urinary concentrations of several caffeine metabolites showed a positive relationship with the urine flow rate. The trend is more noticeable in males and in young subgroups.

Triple-negative tumor cells, a malignant subtype of breast cancer, lack a biologically targeted therapy. Given its DNA repair inhibiting properties, caffeine has been shown to enhance the effectiveness of specific tumor chemotherapies. In this work, we have investigated the effects of caffeine, cisplatin, and a combination of the two as potential treatments in energy metabolism for three cell lines, triple-negative breast cancer (MDA-MB-231), estrogen-receptor lacking breast cancer (MCF7) and breast epithelial cells (MCF10A) using a sensitive label-free approach, phasor-fluorescence lifetime imaging microscopy (phasor-FLIM). We found that solely using caffeine to treat MDA-MB-231 shifts their metabolism towards respiratory-chain phosphorylation with a lower ratio of free to bound NADH, and a similar trend is seen in MCF7. However, MDA-MB-231 cells shifted to a higher ratio of free to bound NADH when cisplatin was added. The combination of cisplatin and caffeine together reduced the survival rate for MDA-MD231 and shifted their energy metabolism to a higher fraction of bound NADH indicative of oxidative phosphorylation. The FLIM and viability results of MCF10A cells demonstrate that the treatments targeted cancer cells over the normal breast tissue. The identification of energy metabolism alteration could open up strategies of improving chemotherapy for malignant breast cancer.

Adenosine receptors mainly control synaptic function, and excessive activation of adenosine receptors may worsen the onset of many neurological disorders. Accordingly, the regular intake of moderate doses of caffeine antagonizes adenosine receptors and affords robust neuroprotection. Although caffeine intake alters brain functional connectivity and multi-omics analyses indicate that caffeine intake modifies synaptic and metabolic processes, it is unclear how caffeine intake affects behavior, synaptic plasticity and its modulation by adenosine. We now report that male mice drinking caffeinated water (0.3 g/L) for 2 weeks were behaviorally indistinguishable (locomotion, mood, memory) from control mice (drinking water) and displayed superimposable synaptic plasticity (long-term potentiation) in different brain areas (hippocampus, prefrontal cortex, amygdala). Moreover, there was a general preservation of the efficiency of adenosine A1 and A2A receptors to control synaptic transmission and plasticity, although there was a tendency for lower levels of endogenous adenosine ensuring A1 receptor-mediated inhibition. In spite of similar behavioral and neurophysiological function, caffeine intake increased the energy charge and redox state of cortical synaptosomes. This increased metabolic competence likely involved a putative increase in the glycolytic rate in synapses and a prospective greater astrocyte–synapse lactate shuttling. It was concluded that caffeine intake does not trigger evident alterations of behavior or of synaptic plasticity but increases the metabolic competence of synapses, which might be related with the previously described better ability of animals consuming caffeine to cope with deleterious stimuli triggering brain dysfunction.

The instinctive rejection of bitter taste has been crucial to the survival of our species and continues to influence food choices. In fact, the bitter taste receptors have evolved to protect the body from the ingestion of foods potentially harmful to health. However, some foods are widely consumed despite their high intensity of bitterness, for example coffee, one of the world’s most popular beverages. Coffee is drunk for its pleasant flavour and aroma as well as for the stimulatory properties arising from its caffeine content. Such properties, as well as the addition of sugar and/or milk, are most likely responsible for our learned preferences for coffee. The aim of this work was to study the relationship between the preference patterns for coffee and the perception of its bitterness. For this purpose, factors relating to both the product – degree of roasting - and the individual - bitterness perception and caffeine metabolism rate - were studied. First, the effect of the roasting temperature on coffee sensory profile and preference was investigated, initially by describing the sensory properties of coffee brews prepared with both under-roasted (140-165°C) and standard roasted (220°C) beans. In addition, seventy-five coffee consumers rated their liking for unsweetened and freely sweetened under-roasted coffee samples. Increasing the bean processing temperature positively affected both the perceived intensity of some sensory attributes specific to coffee and also consumers’ liking. In particular, coffee processed at temperature higher than 150°C were described by the terms “coffee”, “roasted”, “burnt”. Furthermore, no significant differences in the intensity of these attributes were found between samples processed at temperatures higher than 155°C and samples roasted at the standard temperature. In general, samples processed at temperatures higher than 150°C were preferred. However, a subgroup of subjects who liked the samples roasted at lower temperatures was found. These subjects were on average less neophobic than the others, that is, more inclined to consume unfamiliar/unconventional foods. Later, the effects of bitterness sensitivity and caffeine metabolism rate on perception of, and liking for coffee were examined. One hundred and thirty-five regular coffee consumers participated in the study. Subjects were characterised in terms of bitterness sensitivity (fungiform papillae – FP - number and sensitivity to the bitter compound 6-n-propylthiouracil –PROP-); caffeine metabolism rate (slow and fast metabolizers); attitudes and food behaviour (frequency – number of coffees per day- and modality - black, with sugar, with milk- of coffee consumption; preference for and familiarity with bitter foods; self perceived effect of caffeine intake). Caffeine metabolism was investigated by competitive immuno-enzymatic assay. Subjects provided saliva samples after 12 hours of caffeine abstinence (T0) and at 30 and 90 minutes after ingestion of caffeine (100 mg). The individual caffeine metabolism rate in 90 minutes was expressed as a caffeine metabolism index (CmI), computed as the ratio between the amount of residual caffeine in saliva 60 minutes after the adsorption peak and the amount of caffeine at the adsorption peak corrected with the baseline. Subjects rated their liking for six unsweetened and freely sweetened coffee samples selected on the base of their roasting degree, caffeine content and bitterness. The immersive test technique was applied to evaluate the effect of the context on coffee liking. In particular, just before starting the test, subjects were asked to describe the most preferred situation for consuming coffee (time of the day, place, company, etc.) and to imagine that they were doing coffee tasting in that particular situation. In a separate session, subjects evaluated the sourness, bitterness and astringency in the coffee samples. Psychophysical curves were constructed for caffeine and quinine-HCl over 6 concentrations. No significant relationships were found between the FP number, the PROP taster status and the caffeine metabolism rate. Subgroups of subjects were identified based on these indices and differences in preference and sensory responses were explored independently in the subgroups. Both FP density and PROP taster status affected taste sensitivity for bitter compounds in general (caffeine; quinine-HCl) and the use of sugar in coffee. In particular, subjects with a higher FP number rated the bitterness of caffeine and quinine-HCl solutions and sourness of coffees stronger than subjects with a lower FP number. They also added more sugar to, and gave higher liking ratings for, the coffee samples. While coffee liking was unrelated to PROP taster status, PROP non-tasters added more sugar to the coffee samples than did PROP super-tasters. However, super-tasters rated sourness, bitterness and astringency as stronger than non-tasters, both in coffee samples and in standard solutions. Caffeine metabolism was related to bitterness perception both in coffee samples and in standard solutions of caffeine, but not of quinine-HCl. In particular, subjects with a lower caffeine metabolism index rated the bitterness of coffees and of caffeine solutions as stronger than subjects with a higher caffeine metabolism index. Moreover, they added more sugar in coffees and consumed less coffees daily. In general, the results demonstrate that even in high coffee consuming cultures such as Italy, there are clear sensory variations in the coffees that are consumed. Coffee consumption and preference, in terms of frequency and modality, are influenced both by the sensory properties of coffee and the psychological, physiological and metabolic characteristics of consumers. In the coffee production process, the roasting degree is a crucial step towards the development of the sensory properties affecting consumer preference. Furthermore, both the physiological indices – FP number and PROP taster status – and the caffeine metabolism rate play a significant role in taste sensitivity for bitter compounds in general and also in the preference for coffee with or without sugar.

碩士
國立臺灣師範大學
人類發展與家庭學系
101
According the statistics report of Department of Health in Taiwan, diabetes mellitus (DM) is the fifth among the top ten leading causes of death. Among them, 95% of diabetes patients are Type 2 DM, which is characterized by hyperinsulinemia resulted from insulin resistance. Taiwan is becoming to be an aging society and the life expectancy of people is increasing year by year. Thus, the dementia in elderly has been attached great importance to society country. Most dementia is Alzheimer’s disease (AD). The growing evidences indicate that high fat diet is the major risk factor of AD. Furthermore, the protective effect of phenolic acids on hypoglycermia and neuronal has been reported. The result from cell viability test revealed that the maxium safe dosage of phenolic acids is 12.5 μM on neuroblastoma Neuro 2a cells. The insulin resistant cell model was used as a platform for screening the anti-insulin resistance potential phenolic acids. Among the tested samples, caffeic acid exhibited the highest glucose uptake enhancing activity in insulin resistant cells. Then effect of caffeic acid on ameliorating carbohydrate metabolism, insulin resistance and memory impairment and learning ability in high fat diet (HFD)-induced hyperinsulinemic rats were investigated. The results show that orally administered with caffeic acid once a day at a dosage of 30mg/kg B.W. for 30 weeks significantly improved the glucose tolerance and abdominal fat in high-fat diet (HFD) fed male SD rats. The Western blot analysis reveals that caffeic acid increases the expression of glycolysis-associated enzymes, including hexokinase, phosphofructokinase and aldolase in hippocampus and cortex of HFD rats. Moreover, caffeic acid increases the protein expression of insulin signaling-associated proteins, including insulin receptor (IR), phosphatidylinositol-3-kinase (PI3K), AKT/Protein kinase B (AKT/ PKB), glucose transporter-3 (GLUT-3) and insulin degrading enzyme (IDE) in hippocampus and cortex of HFD rats. Additionally, caffeic acid increases the protein expression of leptin signaling-associated proteins, including leptin receptor (LEPR), pJAK2Tyr813/JAK2. The results from passive avoidance test also revealed that caffeic acid significantly improved the memory impairment in HFD rats. Above investigation elucidates that caffeic acid may alleviate brain insulin resistance and improve glucose metabolism thus ameliorate memory impairment and lraening ability in HFD rats.