Coffee drinking has been associated with benefits for various health outcomes, with many attributed to the most prevalent family of polyphenols within coffee, chlorogenic acids (CGA). Whilst reviews of the association between coffee and cognition exist, evidence exploring effects of coffee-specific CGA on cognition has yet to be systematically synthesised. The purpose was to systematically review the current literature investigating the relationship between CGA from coffee and cognitive performance. A further objective was to undertake a meta-analysis of relevant randomised controlled trials (RCT). Observational and intervention studies were included if they considered coffee-based CGA consumption in human participants and applied a standardised measure of cognition. Furthermore, intervention studies were required to define the CGA content and include a control group/placebo. Studies were excluded if they examined CGA alone as an extract or supplement. A search of Scopus, PubMed, Web of Science, ScienceDirect and PsycINFO resulted in including twenty-three papers, six of which were interventions. The evidence from the broader systematic review suggests that CGA from coffee may need to be consumed chronically over a sustained period to produce cognitive benefits. However, the meta-analysis of RCT showed no benefits of coffee CGA intake on cognitive function (d = 0.00, 95% CI −0.05, 0.05). Overall, this review included a limited number of studies, the sample sizes were small, and a wide range of cognitive measures have been utilised. This indicates that further, good-quality interventions and RCT are required to systematically explore the conditions under which coffee CGA may provide benefits for cognitive outcomes.

There is much epidemiological evidence suggesting a reduced risk of development of type 2 diabetes (T2D) in habitual coffee drinkers, however to date there have been few longer-term interventions, directly examining the effects of coffee intake on glucose and lipid metabolism. Previous studies may be confounded by inter-individual variation in caffeine metabolism. Specifically, the rs762551 SNP in the CYP1A2 gene has been demonstrated to influence caffeine metabolism, with carriers of the C allele considered to be of a ‘slow’ metaboliser phenotype. This study investigated the effects of regular coffee intake on markers of glucose and lipid metabolism in coffee-naïve individuals, with novel analysis by rs762551 genotype. Participants were randomised to either a coffee group (n 19) who consumed four cups/d instant coffee for 12 weeks or a control group (n 8) who remained coffee/caffeine free. Venous blood samples were taken pre- and post-intervention. Primary analysis revealed no significant differences between groups. Analysis of the coffee group by genotype revealed several differences. Before coffee intake, the AC genotype (‘slow’ caffeine metabolisers, n 9) displayed higher baseline glucose and NEFA than the AA genotype (‘fast’ caffeine metabolisers, n 10, P<0·05). Post-intervention, reduced postprandial glycaemia and reduced NEFA suppression were observed in the AC genotype, with the opposite result observed in the AA genotype (P<0·05). These observed differences between genotypes warrant further investigation and indicate there may be no one-size-fits-all recommendation with regard to coffee drinking and T2D risk.

This study was conducted to elucidate the effects of decaffeinated green coffee bean extract (GCE) on anthropometric indices, glycaemic control, blood pressure, lipid profile, insulin resistance and appetite in patients with the metabolic syndrome (Mets). Subjects were randomly allocated to consume 400 mg GCE or placebo capsules twice per d for 8 weeks. Both groups were advised to follow an energy balanced diet. After GCE supplementation, systolic blood pressure (SBP) significantly reduced compared with the placebo group (−13·76 (sd 8·48) v. −6·56 (sd 9·58) mmHg, P=0·01). Also, GCE treatment significantly reduced fasting blood glucose (FBS) (−5·15 (sd 60·22) v. 29·42 (sd 40·01) mg/dl (−0·28 (SD 3·34) v. 1·63 (SD 2·22) mmol/l); P=0·03) and homoeostatic model of assessment of insulin resistance in comparison to placebo (−1·41 (sd 3·33) v. 1·23 (sd 3·84), P=0·02). In addition, waist circumference (−2·40 (sd 2·54) v. −0·66 (sd 1·17) cm, P=0·009) and appetite score (−1·44 (sd 1·72) v. −0·2 (sd 1·32), P=0·01) of the individuals supplemented with GCE indicated a significant decline. Besides, weight and BMI reduction in the intervention group was almost twice as much as the placebo group; however, this discrepancy was marginally significant (weight: −2·08 (sd 2·11) v. −0·92 (sd 1·30) kg, P=0·05). No difference was observed in terms of glycated Hb (HbA1c) percentage and lipid profile parameters between the two groups. To sum up, GCE administration had an ameliorating effect on some of the Mets components such as high SBP, high FBS and Mets main aetiological factors including insulin resistance and abdominal obesity. Furthermore, GCE supplementation could reduce appetite level.

Obesity has become a public health concern due to its positive association with the incidence of many diseases, and coffee components including chlorogenic acid (CGA) and caffeine have been demonstrated to play roles in the suppression of fat accumulation. To investigate the mechanism by which CGA and caffeine regulate lipid metabolism, in the present study, forty mice were randomly assigned to four groups and fed diets containing no CGA or caffeine, CGA, caffeine, or CGA+caffeine for 24 weeks. Body weight, intraperitoneal adipose tissue (IPAT) weight, and serum biochemical parameters were measured, and the activities and mRNA and protein expression of lipid metabolism-related enzymes were analysed. There was a decrease in the body weight and IPAT weight of mice fed the CGA+caffeine diet. There was a significant decrease in the serum and hepatic concentrations of total cholesterol, TAG and leptin of mice fed the CGA+caffeine diet. The activities of carnitine acyltransferase (CAT) and acyl-CoA oxidase (ACO) were increased in mice fed the caffeine and CGA+caffeine diets, while the activity of fatty acid synthase (FAS) was suppressed in those fed the CGA+caffeine diet. The mRNA expression levels of AMP-activated protein kinase (AMPK), CAT and ACO were considerably up-regulated in mice fed the CGA+caffeine diet, while those of PPARγ2 were down-regulated. The protein expression levels of AMPK were increased and those of FAS were decreased in mice fed the CGA+caffeine diet. These results indicate that CGA+caffeine suppresses fat accumulation and body weight gain by regulating the activities and mRNA and protein expression levels of hepatic lipid metabolism-related enzymes and that these effects are stronger than those exerted by CGA and caffeine individually.

Postprandial energy metabolism, including postprandial hyperglycaemia, hyperinsulinaemia and hyperlipidaemia, is related to the risk for developing obesity and CVD. In the present study, we examined the effects of polyphenols purified from coffee (coffee polyphenols (CPP)) on postprandial carbohydrate and lipid metabolism, and whole-body substrate oxidation in C57BL/6J mice. In mice that co-ingested CPP with a lipid–carbohydrate (sucrose or starch)-mixed emulsion, the respiratory quotient determined by indirect calorimetry was significantly lower than that in control mice, whereas there was no difference in VO2 (energy expenditure), indicating that CPP modulates postprandial energy partitioning. CPP also suppressed postprandial increases in plasma glucose, insulin, glucose-dependent insulinotropic polypeptide and TAG levels. Inhibition experiments on digestive enzymes revealed that CPP inhibits maltase and sucrase, and, to a lesser extent, pancreatic lipase in a concentration-dependent manner. Among the nine kinds of polyphenols (caffeoyl quinic acids (CQA), di-CQA, feruloyl quinic acids (FQA)) contained in CPP, di-CQA showed more potent inhibitory activity than CQA or FQA on these digestive enzymes, suggesting a predominant role of di-CQA in the regulation of postprandial energy metabolism. These results suggest that CPP modulates whole-body substrate oxidation by suppressing postprandial hyperglycaemia and hyperinsulinaemia, and these effects are mediated by inhibiting digestive enzymes.

Evaluations of molecular mechanisms of dietary plants with their active molecules are essential for the complete exploration of their nutritive and therapeutic value. In the present study, we investigated the effect of chicory (Cichorium intybus) salad leaves in inhibiting protein tyrosine phosphatase 1B (PTP1B), and evaluated their role in modulating the key markers involved in insulin cell signalling and adipogenesis using 3T3-L1 adipocytes. Bioactivity-directed purification studies enlightened the additive effects of chlorogenic acid (CGA) along with other caffeic acid derivatives present in methanolic extract of C. intybus (CME). Incubation of CME and CGA with 3T3-L1 adipocytes significantly enhanced the 2-deoxy-d-3[H]-glucose uptake and inhibited adipogenesis through altering the expressions of insulin signalling and adipogenesis markers. Extending to an in vivo model, the effect of CME was also investigated on insulin sensitivity in high-fat diet with low streptozotocin-induced diabetic rats. Supplementation of CME for 2 weeks reinstated the insulin sensitivity along with plasma metabolic profile. The present results demonstrate that the caffeoyl derivatives of chicory salad leaves show promising pharmacological effect on energy homoeostasis via PTP1B inhibition both in vitro and in vivo.

The absorption and metabolism in the small intestine of chlorogenic acid (5-0-caffeoylquinic acid), the main phenolic acid in the human diet, and of caffeic acid were studied in rats in order to determine whether chlorogenic acid is directly absorbed or hydrolysed in the small intestine. Chlorogenic and caffeic acids were perfused into a segment of ileum plus jejunum during 45;min (50;μm, 0·75sp;ml/min) using an in situ intestinal perfusion rat model with cannulation of the biliary duct, and were quantified together with their metabolites in perfusion effluent, bile and plasma. The net absorption (influent flux minus effluent flux of phenolic acids and their metabolites) accounted for 19·5% and 8% of the perfused caffeic and chlorogenic acids, respectively. A minor fraction of the perfused caffeic acid was metabolized in the intestinal wall and secreted back into the gut lumen in the form of ferulic acid (0·5% of the perfused flux). Part of the chlorogenic acid (1·2% of the perfused flux) was recovered in the gut effluent as caffeic acid, showing the presence of trace esterase activity in the gut mucosa. No chlorogenic acid was detected in either plasma or bile, and only low amounts of phenolic acids (less than 0·4%) were secreted in the bile. The present results show that chlorogenic acid is absorbed and hydrolysed in the small intestine. In contrast to numerous flavonoids, absorbed phenolic acids are poorly excreted in the bile or gut lumen. Their bioavailability therefore appears to be governed largely by their uptake into the gut mucosa.

The developmental regulation and organ-specific expression of shikimate dehydrogenase was studied in seedlings of Capsicum annuum L. during their early development. The results obtained suggest that there is both a developmental regulation and an organ-specific expression of shikimate dehydrogenase in seedlings of C. annuum, seen mainly in the cotyledons. For example, shikimate dehydrogenase isoenzyme 3 was differentially expressed in cotyledons, but not at all in roots or hypocotyls. When the amounts of shikimate dehydrogenase were compared with the end-products of the shikimate pathway, chlorogenic acid and lignins, it was observed that the fall in shikimate dehydrogenase activity in cotyledons coincided with a decrease in the concentrations of phenolics during primary leaf development. However, this did not seem to be the case with the hypocotyls, where the fall in phenolics was not related to the amount of shikimate dehydrogenase but rather to an increase in lignin deposition, supporting the view that chlorogenic acid might act as a precursor of the aromatic moiety of cinnamoyl alcohols during cell wall lignification.