Delphine Curti

Effect of roasting on degradation and structural features of polysaccharides in Arabica coffee beans

The degree and nature of polysaccharide degradation at different roasting levels was determined for three Arabica (Coffea arabica) bean varieties. Between 12 and 40% of the bean polysaccharides were degraded depending on the roasting conditions. The thermal stability of the arabinogalactans, (galacto)mannans and cellulose was markedly different. The arabinogalactans and mannans were degraded up to 60 and 36%, respectively, after a dark roast, while cellulose showed negligible evidence of degradation. Roasting led to increased solubility of both the arabinogalactans and (galacto)mannans from the bean but the structural modifications, which accompanied this change in solubility, were different for each polysaccharide. Despite the moderate degradation of the (galacto)mannans, those remaining in the bean after roasting showed no evidence of change to their molecular weight even after a dark roast. In contrast, arabinogalactans were depolymerised after a light roast both by fission of the galactan backbone and loss of arabinose from the sidechains. The recently discovered covalent link between the coffee bean arabinogalactans and protein survived roasting. The glucuronic acid component of the AG was degraded markedly after a dark roast, but approximately 30% of the original content remained as part of the AG polymer. The results show that polysaccharide degradation during roasting is more marked than previously documented, and points to roasting induced changes to the polysaccharides as major factors in the changing physicochemical profile of the coffee bean during processing.

Coffee bean arabinogalactans: acidic polymers covalently linked to protein.

The arabinogalactan content of green coffee beans (Coffea arabica var. Yellow Caturra) was released by a combination of chemical extraction and enzymatic hydrolysis of the mannan-cellulose component of the wall. Several arabinogalactan fractions were isolated, purified by gel-permeation and ion-exchange chromatography and characterised by compositional and linkage analysis. The AG fractions contained between 6 and 8% glucuronic acid, and gave a positive test for the beta-glucosyl-Yariv reagent, a stain specific for arabinogalactan-proteins. The protein component accounted for between 0.5 and 2.0% of the AGPs and contained between 7 and 12% hydroxyproline. The AG moieties displayed considerable heterogeneity with regard to their degree of arabinosylation and the extent and composition of their side-chains. They possessed a MW average of 650 kDa which ranged between 150 and 2000 kDa. An investigation of the structural features of the major AG fraction, released following enzymatic hydrolysis of the mannan-cellulose polymers, allowed a partial structure of coffee arabinogalactan to be proposed.

Dietary fibre in cocoa shell: characterisation of component polysaccharides

Abstract Polysaccharides were isolated from cocoa shells and characterised by compositional and linkage analysis. The polysaccharide types were diverse and included pectic polysaccharides (∼45%) which were made up of a heterogeneous mixture of rhamnogalacturonans with variable degrees of branching. Hemicelluloses (∼20%) consisted of a mixture of a fucosylated xyloglucan, galactoglucomannans, and glucuronoarabinoxylan. Cellulose accounted for ∼35% of the cell wall polysaccharides. The total dietary fibre content was approximately 40%, not as high as previous reports. This was attributed to the fact that previous studies have included a “Klason Lignin” fraction in estimates of fibre. A solid state NMR study of the cocoa shell “Klason Lignin” fraction provided evidence that it contained little if any lignin and presumably consisted principally of protein–Maillard–tannin complexes.

Cocoa bean carbohydrates: roasting-induced changes and polymer interactions

Abstract Roasting induced change to carbohydrates and cell wall polysaccharides was investigated in three varieties of cocoa beans. The concentrations of glucose and fructose decreased after roasting but levels of the non-reducing sugars, sucrose, raffinose, stachyose and verbascose, were not markedly affected. Approximately 10% of the arabinose content of the polysaccharides was degraded but, overall, the pectic and hemicellulosic polymers remained intact after roasting. The degree of esterification and acetylation of the pectic polysaccharides were unaffected by roasting. Roasting did promote an interaction between polysaccharides, proteins, polyphenolics and Maillard products. This led to the formation of insoluble complexes which co-purified with, and augmented, the levels of cell wall material isolated from roasted compared to unroasted beans. The implications of the results are discussed in relation to the role that “Klason lignin” plays in the formation of these chemical amalgams during roasting.

Physicochemical properties and starch digestibility of whole grain sorghums, millet, quinoa and amaranth flours, as affected by starch and non-starch constituents

Minor grains such as sorghum, millet, quinoa and amaranth can be alternatives to wheat and corn as ingredients for whole grain and gluten-free products. In this study, influences of starch structures and other grain constituents on physicochemical properties and starch digestibility of whole flours made from these grains were investigated. Starches were classified into two groups according to their amylopectin branch chain-length: (i) quinoa, amaranth, wheat (shorter chains); and (ii) sorghum, millet, corn (longer chains). Such amylopectin features and amylose content contributed to the differences in thermal and pasting properties as well as starch digestibility of the flours. Non-starch constituents had additional impacts; proteins delayed starch gelatinization and pasting, especially in sorghum flours, and high levels of soluble fibre retarded starch retrogradation in wheat, quinoa and amaranth flours. Enzymatic hydrolysis of starch was restricted by the presence of associated protein matrix and enzyme inhibitors, but accelerated by endogenous amylolytic enzymes.