Food & Function Blog

New insights into the effect of green tea on the molecular mechanisms of glucose metabolism have recently been reported by Hitoshi Ashida and colleagues.

Tea is one of the world’s most popular beverages and due to its content of polyphenols, particularly catechins, it is considered to possess health promoting effects.  Hitoshi Ashida and his team in Japan have previously showed that catechins in tea decrease glucose uptake in adipose tissue.

In adipose tissue, a membrane protein, GLUT4 is responsible for glucose uptake from the bloodstream.  In the absence of insulin 95% of GLUT4 is located in the cell, but on insulin binding, GLUT4 is translocated to the surface and is able to transport glucose inside.

This current study  published in Food & Function showed that gallate-type catechins reduce insulin-induced glucose uptake by reducing the translocation of GLUT4 to the outside of the cell.  In contrast, the team discovered that in the absence of insulin, when GLUT4 is usually contained intracellularly, a different group of catechins, nongallate-type, increased glucose uptake by increasing the translocation of GLUT4 to the outside of the cell.  An analysis of the signalling pathways involved showed that the gallate-type catechins inhibited the insulin-signalling pathway, but that the nongallate-type catechins were able to increase translocation of GLUT4 without utilising this pathway.

The team from Kobe University and the Central Research Institute have demonstrated that green tea catechins modulate glucose transport in adipose tissue, affecting blood glucose levels.  In a world where the incidence of hypoglycaemia is increasing year by year, insights such as these are invaluable in identifying possible compounds which have the potential to regulate blood glucose levels.

Anna Simpson

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Bacteria in the lower gut are responsible for breaking down of the major cancer fighting chemical in broccoli to release its bioactive form, claim Elizabeth Jeffery and colleagues at the University of Illinois.

Cruciferous vegetables such as broccoli have been shown to reduce cancer risks. Of all the components present in crucifers such as antioxidants and flavonoids, it is believed that a molecule called glucoraphanin (GRP) plays a major role explaining their anticancer properties.  GRP is actually a precursor to the bioactive isothocyanate sulforaphane (SF).  It is hydrolysed to SF by an endogenous enzyme in broccoli called myrosinase.  Upon chewing, the myrosinase gains access to the GRP and catalyses hydrolysis within the gastrointestinal tract, however, in cooked broccoli myrosinase is inactivated yet low levels of SF metabolites appear in urine following ingestion, suggesting hydrolysis has, somehow, occurred.

Evidence exists that gut bacteria are responsible for GRP hydrolysis but this study is the first to report direct evidence of hydrolysis of a GRP to SF in the lower gut. Jeffery and colleagues investigated, in rats, the hydrolysis by gut bacteria and absorption across the cecum (lower intestine) of GRP from broccoli.  Simulated digestion in vitro confirmed that GRP is not destroyed by digestive enzymes therefore reaches the cecum intact.  Introduction of GRP directly to the cecum resulted in the appearance of SF and SF metabolites in the blood travelling away from the abdomen after 2 hours; in contrast, direct introduction of SF resulted in detection of SF and SF metabolites after only 15 minutes. 

These results show for the first time that SF can be absorbed by the cecum, they also indicate that GRP is broken down to SF in the cecum and then absorbed into the bloodstream.  Finally, an ex vivo study showed that GRP was hydrolysed by the rat’s gut bacteria, however, the hydrolysis product was not SF; reasons for the difference in GRP breakdown in and ex vivo are discussed.

Interested in knowing more? Read the full article here:

Glucoraphanin hydrolysis by microbiota in the rat cecum results in sulforaphane absorption
Ren-Hau Lai, Michael Miller and Elizabeth Jeffery
Food Funct., 2010, DOI:10.1039/C0FO00110D