الكاتب: Multiple References

with the consequent induction of enzymes involved in fatty acid synthesis, and that any difference between the metabolism of fructose and glucose is comparatively unimportant as a factor determining the hyperlipidaemic effect of sucrose. To conclude, I will return to the species with which I began. The few sucrose or fructose tolerance tests that have been conducted on human volunteers (Butterfield, Sargeant & Whichelow, 1964; Swann, Davidson & Albrink, 1966) have shown that neither of these sugars, given by mouth, produced as great a rise in blood reducing sugars as did glucose or ‘liquid glucose’ (partially hydrolysed starch) ; the increase in hexose sugars in the bIood after fructose administration was less than half that found with glucose or ‘liquid glucose’, and approximately half of this increase was due to fructose. Furthermore, a significant rise in blood pyruvate was observed with both sucrose and fructose, which may be taken as an indication of augmented throughput of sugars in the Embden-Meyerhof pathway in the liver. It appears, therefore, that in man, as in the rat, a substantial part of ingested sucrose does not reach the systemic blood as monosaccharides but is diverted by the liver, presumably for fat synthesis, and that the hyperlipidaemia encountered in human volunteers consuming sucrose-rich diets may also be explained on this basis.