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The use of fructose in the dietary treatment of diabetes has a very long history [1], but it remains u n solved whether fructose has any place in the dietary treatment of insulin-dependent diabetics today. The saccharine and cyclamate ban in U.S.A. has provoked a renewed interest in the use of fructose as a sweetener for diabetics [2, 3], but still doubt and hesitation prevail. The dietary treatment of insulindependent diabetics is based on a daily supply of significant amounts of slowly absorbed carbohydrates (starch) in a meal pattern, which is repeated from day to day in order to diminish the tendency to hyperglycaemia and or hypoglycaemia between meals. The putative place of fructose in such a dietary scheme should be as a sweetener, i. e. as a substitute for sucrose, not for starch. Because fructose as a sweetener has to be taken in approximately the same amounts as sucrose one problem has been whether fructose causes a smaller rise in blood glucose concentration than sucrose. Such a beneficial effect of fructose has certainly been found [4]. So why do we not recommend fructose? Fructose is very rapidly metabolized in the liver to glucose and lactate in a way which is independent of insulin [5]. Even in the starved state fructose may turn the liver from a lactate clearing organ to a lactate producing organ. The proport ion of fructose which is converted to lactate in the liver is greatly increased by anoxia and a concomitant high glucose concentration (Table 1). Thus fructose metabolism may induce lactate acidosis when there is already insufficient hepatic clearance of peripherally produced lactate. Such an effect has been shown in humans after intravenous administration of fructose and several warnings against this fructose effect have been given in the past 10 years [7, 8, 9]. In fructose infusion studies the arterial concentration of fructose has been about 5 mmol/1 [10, 11, 12]. The effect of fructose on liver metabolism is linearly dependent on the fructose concentration in the low concentration range [13], because of a relatively low affinity for transport across the plasma membrane [14]. Therefore the fructose effects after peroral intake must be anticipated to be strongly dependent on the portal fructose concentration, which has not been measured in humans. However, the following calculation can illustrate what happens after a significant peroral intake of fructose in humans. If 60 g of fructose (330 mmol) are taken perorally within a short time (e. g. 10 min), absorption will be complete in about 1 0 0 m in. Because fructose in humans seems to be absorbed and delivered intact to the portal circulation [15] the average fructose concentration in the absorption period will be about 3.3 mmol/1, provided the portal flow is 1000 ml/min. If the liver weight is 1500 g the average rate of fructose conversion should be 2.2 ptmol/min per g liver, provided no fructose passes completely through the liver. The hepatic extraction of fructose is indeed high [11, 12] in that there are very low (0.2 mmol/1) peripheral fructose concentrations after peroral fructose intake [16]. Thus the average rate of fructose uptake in liver can be estimated to be about 1.75 ,umol/min per g liver. This relationship between concentration and splanchnic hepatic fructose uptake has been confirmed in fructose infusion experiments [11]. Further, it has been shown that 30 g fructose given perorally, increases the rate of ethanol oxidation by about 50% [17]. From this observation two conclusions can bc drawn: first, that the major part of fructose given perorally m u s t be metabolized in the same organ as ethanol, namely in the liver, and second, that the rate of fructose conversion to glucose and lactate must be about 1.7 btmol/min/g liver since in human fructose infusion experiments and pig liver perfusion experiments this rate of fructose metabolism increases the rate of ethanol oxidation by 5 0 -8 0 % [11, 18]. Thus it can be concluded that the rate of fructose metabolism in liver is of the same order of magnitude after peroral intake and after infusion of about 1 g fructose/kg/h. Such a rate of fructose metabolism elicits signifi-

Fructose and the dietary therapy of diabetes mellitus