INSULIN INDEX OF FOODS

1275

lin response to all of the nutrients in the foods as normally

consumed. A standard portion size of 1000 kJ was chosen

because this resulted in realistic serving sizes for most of the

foods except apples, oranges, fish, and potatoes. Although

some of the protein-rich foods may normally be eaten in

smaller quantities, fish, beef, cheese, and eggs still had larger

insulin responses per gram than did many of the foods consist

ing predominantly of carbohydrate. As observed in previous

studies, consumption of protein or fat with carbohydrate in

creases insulin secretion compared with the insulinogenic ef

fect of these nutrients alone (22, 30â€”32). This may partly

explain the markedly high insulin response to baked beans.

Dried hancot beans, which are soaked and boiled, are likely to

have a lower IS than commercial baked beans, which are more

readily digestible.

The results confirm that increased insulin secretion does not

account for the low glycemic responses produced by low-GI

foods such as pasta, porridge, and All-Bran cereal (33). Fur

thermore, equal-carbohydrate servings of foods do not neces

sarily stimulate insulin secretion to the same extent. For exam

ple, isoenergetic servings of pasta and potatoes both contained

=,%50 g carbohydrate, yet the IS for potatoes was three times

greater than that for pasta. Similarly, porridge and yogurt, and

whole-grain bread and baked beans, produced disparate ISs

despite their similar carbohydrate contents. These findings, like

others, challenge the scientific basis of carbohydrate exchange

tables, which assume that portions of different foods containing

10â€”15 g carbohydrate will have equal physiologic effects and

will require equal amounts of exogenous insulin to be metab

olized. It is possible that preprandial insulin doses for patients

with NIDDM could be more scientifically estimated or

matched on the basis of a meal's average insulinemic effect in

healthy individuals, rather than on the basis of the meal's

carbohydrate content or 01. Further research is required to test

this hypothesis. The advent of intensive insulin therapy and the

added risk of hypoglycemia increases the urgency of this

research (34).

Our study was undertaken to test the hypothesis that the

postprandial insulin response was not necessarily proportional

to the blood glucose response and that nutrients other than

carbohydrate influence the overall level of insulinemia. Multi

pIe-regression analysis of the individual results showed that the

glycemic response was a significant predictor of the insulin

response, but it accounted for only 23% of the variability in

insulinemia. The macronutrients (protein or fat, water, sugar,

and starch) were also significant predictors, but together ac

counted for only another 10% of the variability of the insulin

responses. Thus, we can explain only 33% of the variation of

the insulin responses to the 38 foods under examination. The

low R2 value indicates that the macronutrient composition of

foods has relatively limited power for predicting the extent of

postprandial insulinemia. The rate of starch digestion, the

amount of rapidly available glucose and resistant starch, the

degree ofosmolality, the viscosity ofthe gut's contents, and the

rate of gastric emptying must be other important factors influ

encing the degree of postprandial insulin secretion. Further

research is required to examine the relation between postpran

dial insulinemia, food form, and various digestive factors for a

much larger range of foods to produce a regression equation

with greater predictive value.

Dietary guidelines for healthy people and persons with

NIDDM have undergone considerable change and will con

tinue to be modified as our understanding of the relations

between dietary patterns and disease improves. There is con

cern that high-carbohydrate diets may increase triacylglycerol

concentrations and reduce high-density lipoprotein concentra

tions (35, 36). The use of diets high in monounsaturated fat is

an attempt to overcome the undesirable effects of some high

carbohydrate diets on plasma lipids (37â€”39). However, diets

high in monounsaturated fat are unlikely to facilitate weight

loss. A low-fat diet based on less-refined, carbohydrate-rich

foods with relatively low ISs may help enhance satiety and aid

weight loss as well as improve blood glucose and lipid control

(4).

The results of this study are preliminary but we hope they

stimulate discussion and further research. Additional studies are

needed to determine whether the IS concept is useful, reproducible

around the world, predictable in a mixed-meal context, and cliii

ically useful in the treatment of diabetes mellitus, hyperlipidemia,

and overweight. Studies examining the relation between postpran

dial insulinemia and the storage and oxidation of fat, protein, and

carbohydrate may provide further insight into the relation between

fuel metabolism and satiety, and establish whether low-insuline

mic diets can facilitate greater body fat loss than isoenergetic

high-insWinemic diets.

We thank Efi Farmakalidis for her assistancein the planning of this

study and Natasha Porter for her technical assistance with the experimental

work for the carbohydrate-rich food group.

REFERENCES

1. Jenkins DJA, Wolever TMS, Kalmusky J, et al. Low glycemic index

carbohydrate foods in the management of hyperlipidemia. Am J Clin

Nutr 1985;42:604â€”17.

2. Jenkins DJA, Wolever TMS, Vuksan V. et al. Nibbling vs gorging:

metabolic advantages of increased meal frequency. N EngI J Med

1989;32l :929â€”34.

3. Bymes SE, Brand Miller JC, Denyer GS. Development of insulin

resistance in rats after low- vs high-amylose diets. Bachelor of Science

Honours Thesis, Department of Biochemistry, The University of

Sydney, 1993.

4. Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effects of

low-insulin-response, energy-restricted diet on weight loss and plasma

insulin concentrations in hyperinsulinemic obese females. Am J Clin

Nutr l994;60:48â€”53.

5. Lerer-Metzger M, Rizkalla SW, Luo J, et al. Effects of long-term

low-glycaemic index starchy food on plasma glucose and lipid con

centrations and adipose tissue cellularity in normal and diabetic rats.

Br J Nutr 1996;75:723â€”32.

6. Bymes SE, Brand Miller JC, Denyer GS. Amylopectin starch pro

motes the development of insulin resistance in rats. J Nutr

1995;125: 1430â€”7.

7. SalmÃ©ron J, Ascherio A, Rimin EB, et al. Dietary fiber, glycemic load,

and risk of N!DDM in men. Diabetes Care l997;20:545-50.

8. SalmÃ©ron J, Manson JE, Meir J, et al. Dietary fiber, glycemic load, and

risk of non-insulin-dependent diabetes mellitus in women. JAMA

l997;l2:472â€”7.

9. Modan M, Halkin H, Almog 5, et al. Hyperinsutinemia: a link between

hypertension, obesity and glucose intolerance. J Clin Invest

l985;75:809â€”17.

10. Zavaroni I, Bonora E, Pagliara M, et a!. Risk factors for coronary

artely disease in healthy persons with hyperinsulinaemia and normal

glucose tolerance. N Engi J Med l989;320:702â€”6.

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