This review assesses the feasibility of using
glycemic index (GI) as a predictor of
appetite,
hunger and
satiety by surveying published human intervention studies. We also discuss the relationship between GI and two
appetite/
satiety control
hormones,
leptin and
ghrelin.
Ingestion of high-GI food increased
hunger and lowered
satiety in short-term human intervention studies. This effect may be attributed to the rapid decline in
blood glucose level following a hyperinsulinemic response caused by a sharp and transient increase in
blood glucose level that occurs after the
ingestion of high-GI food, which is defined as the glucostatic theory. However,
appetite,
hunger and
satiety after the
ingestion of foods with varying GI were inconsistent among long-term human intervention studies. From the few relevant long-term studies available, we
selected two recent well-designed examples for analysis, but they failed to elicit clear differences in
glycemic and insulinemic responses between high- and low-GI meals (consisting of a combination of different foods or key carbohydrate-rich foods incorporated into habitual diets). One of the reasons that these studies could not predict
glycemic response to mixed meals is presumably that the GI of each particular food was not reflected in that of the mixed meals as a whole. Thus, it is difficult to conclude that the
GI values of foods or mixed meals are a valid long-term predictor for
appetite,
hunger and
satiety. Both
insulin and insulin-mediated
glucose uptake and
metabolism in
adipose tissue affect
blood leptin concentration and its diurnal pattern. Circulating
ghrelin level is suppressed by carbohydrate-rich meals, presumably via
glycemia and insulinemia. Accordingly, low-GI foods may not necessarily increase
satiety or suppress
appetite and/or
hunger because of the lack of insulin-mediated
leptin stimulation and
ghrelin suppression. However, insulin-mediated
leptin stimulation and
ghrelin suppression per se is not consistent among studies; thus we were not able to identify a clear relationship among GI, satietogenic
leptin, and appetitic
ghrelin.
