Biology Reference
In-Depth Information
muscle and liver, and increases lipogenesis in adipose tissue. Simultaneously,
there is suppression of gluconeogenesis, glucose output by liver, and lipolysis.
The rapid absorption of nutrients following a high-GI meal slows down the
rate of entry of exogenous glucose into the circulation. However, the storage
of nutrients continues and glucose mobilization from tissues remains
suppressed due to the effects of high insulin and glucagon levels. This results
in a hypoglycemic episode below fasting levels that triggers release of
counter-regulatory hormones, including glucagon, adrenaline, and growth
hormone. These hormones act to restore circulating fuel levels by increasing
hepatic glucose output and decreasing glucose uptake by skeletal muscle
alongside triggering lipolysis and causing an increase in circulating non-
esterified fatty acid (NEFA) released by adipose tissue (
Wolever, Bentum-
Williams, & Jenkins, 1995
)
. Following the consumption of a low-GI meal,
there is a prolonged and continued absorption of nutrients from the gastro-
intestinal tract, the hypoglycemic episode does not occur, and the return of
blood glucose to the baseline level is delayed. This slower release of nutrients
and gradual drop in blood glucose levels allow adjustment of hepatic glucose
output to maintain circulating glucose levels without dramatic rises and falls,
or a large rebound inNEFA levels. Low-GI diets therefore give a more stable
diurnal profile, reducing postprandial hyperglycemia and hyperinsulinemia,
and attenuating late postprandial rebounds in circulating NEFA, all factors
that
exacerbate various
components of
the metabolic
syndrome
(
Aston, 2006
)
.
Low-GI diets may contribute to modest weight loss or reduction of
weight gain via their effects on reductions in energy intake. Low-GI foods
may increase satiety and delay the return of hunger in comparison with high-
GI foods, which may be translated into reduced energy intake at later meals.
The hormonal environment following a high-GI meal reduces the availabil-
ity of the two major metabolic fuels (glucose and fatty acids), signaling a
fasted state. Hypoglycemia is a signal for hunger, and the rate of change
of blood glucose may also be important, with more rapid falls triggering
more rapid return of hunger (
Pawlak, Ebbeling, & Ludwig, 2002
). The
hypoglycemic undershoot frequently seen following high-GI meals would
therefore be predicted to trigger hunger. In one study by
Ludwig et al.
a subsequent meal with subjects eating more following a high-GI breakfast
than following a low-GI breakfast. The variability in energy intake follow-
ing breakfast of low- and high-GI was predicted also by circulating fatty acid
levels in this study. Initial low levels of NEFA as a result of the high-insulin
response to high-GI foods may also trigger hunger.
Holt and Miller (1994)
