The main blood sugar of locusts is trehalose, which
is hydrolysed to two glucose units by trehalase.
Homogenates of locust flight muscles are rich in trehalase
activity, which is bound to membranes. A minor fraction
of trehalase is in an overt form while the remainder is
latent, i.e. active only after impairing membrane integrity.
Trehazolin, an antibiotic pseudosaccharide, inhibits locust
flight muscle trehalase with apparent Ki- and EC50 values
of 10–8mol l–1 and 10–7mol l–1, respectively. Trehazolin is
insecticidal: 50µg injected into locusts completely and
selectively blocked the overt form of muscle trehalase
(with little effect on latent activity) and killed 50% of the
insects within 24 h. Here, it is demonstrated for the first
time that trehazolin causes dramatic hypoglycaemia.
Injection of 10µg trehazolin caused glucose levels to fall
by over 90% in 24 h, from 2.8 mmol l–1 to 0.23 mmol l–1,
while trehalose increased from 61 mmol l–1 to 111 mmol l–1.
Feeding glucose to the locusts fully neutralized the effects
of a potentially lethal dose of trehazolin. This indicates
that hypertrehalosaemia is not acutely toxic, whereas lack
of glucose causes organ failure (presumably of the nervous
system), and that sufficient haemolymph glucose can only
be generated from trehalose by trehalase. The results also
suggest that overt flight muscle trehalase is located in the
plasma membrane with the active site accessible to the
haemolymph. Trehalase inhibitors are valuable tools for
studying the molecular physiology of trehalase function
and sugar metabolism in insects.