Inhibition of flight in Periplaneta americana (Linn.) by a trehalase inhibitor, validoxylamine A

Kono, Yoshiaki; Takahashi, M.; Matsushita, Kazuhiro; Nishina, Masami; Kameda, Yukihiko; Hori, Eitaro

doi:10.1016/0022-1910(94)90117-1

Cited by 35 publications

(20 citation statements)

References 11 publications

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“…The cockroach (Periplaneta americana) which uses glucose as its primary flying fuel [42], opts for trehalose as a high energy substrate for prolonged flights. Administration of an inhibitor of trehalase (the enzyme involved in trehalose breakdown) significantly decreases cockroach flight time [43]. Many other long distance fliers, like locusts, also use trehalose [36].…”

Section: Trehalose's Role As Energy Sourcementioning

confidence: 99%

Carbohydrate Metabolism in Drosophila: Reliance on the Disaccharide Trehalose

Reyes-DelaTorre¹,

Peña-Rangel²,

Riesgo-Escovar³

2012

Carbohydrates - Comprehensive Studies on Glycobiology and Glycotechnology

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Section: Trehalose's Role As Energy Sourcementioning

confidence: 99%

Carbohydrate Metabolism in Drosophila: Reliance on the Disaccharide Trehalose

Reyes-DelaTorre¹,

Peña-Rangel²,

Riesgo-Escovar³

2012

Carbohydrates - Comprehensive Studies on Glycobiology and Glycotechnology

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“…These inhibitors, such as trehazolin (Ando et al, 1991) or validoxylamine A (Asano et al, 1990;Asano, 2003), are analogues of trehalose of bacterial origin that bind tightly to trehalase. When injected into insects, these inhibitors affect motor activity, feeding, metabolism, growth, development, reproduction and flight (Kono et al, 1993;Kono et al, 1994a;Kono et al, 1994b;Ando et al, 1995a;Tanaka et al, 1998), thus indicating that trehalose metabolism is involved in many aspects of insect physiology. The inhibitors interfere specifically with the hydrolysis of trehalose (Ando et al, 1995b) but apparently do not block its production and release into the haemolymph by the fat body (Kono et al, 1995;Wegener et al, 2003;Liebl et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Long-term effects of the trehalase inhibitor trehazolin on trehalase activity in locust flight muscle

Wegener

Macho

Schlöder

et al. 2010

Journal of Experimental Biology

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SUMMARY Trehalase (EC 3.2.1.28) hydrolyzes the main haemolymph sugar of insects, trehalose, into the essential cellular substrate glucose. Trehalase in locust flight muscle is bound to membranes that appear in the microsomal fraction upon tissue fractionation, but the exact location in vivo has remained elusive. Trehalase has been proposed to be regulated by a novel type of activity control that is based on the reversible transformation of a latent (inactive) form into an overt (active) form. Most trehalase activity from saline-injected controls was membrane-bound (95%) and comprised an overt form (∼25%) and a latent form (75%). Latent trehalase could be assayed only after the integrity of membranes had been destroyed. Trehazolin, a potent tight-binding inhibitor of trehalase, is confined to the extracellular space and has been used as a tool to gather information on the relationship between latent and overt trehalase. Trehazolin was injected into the haemolymph of locusts, and the trehalase activity of the flight muscle was determined at different times over a 30-day period. Total trehalase activity in locust flight muscle was markedly inhibited during the first half of the interval, but reappeared during the second half. Inhibition of the overt form preceded inhibition of the latent form, and the time course suggested a reversible precursor–product relation (cycling) between the two forms. The results support the working hypothesis that trehalase functions as an ectoenzyme, the activity of which is regulated by reversible transformation of latent into overt trehalase.

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“…The low glucose content in insect haemolymph is probably the reason why the inhibitor-induced dramatic decrease in haemolymph glucose has escaped notice for so long. In previous studies, the effects of trehalase inhibitors on haemolymph constituents were usually analysed by NMR-spectroscopy (Kono et al, 1993(Kono et al, , 1994a(Kono et al, ,b, 1999Takahashi et al, 1995). This powerful method can detect many compounds simultaneously, yet is not sensitive enough to follow a decrease in glucose content.…”

Section: Hypertrehalosaemic and Hypoglycaemic Effects Of Trehalase Inmentioning

confidence: 99%

“…(6) Locusts must possess vital organs (cells) that require glucose for proper functioning. This is backed up by reports that fuel other than glucose, such as lipids and amino acids, which are prominent in insect haemolymph (Mullins, 1985), is not depleted in insects injected with trehalase inhibitors (Kono et al, 1993(Kono et al, , 1994a(Kono et al, ,b, 1999. It is not known which organ failure proves to be fatal, but the behaviour of the trehazolin-poisoned locusts preceding death suggests that the central nervous system is the most likely candidate.…”

Section: Haemolymph Glucose Is Derived From Trehalose and Ismentioning

confidence: 99%

The toxic and lethal effects of the trehalase inhibitor trehazolin in locusts are caused by hypoglycaemia

Wegener

Tschiedel

Schlöder

et al. 2003

Journal of Experimental Biology

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SUMMARY 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 10–8 mol l–1and 10–7 mol l–1, respectively. Trehazolin is insecticidal: 50 μg 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 10 μg 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.

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Inhibition of flight in Periplaneta americana (Linn.) by a trehalase inhibitor, validoxylamine A

Cited by 35 publications

References 11 publications

Carbohydrate Metabolism in Drosophila: Reliance on the Disaccharide Trehalose

Carbohydrate Metabolism in Drosophila: Reliance on the Disaccharide Trehalose

Long-term effects of the trehalase inhibitor trehazolin on trehalase activity in locust flight muscle

The toxic and lethal effects of the trehalase inhibitor trehazolin in locusts are caused by hypoglycaemia

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