Abstract
Adipokinetic hormone (AKH), an analog of mammalian glucagon, functions in supplying the required energy by releasing lipids and carbohydrates from the fat body into the hemolymph. Our previous study showed that AKH receptor (AKHR) knockdown in the two-spotted cricket Gryllus bimaculatus decreased hemolymph lipid levels and increased its feeding frequency. To reveal underlying mechanisms by which AKH signaling modulates lipid homeostasis, we analyzed the fatty acid composition as the lipid structure in the crickets. AKH administration significantly increased the proportion of unsaturated fatty acids (USFAs) to total fatty acids with decrease of the saturated fatty acids (SFAs) in hemolymph, while these proportions were inversely changed in RNA interference-mediated AKHR-knockdowned (AKHRRNAi) crickets. Interestingly, knockdown of hormone-sensitive lipase (Hsl) by RNAi (HslRNAi) affected the proportion of USFAs and SFAs in a similar manner to that observed in AKHRRNAi crickets. AKH administration in HslRNAi crickets did not change hemolymph fatty acid composition, indicating that AKH signaling critically altered fatty acid composition in the hemolymph through Hsl. In addition, a choice assay revealed that AKHRRNAi significantly increases the preference of USFAs. These data indicate that hemolymph lipid level and composition were modulated by AKH signaling with a complementary feeding behavior toward USFAs.
Highlights
IntroductionThe fat body, plays a crucial role in lipid biosynthesis, metabolism, and energy storage
Insect adipose tissue, the fat body, plays a crucial role in lipid biosynthesis, metabolism, and energy storage
We first confirmed the effects of Adipokinetic hormone (AKH) injection on adult crickets, which triggered a significant increase in hemolymph lipid level compared with those of no treatment, while the lipid level of Phosphate-buffered saline (PBS)-injected crickets did not alter (Fig. 1A)
Summary
The fat body, plays a crucial role in lipid biosynthesis, metabolism, and energy storage. Energy is acquired by consuming dietary nutrients by feeding and by catabolizing lipids and glycogen in the fat body, which are mobilized into the circulating system (hemolymph) similar to that observed in other animals[3,4]. Such energy demands, including lipid mobilization, are under endocrine control involving adipokinetic hormone (AKH), an analog of mammalian glucagon[5,6]. AKH signaling must modulate lipid biosynthesis and metabolism, eventually causing changes in the fatty acid composition, according to the nutritional state following feeding behavior
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