Lipid metabolism is fundamental to life. In insects, it is critical, during reproduction, flight, starvation, and diapause. The coordination center for insect lipid metabolism is the fat body, which is analogous to the vertebrate adipose tissue and liver. Fat body contains various different cell types; however, adipocytes and oenocytes are the primary cells related to lipid metabolism. Lipid metabolism starts with the hydrolysis of dietary lipids, absorption of lipid monomers, followed by lipid transport from midgut to the fat body, lipogenesis or lipolysis in the fat body, and lipid transport from fat body to other sites demanding energy. Lipid metabolism is under the control of hormones, transcription factors, secondary messengers and posttranscriptional modifications. Primarily, lipogenesis is under the control of insulin‐like peptides that activate lipogenic transcription factors, such as sterol regulatory element‐binding proteins, whereas lipolysis is coordinated by the adipokinetic hormone that activates lipolytic transcription factors, such as forkhead box class O and cAMP‐response element‐binding protein. Calcium is the primary–secondary messenger affecting lipid metabolism and has different outcomes depending on the site of lipogenesis or lipolysis. Phosphorylation is central to lipid metabolism and multiple phosphorylases are involved in lipid accumulation or hydrolysis. Although most of the knowledge of insect lipid metabolism comes from the studies on the model Drosophila; other insects, in particular those with obligatory or facultative diapause, also have great potential to study lipid metabolism. The use of these models would significantly improve our knowledge of insect lipid metabolism.

Calcium (Ca2+) homeostasis is vital for insect development and metabolism, and the endoplasmic reticulum (ER) is a major intracellular reservoir for Ca2+. The inositol 1,4,5- triphosphate receptor (IP3R) and ryanodine receptor (RyR) are large homotetrameric channels associated with the ER and serve as two major actors in ER-derived Ca2+ supply. Most of the knowledge on these receptors derives from mammalian systems that possess three genes for each receptor. These studies have inspired work on synonymous receptors in insects, which encode a single IP3R and RyR. In the current review, we focus on a fundamental, common question: “why do insect cells possess two Ca2+ channel receptors in the ER?”. Through a comparative approach, this review covers the discovery of RyRs and IP3Rs, examines their structures/functions, the pathways that they interact with, and their potential as target sites in pest control. Although insects RyRs and IP3Rs share structural similarities, they are phylogenetically distinct, have their own structural organization, regulatory mechanisms, and expression patterns, which explains their functional distinction. Nevertheless, both have great potential as target sites in pest control, with RyRs currently being targeted by commercial insecticide, the diamides.

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Molecular chaperones are crucial for the correct folding of newly synthesized polypeptides, in particular, under stress conditions. Various studies have revealed the involvement of molecular chaperones, such as heat shock proteins, in diapause maintenance and starvation; however, the role of other chaperones in diapause and starvation relatively is unknown. In the current study, we identified two lectintype chaperones with calcium affinity, a calreticulin (LdCrT) and a calnexin (LdCnX), that were present in the fat body of the Colorado potato beetle, Leptinotarsa decemlineata (Coleoptera: Chrysomelidae) during diapause. Both proteins possessed an N-globular domain, a P-arm domain, and a highly charged C-terminal domain, while an additional transmembrane domain was present in LdCnX. Phylogenetic analysis revealed distinction at the order level. Both genes were expressed in multiple tissues in larval and adult stages, and constitutively throughout development, though a starvation response was detected only for LdCrT. In females, diapause-related expression analysis in the whole body revealed an upregulation of both genes by post-diapause, but a downregulation by diapause only for LdCrT. By contrast, males revealed no alteration in their