FB2026_02 , released June 18, 2026
FB2026_02 , released June 18, 2026
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Citation
Toprak, U. (2026). Lipid Metabolism in Relation to Calcium Homeostasis.  Adv. Exp. Med. Biol. 1494(): 217--237.
FlyBase ID
FBrf0264348
Publication Type
Review
Abstract
Calcium (Ca[2+]) homeostasis is a critical regulator of insect cellular functions, influencing neurotransmission, muscle contraction, hormone signaling, and lipid metabolism. This chapter explores the intricate relationship between Ca[2+] signaling and lipid metabolism, emphasizing key molecular components that mediate this interaction. Store-operated calcium entry (SOCE) mechanisms, involving sarco/endoplasmic reticulum Ca[2+]-ATPase (SERCA), inositol 1,4,5-trisphosphate receptor (IP3R), ryanodine receptor (RyR), stromal interaction molecule (STIM), and Orai1, coordinate intracellular Ca[2+] fluxes that regulate lipid storage, mobilization, and utilization. Other Ca[2+]-binding proteins, such as calmodulin (CaM), calcineurin (CaN), regucalcin (RgN), calreticulin (CrT), and calnexin (CnX), further modulate Ca[2+] homeostasis and impact lipid metabolism by influencing lipolysis, lipogenesis, and lipid droplet dynamics. This chapter also highlights the role of hepatocyte-like oenocytes in lipid metabolism. These cells, analogous to mammalian hepatocytes, regulate lipid processing and mobilization during fasting, forming a metabolic axis with fat body adipocytes. While Ca[2+] signaling is well characterized in adipocytes, its role in oenocyte lipid metabolism remains largely unexplored. However, Ca[2+]-dependent regulation of lipid metabolism in mammalian hepatocytes suggests a similar involvement in insect oenocytes. A central theme is the bidirectional relationship between Ca[2+] homeostasis and lipid metabolism. While Ca[2+] signaling regulates lipid accumulation and hydrolysis, impaired lipid metabolism can disrupt Ca[2+] homeostasis. For instance, Drosophila melanogaster seipin mutants with defective lipid storage exhibit reduced SERCA activity, leading to lower ER and mitochondrial Ca[2+] levels, which impair lipogenesis. Additionally, CaN promotes lipogenesis, whereas STIM and IP3R serve as lipolytic regulators. This metabolic feedback loop is essential for maintaining energy balance. Understanding the Ca[2+]-lipid interplay in insects provides insights into metabolic regulation, with implications for pest management and metabolic disease research. Future studies should further investigate Ca[2+]-dependent mechanisms governing oenocyte function and systemic lipid homeostasis.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Adv. Exp. Med. Biol.
    Title
    Advances in Experimental Medicine and Biology
    Publication Year
    1976-
    ISBN/ISSN
    0065-2598
    Data From Reference