Lipid Metabolism in Relation to Calcium Homeostasis


TOPRAK U.

Advances in Experimental Medicine and Biology, Springer, ss.217-237, 2026 identifier

  • Yayın Türü: Kitapta Bölüm / Araştırma Kitabı
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1007/978-3-032-04842-4_875
  • Yayınevi: Springer
  • Sayfa Sayıları: ss.217-237
  • Anahtar Kelimeler: Calcium, Ip3r, Lipid, ORAI, SERCA, SOCE, STIM
  • Ankara Üniversitesi Adresli: Evet

Özet

Calcium (Ca2+) 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 Ca2+ signaling and lipid metabolism, emphasizing key molecular components that mediate this interaction. Store-operated calcium entry (SOCE) mechanisms, involving sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), inositol 1,4,5-trisphosphate receptor (IP3R), ryanodine receptor (RyR), stromal interaction molecule (STIM), and Orai1, coordinate intracellular Ca2+ fluxes that regulate lipid storage, mobilization, and utilization. Other Ca2+-binding proteins, such as calmodulin (CaM), calcineurin (CaN), regucalcin (RgN), calreticulin (CrT), and calnexin (CnX), further modulate Ca2+ 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 Ca2+ signaling is well characterized in adipocytes, its role in oenocyte lipid metabolism remains largely unexplored. However, Ca2+-dependent regulation of lipid metabolism in mammalian hepatocytes suggests a similar involvement in insect oenocytes. A central theme is the bidirectional relationship between Ca2+ homeostasis and lipid metabolism. While Ca2+ signaling regulates lipid accumulation and hydrolysis, impaired lipid metabolism can disrupt Ca2+ homeostasis. For instance, Drosophila melanogaster seipin mutants with defective lipid storage exhibit reduced SERCA activity, leading to lower ER and mitochondrial Ca2+ 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 Ca2+-lipid interplay in insects provides insights into metabolic regulation, with implications for pest management and metabolic disease research. Future studies should further investigate Ca2+-dependent mechanisms governing oenocyte function and systemic lipid homeostasis.