scholarly journals Torso-like is a component of the hemolymph and regulates the insulin signalling pathway in Drosophila

2018 ◽  
Author(s):  
Michelle A. Henstridge ◽  
Lucinda Aulsebrook ◽  
Takashi Koyama ◽  
Travis K. Johnson ◽  
James C. Whisstock ◽  
...  
Keyword(s):  
Body Size ◽  
Insulin Signalling ◽  
Steroid Hormone ◽  
The Body ◽  
Signalling Pathway ◽  
Prothoracic Gland ◽  
Signalling Pathways ◽  
Mature Adult ◽  
Developmental Transitions ◽  
Insulin Signalling Pathway

ABSTRACTIn Drosophila key developmental transitions are governed by the steroid hormone ecdysone. A number of neuropeptide-activated signalling pathways control ecdysone production in response to environmental signals, including the insulin signalling pathway, which regulates ecdysone production in response to nutrition. Here, we find that the Membrane Attack Complex/Perforin-like protein Torso-like, best characterised for its role in activating the Torso receptor tyrosine kinase in early embryo patterning, also regulates the insulin signalling pathway in Drosophila. We previously reported that the small body size and developmental delay phenotypes of torso-like null mutants resemble those observed when insulin signalling is reduced. Here we report that, in addition to growth defects, torso-like mutants also display metabolic and nutritional plasticity phenotypes characteristic of mutants with impaired insulin signalling. We further find that in the absence of torso-like the expression of insulin-like peptides is increased, as is their accumulation in the insulin-producing cells. Finally, we show that Torso-like is a component of the hemolymph and that it is required in the prothoracic gland to control developmental timing and body size. Taken together, our data suggest that the secretion of Torso-like from the prothoracic gland influences the activity of insulin signalling throughout the body in Drosophila.ARTICLE SUMMARYIn many animals distinct developmental transitions are crucial for the coordinated progression from the juvenile stage to adulthood. In Drosophila, the transition from an immature larva into a reproductively mature adult is controlled by the steroid hormone ecdysone. Several neuropeptide-activated signalling pathways, including the insulin signalling pathway, regulate ecdysone production in response to environmental cues. Here we find that the perforin-like protein Torso-like regulates the insulin signalling pathway. We show that Torso-like is secreted into circulation where it acts to influence insulin-like peptide activity, revealing a novel mechanism for the regulation of insulin signalling in Drosophila.

scholarly journals Neuropeptide F receptor acts in the Drosophila prothoracic gland to regulate growth and developmental timing

2019 ◽  
Author(s):  
Jade R. Kannangara ◽  
Michelle A. Henstridge ◽  
Linda M. Parsons ◽  
Shu Kondo ◽  
Christen K. Mirth ◽  
...  
Keyword(s):  
Body Size ◽  
Feeding Behaviour ◽  
Insulin Signalling ◽  
Steroid Hormone ◽  
Prothoracic Gland ◽  
Environmental Cues ◽  
Feeding Period ◽  
Animal Development ◽  
Insulin Signalling Pathway ◽  
Neuropeptide F

SUMMARYAs juvenile animals grow, their behaviour, physiology, and development need to be matched to environmental conditions to ensure they survive to adulthood. However, we know little about how behaviour and physiology are integrated with development to achieve this outcome. Neuropeptides are prime candidates for achieving this due to their well-known signalling functions in controlling many aspects of behaviour, physiology and development in response to environmental cues. In the growing Drosophila larva, while several neuropeptides have been shown to regulate feeding behaviour, and a handful to regulate growth, it is unclear if any of these play a global role in coordinating feeding behaviour with developmental programs. Here, we demonstrate that Neuropeptide F Receptor (NPFR), best studied as a conserved regulator of feeding behaviour from insects to mammals, also regulates development in Drosophila. Knocking down NPFR in the prothoracic gland, which produces the steroid hormone ecdysone, generates developmental delay and an extended feeding period, resulting in increased body size. We show that these effects are due to decreased ecdysone production, as these animals have reduced expression of ecdysone biosynthesis genes and lower ecdysone titres. Moreover, these phenotypes can be rescued by feeding larvae food supplemented with ecdysone. Further, we show that NPFR negatively regulates the insulin signalling pathway in the prothoracic gland to achieve these effects. Taken together, our data demonstrate that NPFR signalling plays a key role in regulating animal development and may thus play a global role in integrating feeding behaviour and development in Drosophila.

scholarly journals Grape seed extract supplementation prevents high-fructose diet-induced insulin resistance in rats by improving insulin and adiponectin signalling pathways

2011 ◽  
Vol 106 (8) ◽  
pp. 1173-1181 ◽  
Author(s):  
Aramsri Meeprom ◽  
Weerachat Sompong ◽  
Wannaporn Suwannaphet ◽  
Sirintorn Yibchok-anun ◽  
Sirichai Adisakwattana
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Mrna Expression ◽  
Glycogen Synthase ◽  
Insulin Signalling ◽  
Grape Seed ◽  
Signalling Pathway ◽  
Signalling Pathways ◽  
High Fructose ◽  
Insulin Signalling Pathway

Recent evidence strongly supports the contention that grape seed extract (GSE) improves hyperglycaemia and hyperinsulinaemia in high-fructose-fed rats. To explore the underlying molecular mechanisms of action, we examined the effects of GSE on the expression of muscle proteins related to the insulin signalling pathway and of mRNA for genes involved in the adiponectin signalling pathway. Compared with rats fed on a normal diet, high-fructose-fed rats developed pathological changes, including insulin resistance, hyperinsulinaemia, hypertriacylglycerolaemia, a low level of plasma adiponectin and a high level of plasma fructosamine. These disorders were effectively attenuated in high-fructose-fed rats supplemented with GSE. A high-fructose diet causes insulin resistance by significantly reducing the protein expression of insulin receptor, insulin receptor substrate-1, Akt and GLUT4, and the mRNA expression of adiponectin, adiponectin receptor R1 (AdipoR1) and AMP-activated protein kinase (AMPK)-α in the skeletal muscle. Supplementation of GSE enhanced the expression of insulin signalling pathway-related proteins, including Akt and GLUT4. GSE also increased the mRNA expression of adiponectin, AdipoR1 and AMPK-α. In addition, GSE increased the mRNA levels of glycogen synthase and suppressed the mRNA expression of glycogen synthase kinase-3-α, causing an increase in glycogen accumulation in the skeletal muscle. These results suggest that GSE ameliorates the defective insulin and adiponectin signalling pathways in the skeletal muscle, resulting in improved insulin resistance in fructose-fed rats.

scholarly journals Autocrine regulation of ecdysone synthesis by β3-octopamine receptor in the prothoracic gland is essential for Drosophila metamorphosis

2015 ◽  
Vol 112 (5) ◽  
pp. 1452-1457 ◽  
Author(s):  
Yuya Ohhara ◽  
Yuko Shimada-Niwa ◽  
Ryusuke Niwa ◽  
Yasunari Kayashima ◽  
Yoshiki Hayashi ◽  
...  
Keyword(s):  
Body Size ◽  
Signaling Pathways ◽  
G Protein ◽  
Steroid Hormone ◽  
Prothoracic Gland ◽  
Autocrine Signaling ◽  
Developmental Transitions ◽  
Autocrine Regulation ◽  
Octopamine Receptor ◽  
G Protein Coupled

In Drosophila, pulsed production of the steroid hormone ecdysone plays a pivotal role in developmental transitions such as metamorphosis. Ecdysone production is regulated in the prothoracic gland (PG) by prothoracicotropic hormone (PTTH) and insulin-like peptides (Ilps). Here, we show that monoaminergic autocrine regulation of ecdysone biosynthesis in the PG is essential for metamorphosis. PG-specific knockdown of a monoamine G protein-coupled receptor, β3-octopamine receptor (Octβ3R), resulted in arrested metamorphosis due to lack of ecdysone. Knockdown of tyramine biosynthesis genes expressed in the PG caused similar defects in ecdysone production and metamorphosis. Moreover, PTTH and Ilps signaling were impaired by Octβ3R knockdown in the PG, and activation of these signaling pathways rescued the defect in metamorphosis. Thus, monoaminergic autocrine signaling in the PG regulates ecdysone biogenesis in a coordinated fashion on activation by PTTH and Ilps. We propose that monoaminergic autocrine signaling acts downstream of a body size checkpoint that allows metamorphosis to occur when nutrients are sufficiently abundant.

scholarly journals The insulin signalling pathway

2002 ◽  
Vol 12 (7) ◽  
pp. R236-R238 ◽  
Author(s):  
Jose M. Lizcano ◽  
Dario R. Alessi
Keyword(s):  
Insulin Signalling ◽  
Signalling Pathway ◽  
Insulin Signalling Pathway

Effect of food restriction on the insulin signalling pathway in rat skeletal muscle and adipose tissue

2005 ◽  
Vol 16 (10) ◽  
pp. 602-609 ◽  
Author(s):  
Ana Alonso ◽  
Yolanda Fernández ◽  
Rebeca Fernández ◽  
Patricia Ordóñez ◽  
María Moreno ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Food Restriction ◽  
Insulin Signalling ◽  
Signalling Pathway ◽  
Rat Skeletal Muscle ◽  
Insulin Signalling Pathway ◽  
Effect Of Food

scholarly journals Mulberry leaf reduces inflammation and insulin resistance in type 2 diabetic mice by TLRs and insulin Signalling pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Simin Tian ◽  
Min Wang ◽  
Chenyue Liu ◽  
Hongbin Zhao ◽  
Baosheng Zhao
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Insulin Signalling ◽  
Signalling Pathway ◽  
Inflammatory Factor ◽  
Diabetic Mice ◽  
Mulberry Leaf ◽  
Insulin Signalling Pathway ◽  
Tnf Α ◽  
Necrosis Factor

Abstract Background It has been testified that Diabetes mellitus (DM) has a close association with chronic inflammation and Toll-like Receptors (TLRs), and DM could be prevented by mulberry leaf. Therefore, a hypothesis came into being that mulberry leaf could ameliorate proinflammation and insulin resistance (IR) through TLRs and insulin signalling pathways. Methods Water extracts of mulberry leaf (WEM) was given to diabetic mice by gavage for 10 weeks, and the diabetic mice was injected with low-dose streptozocin, fed with high-fat and high-sugar diet. Oral glucose tolerance tests (OGTTs) were conducted. At the same time, homeostasis model assessment of insulin (HOMA-IR) and the level of the inflammatory factor, tumour necrosis factor-α (TNF-α) was measured. The expressions of critical nodes of TLRs and insulin signalling pathway were also examined. Results WEM contributed to a significant decrease in fasting blood glucose, AUC from the investigation of OGTTs and HOMA-IR. The levels of the inflammatory factor, tumour necrosis factor-α (TNF-α) also declined. Moreover, WEM suppressed the expression of TLR2, myeloid differentiation primary-response protein 88 (MyD88), tumour-necrosis-factor receptor-associated factor 6 (TRAF6), nuclear factor kappa B (NF-κB) in the skeletal muscle. WEM could up-regulate the expression of insulin receptor (InsR) and insulin receptor substrate 1 (IRS1), and down-regulate the phosphorylation of IRS1 in adipose tissue. Conclusion Through this study, a conclusion could be made that WEM mitigates hyperglycemia, IR, and inflammation through the interactions among TLR2 signalling pathway, insulin signalling pathway and TNF-α.

scholarly journals Agonists for endothelial P2 purinoceptors trigger a signalling pathway producing Ca2+ responses in lymphocytes adherent to endothelial cells

1995 ◽  
Vol 311 (2) ◽  
pp. 589-594 ◽  
Author(s):  
J S Wiley ◽  
J R Chen ◽  
G P Jamieson ◽  
P J Thurlow
Keyword(s):  
Endothelial Cells ◽  
Lymphocytic Leukaemia ◽  
Umbilical Vein ◽  
Cell Types ◽  
The Body ◽  
Signalling Pathway ◽  
Signalling Pathways ◽  
Transient Rise ◽  
Umbilical Vein Endothelial Cells ◽  
Stimulation Of

Recirculation of lymphocytes through the body involves their frequent adhesion to endothelial cells but little is known of the signalling pathways between these two cell types. Lymphocytes from patients with chronic lymphocytic leukaemia were loaded with the Ca(2+)-sensitive indicator, fura 2, and allowed to adhere to either glass or monolayers of human umbilical-vein endothelial cells. Addition of ATP or UTP (1-10 microM) to the superfusate produced a transient rise in cytosolic Ca2+ concentration in the lymphocytes adherent to endothelium (24 of 35 cells). In contrast, ATP or UTP (1-10 microM) had no effect on the cytosolic Ca2+ of lymphocytes attached to glass. As the only lymphocyte receptor for ATP (P2Z class) requires higher ATP concentrations (> 50 microM) for Ca2+ influx and is unresponsive to UTP, the involvement of a lymphocyte P2Z purinoceptor is unlikely. Various agonists including ATP, UTP, 2-methylthioATP, ADP and histamine all stimulated increases in endothelial cytosolic Ca2+ but only ATP and UTP (both agonists for endothelial P2U purinoceptors) triggered Ca2+ transients in adherent lymphocytes. Removal of extracellular Ca2+ did not abolish the ATP-induced rise in cytosolic Ca2+ concentration in lymphocytes adherent to endothelial cells. These findings show that stimulation of endothelial P2U purinoceptors triggers an endothelial-lymphocyte signalling pathway which releases internal Ca2+ in adherent lymphocytes.

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