Cellular Insulin signaling shows a remarkable high molecular and functional conservation. Insulin-producing cells respond directly to nutritional cues in circulation and receive modulatory input from connected neuronal networks. Neuronal control integrates a wide range of variables including dietary change or environmental temperature. Although it is shown that neuronal input is sufficient to regulate Insulin-producing cells, the physiological relevance of this network remains elusive. In , Insulin-like peptide7-producing neurons are wired with Insulin-producing cells. We found that the former cells regulate the latter to facilitate larval development at high temperatures, and to regulate systemic Insulin signaling in adults feeding on calorie-rich food lacking dietary yeast. Our results demonstrate a role for neuronal innervation of Insulin-producing cells important for fruit flies to survive unfavorable environmental conditions.
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http://dx.doi.org/10.3389/fphys.2021.630390 | DOI Listing |
Stem Cell Res Ther
December 2024
Department of Central Laboratory, Shenzhen Hospital, Beijing University of Chinese Medicine, Shenzhen, Guangdong, China.
Background: The simultaneous differentiation of human pluripotent stem cells (hPSCs) into both endodermal and mesodermal lineages is crucial for developing complex, vascularized tissues, yet poses significant challenges. This study explores a method for co-differentiation of mesoderm and endoderm, and their subsequent differentiation into pancreatic progenitors (PP) with endothelial cells (EC).
Methods: Two hPSC lines were utilized.
Stem Cell Res
December 2024
Guangzhou National Laboratory, Guangzhou 510005, China; School of Biomedical Engineering, Guangzhou Medical University, Guangzhou 510180, China; Bioland Laboratory, Guangzhou 510005, China.
As a member of the single-fluorophore genetically encoded calcium indicators (GECIs), jGCaMP7f is widely applied to investigate intracellular Ca concentrations. Here, we established an INS-jGCaMP7f knock-in H1 human embryonic stem cell (hESC) line by integrating jGCaMP7f gene into insulin locus via CRISPR/Cas9 system. The reporter cell line not only effectively labelled the insulin-producing cells induced from hESC, but also reflected the cytosolic change of Ca level in response to different stimuli.
View Article and Find Full Text PDFClin Transl Med
December 2024
Andalusian Center of Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucía-University of Pablo de Olavide-University of Seville-CSIC, Seville, Spain.
Background: The complex aetiology of type 1 diabetes (T1D), characterised by a detrimental cross-talk between the immune system and insulin-producing beta cells, has hindered the development of effective disease-modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can reverse hyperglycaemia in mouse models of T1D by attenuating the autoimmune attack coupled to beta cell survival/regeneration prompted us to investigate whether immune tolerisation could be translated to individuals with T1D by LRH-1/NR5A2 activation and improve islet survival.
Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from individuals with and without T1D and derived into various immune cells, including macrophages and dendritic cells.
Methods Mol Biol
December 2024
Precision Health Program, Michigan State University, East Lansing, MI, USA.
Pancreatic islet transplantation is a promising cell replacement therapy for patients with type 1 diabetes (T1D), an autoimmune disease that destroys insulin-producing islet β cells. However, the shortage of donor pancreatic islets significantly limits the widespread use of this strategy as a routine therapy. Pluripotent stem cell-derived insulin-producing islet organoids present a promising alternative β cell source for T1D patients.
View Article and Find Full Text PDFCurr Pharm Des
December 2024
Department of Pharmacy, Guru Ghasidas Vishwavidyalaya, Bilaspur (C.G.) 495009, India.
Type 1 Diabetes is an autoimmune disease characterized by the destruction of insulin-producing pancreatic β-cells, leading to hyperglycemia and various complications. Despite insulin replacement therapy, there is a need for therapies targeting the underlying autoimmune response. This review aims to explore the mechanistic insights into T1D pathogenesis and the impact of delivery systems on immunotherapy.
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