The avian pancreas has three or four lobes and develops from a dorsal and two ventral buds. The cells that will contribute to formation of the dorsal bud are at first located in the mid-dorsal endoderm, those of the ventral buds in the floor of the foregut. The determination of endoderm to form dorsal and ventral bud derivatives occurs before formation of the buds. The highest concentration of endocrine tissue is in the splenic lobe. The lobes contain A and B islets in which glucagon and insulin cells, respectively, predominate. Islets contain somatostatin and pancreatic polypeptide (PP) cells, both of which also occur scattered in the exocrine parenchyma. Pancreatic endocrine cells arise from endoderm: glucagon, insulin, and somatostatin cells differentiate early, PP cells later. To establish culture conditions suitable for avian insulin cells, the epithelial component of dorsal buds of 5-day chick embryos was cultured under various conditions. At the end of 7 days the proportion of insulin cells was determined. In raising the proportion of insulin cells, Matrigel was superior to collagen gel and a serum-free medium (incorporating insulin, transferrin, and selenium) was superior to a serum-containing medium. Modifications to the serum-free medium were tested. Raising the level of glucose or of glucose and essential amino acids increased the proportion of insulin cells. This proportion was also increased by replacement of insulin by insulin-like growth factor-I, whereas addition of transforming growth factor beta1 reduced the proportion. Transfer of explants from poor to favourable culture conditions showed that the improved conditions stimulated quiescent insulin progenitor cells to develop.
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http://dx.doi.org/10.1002/(SICI)1097-0029(19981115)43:4<292::AID-JEMT3>3.0.CO;2-X | DOI Listing |
Circ Res
January 2025
British Heart Foundation Centre for Research Excellence, School of Cardiovascular and Metabolic Medicine and Sciences, James Black Centre, King's College London, United Kingdom (C.Y.H., M.-Y.W., J.T., S.A., L.D., G.A., R.H., C.M.S.).
Background: Vascular calcification is a detrimental aging pathology markedly accelerated in patients with chronic kidney disease. Prelamin A is a biomarker of vascular smooth muscle cell aging that accelerates calcification however the mechanisms remain undefined.
Methods: Vascular smooth muscle cells were transduced with prelamin A using an adenoviral vector and epigenetic modifications were monitored using immunofluorescence and targeted polymerase chain reaction array.
J Ovarian Res
January 2025
The First Affiliated Hospital, Gynecology&Obstetrics and Reproductive Medical Center, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Objective: Polycystic Ovary Syndrome (PCOS) is a prevalent endocrinopathy in reproductive-aged women, contributing to 75% of infertility cases due to ovulatory dysfunction. The condition poses significant health and psychological challenges, making the study of its pathogenesis and treatment a research priority. This study investigates the effects of Mogroside V (MV) on PCOS, focusing on its anti-inflammatory and anti-insulin resistance properties.
View Article and Find Full Text PDFRev Endocr Metab Disord
January 2025
Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Illinois at Chicago, Chicago, IL, USA.
This review focuses on our current understanding of how growth hormone releasing hormone (GHRH): 1) stimulates GH release and synthesis from pituitary growth hormone (GH)-producing cells (somatotropes), 2) drives somatotrope proliferation, 3) is negatively regulated by somatostatin (SST), GH and IGF1, 4) is altered throughout lifespan and in response to metabolic challenges, and 5) analogues can be used clinically to treat conditions of GH excess or deficiency. Although a large body of early work provides an underpinning for our current understanding of GHRH, this review specifically highlights more recent work that was made possible by state-of-the-art analytical tools, receptor-specific agonists and antagonists, high-resolution in vivo and ex vivo imaging and the development of tissue (cell) -specific ablation mouse models, to paint a more detailed picture of the regulation and actions of GHRH.
View Article and Find Full Text PDFInt J Obes (Lond)
January 2025
Department of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston Salem, NC, 27101, USA.
Previous studies have identified G protein-coupled receptor (GPCR) kinase 5 (GRK5) as a genetic factor contributing to obesity pathogenesis, but the underlying mechanism remains unclear. We demonstrate here that Grk5 mRNA is more abundant in stromal vascular fractions of mouse white adipose tissue, the fraction that contains adipose progenitor cells, or committed preadipocytes, than in adipocyte fractions. Thus, we generated a GRK5 knockout (KO) 3T3-L1 preadipocyte to further investigate the mechanistic role of GRK5 in regulating adipocyte differentiation.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Traditional Chinese Medicine Integrated Department of Nephrology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China; Research Institute of Nephrology, Zhengzhou University, Zhengzhou, Henan province, China; Henan Province Research Center for Kidney Disease, Zhengzhou, Henan Province, China; Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province, Zhengzhou, Henan Province, China; Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, China; Innovation Center of Basic Research for Metabolic-Associated Fatty Liver Disease, Ministry of Education of China, Zhengzhou, Henan Province, China. Electronic address:
Acute kidney injury (AKI) involves a series of syndromes characterized by a rapid increase in creatinine levels. Ferroptosis, as an iron-dependent mode of programmed cell death, reportedly participates in the pathogenesis of AKI. Methyltransferase-like 3 (METTL3)-mediated m6A modification has been recently associated with various kidney diseases; however, the mechanism of METTL3 crosstalk with the molecules involved in ferroptosis is not clearly understood.
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