Glucagon has been suggested to be a mediator of intra-islet paracrine effect of insulin and somatostatin during nutritive stimulation. The aim of this study was to reveal possible intra-islet interactions between insulin, somatostatin and glucagon in a batch stimulation model with isolated pancreatic islets. Such interactions may influence stimulus-secretion experiments in this experimental model. In our hands arginine stimulated somatostatin secretion only in the presence of insulin antiserum. Furthermore, arginine-induced glucagon secretion was greatly increased following addition of insulin antiserum. The addition of glucagon antiserum inhibited these effects of insulin antiserum on somatostatin secretion. In conclusion, glucagon apparently represents the central mediator of arginine effects on somatostatin secretion in isolated rat pancreatic islets in batch stimulation experiments.
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http://dx.doi.org/10.3109/00365519209088773 | DOI Listing |
Background: A significant proportion of individuals maintain healthy cognitive function despite having extensive Alzheimer's disease (AD) pathology, known as cognitive resilience. Understanding the molecular mechanisms that protect these individuals can identify therapeutic targets for AD dementia. This study aims to define molecular and cellular signatures of cognitive resilience, protection and resistance, by integrating genetics, bulk RNA, and single-nucleus RNA sequencing data across multiple brain regions from AD, resilient, and control individuals.
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January 2025
1 Pécsi Tudományegyetem, Általános Orvostudományi Kar, Klinikai Központ, Aneszteziológiai és Intenzív Terápiás Intézet Pécs, Ifjúság u. 13., 7624 Magyarország.
Life (Basel)
January 2025
Laboratory of Nervous System Development, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution "Petrovsky National Research Centre of Surgery", Tsurupi Street, 3, 117418 Moscow, Russia.
Type 1 diabetes (T1D) is related to the autoimmune destruction of β-cells, leading to their almost complete absence in patients with longstanding T1D. However, endogenous insulin secretion persists in such patients as evidenced by the measurement of plasma C-peptide. Recently, a low level of insulin has been found in non-β islet cells of patients with longstanding T1D, indicating that other islet cell types may contribute to persistent insulin secretion.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Endocrinology Unit, Department of Internal Medicine and Medical Specialties, School of Medical and Pharmaceutical Sciences, University of Genova, 16132 Genova, Italy.
Acromegaly is a rare endocrine disorder caused by excessive growth hormone (GH) production, due, in the vast majority of cases, to the presence of a GH-secreting pituitary tumour. The chronic elevation of GH and the resulting high circulating levels of insulin-like growth factor-1 (IGF-1) cause the characteristic tissue overgrowth and a number of associated comorbidities, including several metabolic changes, such as glucose intolerance and overt diabetes mellitus (DM). Elevated GH concentrations directly attenuate insulin signalling and stimulate lipolysis, decreasing glucose uptake in peripheral tissues, thus leading to the development of impaired glucose tolerance and DM.
View Article and Find Full Text PDFFront Oncol
January 2025
Department of Nuclear Medicine, Mount Sinai Hospital at Icahn School of Medicine, New York, NY, United States.
Peptide receptor radionuclide therapy (PRRT) is used for the management of neuroendocrine tumors (NETs) not responsive to somatostatin analogs. In this case series, we report two patients with pancreatic vasoactive intestinal peptide (VIP)-secreting NETs (VIPomas) not responsive to any other therapies who achieved symptomatic control and a significant decrease in serum VIP levels with PRRT during their hospital stay. Two patients with VIPomas were admitted to the hospital with multiple prior hospital admissions after going through multiple lines of therapy.
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