Somatic hybridization was employed for obtaining 335 hybridomas producing monoclonal antibodies to insulin. Twelve hybridomas were cloned by a method of maximum dilutions, and specific immunoglobulins, secreted by them, were characterized by solid phase immunoenzyme assay. Monoclonal antibodies possessed different activity with relation to human, porcine and cattle insulins, indicating their specificity to different epitopes on the insulin molecule. Antibodies of IN-2 and IN-3 clones were capable of inhibiting insulin biological activity in vivo. In experiments on rabbits antibodies of IN-2 clone decreased a 3-fold insulin hypoglycemic action, and antibodies of IN-3 clone caused an increase in the life span of mice after administration of insulin at high doses to them.
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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 PDFMetabolites
January 2025
Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, 40-752 Katowice, Poland.
Untreated hyperprolactinemia and autoimmune thyroiditis (Hashimoto's disease) seem to increase cardiometabolic risk. The cardiometabolic effects of cabergoline were less significant in young women with concurrent euthyroid Hashimoto's illness. This study sought to investigate if the detrimental effects of this condition on cabergoline efficacy are also evident in postmenopausal women.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Section on Growth and Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD, United States.
Recombinant human IGF-1 is used to treat severe primary IGF-1 deficiency, but this treatment requires twice-daily injection, often does not fully correct the growth deficit, and has important off-target effects. We therefore sought to target IGF-1 to growth plate cartilage by generating fusion proteins combining IGF-1 with single-chain human antibody fragments that target matrilin-3, a cartilage matrix protein. We previously showed that this cartilage-targeting IGF-1 fusion protein (CV1574-1) promoted growth plate function in a GH-deficient (lit) mouse model.
View Article and Find Full Text PDFDiabetologia
January 2025
Department of Chemical and Biological Engineering, Colorado School of Mines, Golden, CO, USA.
Type 1 diabetes is an autoimmune disease characterised by the destruction of pancreatic beta cells, resulting in lifelong insulin dependence. Although exogenous insulin can maintain glycaemic control, this approach does not protect residual or replacement pancreatic beta cells from immune-mediated death. Current therapeutics designed to protect functional beta cell mass or promote beta cell proliferation and regeneration can have off-target effects, resulting in higher dose requirements and adverse side effects.
View Article and Find Full Text PDFCirc 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.
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