The interference of adrenal hormones with the oestradiol-induced modifications of endocrine pancreatic function remains controversial. For this reason, we compared sham-operated, ovariectomized and adrenalectomized-ovariectomized female rats. In each group, control and 17-beta-oestradiol-treated rats (0.1 mg/day for 14 days) were studied, the latter group being compared with similar rats treated with corticosterone (0.4 mg/day). Oestradiol treatment induced hypoglycaemia and hyperinsulinism in basal and glucose-stimulated states, and hypoglucagonaemia. The presence of adrenal glands was necessary for the full expression of oestradiol effects on pancreatic islet B cells: in adrenalectomized-ovariectomized rats, oestradiol treatment induced an unexpected decrease in insulin response to intravenous glucose, and in pancreatic insulin content. Corticosterone treatment partly restored the oestradiol-induced rise of plasma insulin, and restored the B cell response to intravenous glucose. A permissive action of glucocorticoids may be a prerequisite for the effect of oestrogens on B cells. Since oestrogens by themselves augment the plasma corticosterone level, the insulinotropic effect of oestrogens may be partly mediated by the increase in endogenous corticosteroids. In contrast, oestradiol seems to suppress islet A cell function.
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http://dx.doi.org/10.1007/BF00297394 | DOI Listing |
J Gastroenterol
January 2025
Department of Gastroenterological, Breast and Endocrine Surgery, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Elife
January 2025
Neurobiology and Genetics, Theodor-Boveri-Institute, Biocenter, Julius-Maximilians-University of Würzburg, Würzburg, Germany.
Insulin plays a key role in metabolic homeostasis. insulin-producing cells (IPCs) are functional analogues of mammalian pancreatic beta cells and release insulin directly into circulation. To investigate the in vivo dynamics of IPC activity, we quantified the effects of nutritional and internal state changes on IPCs using electrophysiological recordings.
View Article and Find Full Text PDFIntroduction: Type 1 diabetes is often accompanied by autoimmune thyroid disease. We aimed to investigate the clinical characteristics of Japanese patients with acute-onset type 1 diabetes and thyroid autoantibodies, focusing on decreased endogenous insulin secretion.
Materials And Methods: We examined 80 patients with acute-onset type 1 diabetes, classifying them into two groups with and without thyroid autoantibodies and compared the clinical characteristics of the two groups.
Cell Mol Life Sci
January 2025
Department of Endocrinology, Central South University Third Xiangya Hospital, Changsha, China.
Pancreatic β-cell damage is a critical pathological mechanism in the progression of obese type 2 diabetes mellitus (T2DM). However, the exact underlying mechanism remains unclear. We established an obese T2DM mouse model via high-fat diet feeding.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
January 2025
Université Paris Cité, Institut Cochin, CNRS, INSERM, Paris, France.
Context: Type 1 diabetes (T1D) is characterized by the presence of autoantibodies on a genetic background largely determined by HLA class II haplotypes. Stage 1 T1D is characterized by the presence of multiple autoantibodies and normoglycemia.
Objective: To investigate the prevalence of high-risk HLA-DQB1 haplotypes and the extent of islet autoimmunity in pancreatic tissues from non-diabetic organ donors with autoantibodies.
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