10 compounds from the 2.4- and 3.4-difluorinated phenylethanol-amines series were tested for their antagonistic action against a hyperglycemia induced by catecholamines in rats, and the ED50 and AD50 values were determined. All the substances acted beta-adrenolytically, with the glycogenolysis enhanced by isoproterenol being blocked more potently by 3.4-difluorophenylethanolamines than by the corresponding 2.4-difluoroderivatives. An exception in the series is 2.4-difluoro-n-butylnoradrenalin, which acts 10fold more beta-adrenolytically than the 3.4-difluoroderivative, and has 3 times the effect of the comparative substance dichloroisoproterenol.
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Pharmacol Rep
January 2025
Department of Gynaecological Oncology, Poznań University Clinical Hospital, Szamarzewskiego 84, Poznań, Poland.
Background: Olaparib is a relatively new poly(ADP-ribose) polymerase inhibitor (PARPi) administered to ovarian cancer (OC) patients with a complete or partial response to first-line chemotherapy. One of the metabolic side effects of olaparib is the disruption of glucose homeostasis, often resulting in hyperglycemia The study was a retrospective analysis of olaparib-induced hyperglycemia in OC patients with initial normoglycemia following the first, second, and third month of olaparib treatment METHODS: The study involved 32 OC patients, classified into three groups according to their Body Mass Index (BMI): normal BMI (BMI 18.5-24.
View Article and Find Full Text PDFJ Mol Histol
January 2025
Clinical Pharmacology Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt.
Type 2 diabetes mellitus (T2DM) adversely affects various organs, including the brain and its blood barrier. In addition to the brain, hyperglycemia damages the testes. The testes possess blood-tissue barriers that share common characteristics and proteins with the blood-brain barrier (BBB), including breast cancer-resistant protein (BCRP).
View Article and Find Full Text PDFClin Neuroradiol
January 2025
Department of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Background: Cardiovascular risk management is beneficial, but stringent glycemic control does not prevent the progression of distal sensorimotor polyneuropathy (DSPN). Persistent hyperglycemia-induced alterations and cardiovascular factors may contribute to diabetes-associated nerve damage. This study aimed to evaluate the correlation between skin auto-fluorescence (sAF), an indicator of dermal advanced glycation end-product (AGE) accumulations, cardiovascular risk, and changes in peripheral nerve integrity.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, Pennsylvania 17033. Electronic address:
Increasing evidence supports the role of an augmented immune response in the early development and progression of renal complications caused by diabetes. We recently demonstrated that podocyte-specific expression of stress response protein regulated in development and DNA damage response 1 (REDD1) contributes to activation of the pro-inflammatory transcription factor NF-κB in the kidney of diabetic mice. The studies here were designed to define the specific signaling events whereby REDD1 promotes NF-κB activation in the context of diabetic nephropathy.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Division of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Hyogo, 650-0017, Japan. Electronic address:
The condition in which the insulin secretory ability of pancreatic β-cells decreases in diabetes is extremely important, but there are currently no biomarkers that reflect pancreatic β-cell failure. Therefore, we conducted a search for biomarkers, using pancreatic β-cell-specific 3-Phosphoinositide-dependent protein kinase 1 (PDK1) knockout mice, which develop severe hyperglycemia due to a decrease in pancreatic β-cell mass without insulin resistance. The analysis was performed in young mice when metabolic abnormalities were not yet apparent.
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