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Chronic inorganic nitrate supplementation does not improve metabolic health and worsens disease progression in mice with diet-induced obesity.
Am J Physiol Endocrinol Metab
December 2024
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 3EG, UK.
Inorganic nitrate (NO) has been proposed to be of therapeutic use as a dietary supplement in obesity and related conditions including the Metabolic Syndrome (MetS), type-II diabetes and metabolic dysfunction associated steatotic liver disease (MASLD). Administration of NO to endothelial nitric oxide synthase-deficient mice reversed aspects of MetS, however the impact of NO supplementation in diet-induced obesity is not well understood. Here we investigated the whole-body metabolic phenotype and cardiac and hepatic metabolism in mice fed a high-fat high-sucrose (HFHS) diet for up to 12-months of age, supplemented with 1 mM NaNO (or NaCl) in their drinking water.
View Article and Find Full Text PDFPharmacological induction of diabetes mellitus in pregnant female mice: a comparison of two doses and routes of administration.
Eur Rev Med Pharmacol Sci
April 2024
Laboratorio de Investigación en Nutrición, Facultad de Medicina, Universidad Autónoma del Estado de México, Paseo Tollocan esquina Jesús Carranza S/N, Colonia Moderna de la Cruz, Toluca, México.
Unlabelled: OBJECTIVE: This study aimed to compare two routes of administration and different dosages of streptozotocin (STZ) for the pharmacological induction of gestational diabetes mellitus (GDM) in pregnant CD1 females. MATERIALS AND METHODS: 35 female CD1 mice were divided into 5 groups (n = 7). Diabetes mellitus (DM) was induced with STZ by two routes and two doses: 1) Control Group without administration of STZ (CL), 2) Intraperitoneal Group with 200 mg of STZ/Kg of weight (IP200), 3) Intraperitoneal Group with 230 mg of STZ/Kg of weight (IP230), 4) Subcutaneous Group with 200 mg of STZ/Kg of weight (SC200) and 5) Subcutaneous Group with 230 mg of STZ/Kg of weight (SC230).
View Article and Find Full Text PDFHLA-DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients.
J Diabetes
July 2023
Indian Council of Medical Research (ICMR)-National Institute of Pathology, Safdarjung Hospital Campus, New Delhi, India.
Aim: We planned this study to identify diabetogenic glutamic acid decarboxylase (GAD65) peptides possibly responsible for human leucocyte antigen (HLA)-DR3/DQ2-mediated activation of GAD65-specific CD4 T cells in type 1 diabetes (T1D).
Methods: Top 30 GAD65 peptides, found to strongly bind in silico with HLA-DR3/DQ2 molecules, were selected and grouped into four pools. The peptides were used to stimulate CD4 T cells of study subjects in 16-h peripheral blood mononuclear cell culture.
Glucoregulatory disruption in male mice offspring induced by maternal transfer of endocrine disrupting brominated flame retardants in DE-71.
Front Endocrinol (Lausanne)
April 2023
Department of Molecular, Cell and Systems Biology, University of California Riverside, Riverside, CA, United States.
Introduction: Polybrominated diphenyl ethers (PBDEs) are commercially used flame retardants that bioaccumulate in human tissues, including breast milk. PBDEs produce endocrine and metabolic disruption in experimental animals and have been associated with diabetes and metabolic syndrome (MetS) in humans, however, their sex-specific diabetogenic effects are not completely understood. Our past works show glucolipid dysregulation resulting from perinatal exposure to the commercial penta-mixture of PBDEs, DE-71, in C57BL/6 female mice.
View Article and Find Full Text PDFEffects of statin therapy on glycemic control and insulin resistance: A systematic review and meta-analysis.
Eur J Pharmacol
May 2023
Exercise Physiology Lab at Toledo, Sports Science Department, University of Castilla-La Mancha, 45004, Toledo, Spain. Electronic address:
Aims: To update the evidence about the diabetogenic effect of statins.
Methods: We searched for randomized-controlled trials reporting the effects of statin therapy on glycosylated hemoglobin (HbA1c) and/or homeostatic model insulin resistance (i.e.
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