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Hereditary hemochromatosis occurs due to genetic mutations, namely, cysteine-to-tyrosine substitution at amino acid 282 (C282Y) and histidine-to-aspartic acid substitution at 63 (H63D) mutations. The role of H63D mutation in hemochromatosis is less clear, and its penetrance is low even in homozygotes. Therefore, iron overload in H63D heterozygotes is extremely rare and scarcely reported.

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Synthesis of Alkyl α-Amino-benzylphosphinates by the Aza-Pudovik Reaction; The Preparation of the Butyl Phenyl--phosphinate Starting P-Reagent.

Molecules

January 2025

Department of Organic Chemistry and Technology, Faculty of Chemical Technology and Biotechnology, Budapest University of Technology and Economics, Műegyetem rkp. 3, 1111 Budapest, Hungary.

Butyl phenyl--phosphinate that is not available commercially was prepared from phenyl--phosphinic acid by three methods: by alkylating esterification (i), by microwave-assisted direct esterification (ii), and unexpectedly, by thermal esterification (iii). Considering the green aspects, selectivity and scalability, the thermal variation seemed to be optimal. However, there was need for prolonged heating.

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A comprehensive atlas of multi-tissue metabolome and microbiome shifts: Exploring obesity and insulin resistance induced by perinatal bisphenol S exposure in high-fat diet-fed offspring.

J Hazard Mater

December 2024

College of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, China; Research Unit Analytical BioGeoChemistry, Helmholtz Munich, Neuherberg 85764, Germany; Xiamen Key Laboratory of Marine Functional Food, Xiamen 361021, China. Electronic address:

Bisphenol S (BPS) is widely used as a substitute for Bisphenol A (BPA). While perinatal BPS exposure is suspected to increase susceptibility to high-caloric diet-induced adipogenesis, how BPS affects offspring remains largely unknown. This study explored effects of prenatal BPS exposure on adiposity and insulin resistance in high-fat diet (HFD)-fed C57BL/6 offspring, revealing significant changes in body weight, glucose tolerance, insulin sensitivity, and histopathology.

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Introduction: The progression of type 2 diabetes in humans appears to be linked to the loss of insulin-producing β-cells. One of the major contributors to β-cell loss is the formation of toxic human IAPP amyloid (hIAPP, Islet Amyloid Polypeptide, amylin) in the pancreas. Inhibiting the formation of toxic hIAPP amyloid could slow, if not prevent altogether, the progression of type 2 diabetes.

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Article Synopsis
  • Recent advancements in food safety have prompted this study to develop better predictive models for the effects of food additives like sugar substitutes and pigments on human health.
  • The research introduces a pancreas islet-on-a-chip system that maintains high cell viability and promotes growth in a dynamic 3D cell culture environment, significantly enhancing factors important for islet development.
  • Results indicate that unlike sugar substitutes erythritol and sucralose, certain treatments like GLP-1 and curcumin notably increase insulin secretion, paving the way for innovative evaluations of food additives and diabetes treatments.
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