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In JoVE (1)
Other Publications (2)
Articles by Thomas A. Lutz in JoVE
JoVE Clinical and Translational Medicine
Roux-en-Y Gastric Bypass Operation in Rats
1Department of Surgery, University Hospital Zürich, 2Zürich Centre for Integrative Human Physiology, University of Zürich, 3Institute of Veterinary Physiology, Vetsuisse Faculty, University of Zürich, 4Imperial Weight Centre, Department of Investigative Medicine, Imperial College London
Numerous studies using gastric bypass rat models have been recently conducted to uncover the underlying physiological mechanisms of Roux-en-Y gastric bypass operations. This article aims to demonstrate and discuss the technical and experimental details of our published gastric bypass rat model to understand advantages and limitations of this experimental tool.
Other articles by Thomas A. Lutz on PubMed
Biological Importance of the Peptides of the Calcitonin Family As Revealed by Disruption and Transfer of Corresponding Genes
The hormone calcitonin (CT) of thyroid C-cell origin, the neuropeptides alpha- and beta-calcitonin gene-related peptide (CGRP), the widely expressed hormone and tissue factor adrenomedullin (AM), and amylin (AMY) that is co-produced with insulin in pancreatic beta-cells, are structurally related peptides. They have in common six or seven amino acid ring structures, linked by disulfide bridges between cysteine residues, and amidated carboxyl termini that are both required for biological activity. The actions of the peptides in vivo have traditionally been studied after intravenous and intracerebroventricular administration. As a result, CT lowers serum calcium and reduces pain perception. alpha- and beta CGRP and AM are highly potent vasodilatory peptides. AMY inhibits food intake through its action in the area postrema of the brain. Physiological actions of the peptides summarized in the present review have been defined through gene knockout and overexpression strategies.
Feline Pancreatic Islet-like Clusters and Insulin Producing Cells Express Functional Toll-like Receptors (TLRs)
Toll-like receptors (TLRs) are cellular receptors that recognize molecules derived from pathogens, endogenous molecules generated after cellular stress, and free fatty acids. TLR activation leads to a proinflammatory reaction that is fundamental in the initiation of an innate immune response and subsequent adaptive responses but also can damage tissues. TLRs are not only expressed within the immune system, but also in most other organ systems including the pancreas. TLR4 is expressed in pancreatic β-cells of rodents and humans and its stimulation affects insulin secretion in response to glucose. A low-grade inflammation is often associated with disturbed performance of β-cells and insulin resistance, the cardinal metabolic event of type-2 diabetes. Feline diabetes mellitus shares many similarities with type-2 diabetes in humans. Our objective was to elucidate the role of TLRs in feline pancreatic islets and islet-like clusters (ILC) that consist of islets with their adjacent tissue. We tested whether TLRs are triggered by their agonists and lead to the expression of inflammatory cytokines. We confirmed the expression of all known feline TLRs in pancreas and ILC. Furthermore, stimulation with TLR agonists increased IL-6 mRNA and protein content and the expression of other proinflammatory cytokines indicating a clear proinflammatory response. The reactivity to TLR ligands was stronger in β-cell enriched populations obtained after sorting by FACS indicating that inflammatory stimuli can also be generated within β-cells. We conclude that the microenvironment of feline β-cells harbor the potential for inflammatory reactions, that can be initiated by molecules released from bacteria or viruses or other molecules recognized by TLRs. Therefore infections associated with bacteriemia and viremia can induce inflammation in islets and damage the endocrine pancreatic tissue.
