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      Brunner's Gland Hyperplasia in a Patient after Roux-Y Gastric Bypass: An Important Pitfall in GLP-1 Receptor Imaging

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          Abstract

          Severe cases of postprandial hypoglycaemia after bariatric surgery can be a diagnostic and therapeutic challenge. The diagnostic role of 68Ga-DOTA-Exendin-4 PET/CT in postbariatric hypoglycaemia for further treatment decisions is unclear. We present a case of a 50-year-old woman with frequent and severe postprandial hypoglycaemic (≤2.5 mmol/L) episodes starting three years after Roux-Y gastric bypass. Despite strict dietary adherence and several medical therapies, the patient remained severely affected, and 68Ga-DOTA-Exendin-4 PET/CT was performed to exclude atypical presentation of an insulinoma or nesidioblastosis. No pancreatic abnormalities were found, but intensive tracer accumulation in the first and second part of the duodenum was detected, which proved to be hyperplastic Brunner's glands on histology and were strongly positive for the glucagon-like peptide-1 receptor. This case provides histopathological verification that duodenal 68Ga-DOTA-Exendin-4 uptake is caused by uptake in Brunner's glands and points to a potential relationship between bariatric surgery and Brunner's glands.

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          GLP-1 receptor expression in human tumors and human normal tissues: potential for in vivo targeting.

          Martin Stöckli, Meike Körner, Jean Claude Reubi … (2007)
          Peptide hormone receptors overexpressed in human tumors, such as somatostatin receptors, can be used for in vivo targeting for diagnostic and therapeutic purposes. A novel promising candidate in this field is the GLP-1 receptor, which was recently shown to be massively overexpressed in gut and lung neuroendocrine tumors--in particular, in insulinomas. Anticipating a major development of GLP-1 receptor targeting in nuclear medicine, our aim was to evaluate in vitro the GLP-1 receptor expression in a large variety of other tumors and to compare it with that in nonneoplastic tissues. The GLP-1 receptor protein expression was qualitatively and quantitatively investigated in a broad spectrum of human tumors (n=419) and nonneoplastic human tissues (n=209) with receptor autoradiography using (125)I-GLP-1(7-36)amide. Pharmacologic competition experiments were performed to provide proof of specificity of the procedure. GLP-1 receptors were expressed in various endocrine tumors, with particularly high amounts in pheochromocytomas, as well as in brain tumors and embryonic tumors but not in carcinomas or lymphomas. In nonneoplastic tissues, GLP-1 receptors were present in generally low amounts in specific tissue compartments of several organs--namely, pancreas, intestine, lung, kidney, breast, and brain; no receptors were identified in lymph nodes, spleen, liver, or the adrenal gland. The rank order of potencies for receptor binding--namely, GLP-1(7-36)amide = exendin-4 > GLP-2 = glucagon(1-29)--provided proof of specific GLP-1 receptor identification. The GLP-1 receptors may represent a novel molecular target for in vivo scintigraphy and targeted radiotherapy for a variety of GLP-1 receptor-expressing tumors. For GLP-1 receptor scintigraphy, a low-background signal can be expected, on the basis of the low receptor expression in the normal tissues surrounding tumors.
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            Oxyntomodulin and glucagon-like peptide-1 differentially regulate murine food intake and energy expenditure.

            Laurie L. Baggio, Daniel Drucker, Qingling Huang … (2004)
            Gut-derived peptides including ghrelin, cholecystokinin (CCK), peptide YY (PYY), glucagon-like peptide (GLP-1), and GLP-2 exert overlapping actions on energy homeostasis through defined G-protein-coupled receptors (GPCRs). The proglucagon-derived peptide (PGDP) oxyntomodulin (OXM) is cosecreted with GLP-1 and inhibits feeding in rodents and humans; however, a distinct receptor for OXM has not been identified. We examined the mechanisms mediating oxyntomodulin action using stable cell lines expressing specific PGDP receptors in vitro and both wild-type and knockout mice in vivo. OXM activates signaling pathways in cells through glucagon or GLP-1 receptors (GLP-1R) but transiently inhibits food intake in vivo exclusively through the GLP-1R. Both OXM and the GLP-1R agonist exendin-4 (Ex-4) activated neuronal c-fos expression in the paraventricular nucleus of the hypothalamus, the area postrema, and the nucleus of the solitary tract following intraperitoneal (i.p.) injection. However, OXM transiently inhibited food intake in wild-type mice following intracerebroventricular (i.c.v.) but not i.p. administration, whereas Ex-4 produced a more potent and sustained inhibition of food intake following both i.c.v. and i.p. administration. The anorectic effects of OXM were preserved in Gcgr(-/-) mice but abolished in GLP-1R(-/-) mice. Although central Ex-4 and OXM inhibited feeding via a GLP-1R-dependent mechanism, Ex-4 but not OXM reduced VO2 and respiratory quotient in wild-type mice. These findings demonstrate that structurally distinct PGDPs differentially regulate food intake and energy expenditure by interacting with a GLP-1R-dependent pathway. Hence ligand-specific activation of a common GLP-1R increases the complexity of gut-central nervous system pathways regulating energy homeostasis and metabolic expenditure.
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              Glucagon-like peptide-1 receptor imaging for localization of insulinomas.

              Helmut R. Maecke, Jean Claude Reubi, Emanuel Christ … (2009)
              The surgical removal of insulinomas is hampered by difficulties to localize it using conventional radiological procedures. Recently these tumors were shown to exhibit a very high density of glucagon-like peptide-1 receptors (GLP-1R) in vitro that may be used as specific targets for in vivo receptor radiolabeling. The objective of the study was to test the 111In-labeled GLP-1R agonist 111In-DOTA-exendin-4 in localizing insulinomas using single photon emission computed tomography in combination with computed tomography images. This was a prospective open-label investigation. The study was conducted at three tertiary referral centers in Switzerland. Patients included six consecutive patients with proven clinical and biochemical endogenous hyperinsulinemic hypoglycemia. (111)In-DOTA-exendin-4 was administered iv at a dose of about 90 MBq (30 microg peptide) over 5 min. Whole-body planar images of the abdomen were performed at 20 min, 4 h, 23 h, 96 h, and up to 168 h after injection. After surgical removal of the insulinomas, GLP-1R expression was assessed in the tumor tissue in vitro by GLP-1R autoradiography. The detection rate of insulinomas was measured. In all six cases, the GLP-1R scans successfully detected the insulinomas identified using conventional methods in four cases. By using a gamma-probe intraoperatively, GLP-1R detection permitted a successful surgical removal of the tumors in all patients, diagnosed histopathologically as five pancreatic and one extrapancreatic insulinomas. In vitro GLP-1R autoradiography showed a high density of GLP-1R in all tested insulinomas. In vivo GLP-1R imaging is an innovative, noninvasive diagnostic approach that successfully localizes small insulinomas pre- and intraoperatively and that may in the future affect the strategy of insulinoma localization.
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                Author and article information

                Contributors
                Emanuel R. Christ:
                ORCID: https://orcid.org/0000-0002-5604-4606
                Journal
                Journal ID (nlm-ta): Case Rep Endocrinol
                Journal ID (iso-abbrev): Case Rep Endocrinol
                Journal ID (publisher-id): CRIE
                Title: Case Reports in Endocrinology
                Publisher: Hindawi
                ISSN (Print): 2090-6501
                ISSN (Electronic): 2090-651X
                Publication date Collection: 2020
                Publication date (Electronic): 3 April 2020
                Volume: 2020
                Electronic Location Identifier: 4510910
                Affiliations
                1Division of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Petersgraben 4, 4053 Basel, Switzerland
                2Clinic of Endocrinology, Cantonal Hospital Olten, Basler Strasse 150, 4600 Olten, Switzerland
                3Division of Nuclear Medicine, University Hospital Basel, Petersgraben 4, 4053 Basel, Switzerland
                4Institute of Pathology, University of Berne, Berne, Switzerland
                5Center for Neuroendocrine and Endocrine Tumors, University Hospital Basel, Petersgraben 4, 4053 Basel, Switzerland
                Author notes

                Academic Editor: J. Paul Frindik

                Author information
                https://orcid.org/0000-0002-6905-6235
                https://orcid.org/0000-0002-5604-4606
                Article
                DOI: 10.1155/2020/4510910
                PMC ID: 7160728
                PubMed ID: 32313706
                SO-VID: 4cd2028f-71d8-47b3-8cf8-30b98360aa6d
                Copyright © Copyright © 2020 Matthias Hepprich et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 December 2019
                Date revision received : 10 February 2020
                Date accepted : 20 February 2020
                Funding
                Funded by: Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
                Award ID: 320030
                Award ID: 152938
                Funded by: Desirée and Niels Yde's Foundation
                Award ID: 389-12
                Categories
                Subject: Case Report

                Data availability:

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