15
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Diabetes mellitus remission in three cats with hypersomatotropism after cabergoline treatment

      case-report

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Case summary

          Three diabetic cats presented with polyuria, polydipsia, polyphagia and poor glycemic control. Cat 1 displayed prognathia inferior and had a body condition score (BCS) of 4/5; cat 2 had a BCS of 5/5; and cat 3 had broad facial features. Serum insulin-like growth factor 1 concentrations were compatible with hypersomatotropism in cat 1 and cat 2 (>1500 ng/ml and 1200 ng/ml, respectively) and just below the cut-off of 1000 ng/ml (947 ng/ml) in cat 3; in this last cat diagnosis was further supported by the presence of pituitary enlargement on MRI. Oral cabergoline (10 μg/kg q48h) was initiated. Insulin requirements progressively reduced, as evidenced by daily blood glucose monitoring and weekly blood glucose curves. Diabetic remission occurred in all three cats between the second and third months of cabergoline treatment. At the time of writing, remission has persisted thus far (cat 1: 23 months; cat 2: 14 months; cat 3: 38 months).

          Relevance and novel information

          To our knowledge, these are the first reported cases of diabetic remission in cats with hypersomatotropism after cabergoline treatment, despite previous reports of this being an ineffective treatment. Further work is indicated to determine why some cats do, and others do not, respond to this treatment.

          Related collections

          Most cited references26

          • Record: found
          • Abstract: found
          • Article: not found

          What can we learn from rodents about prolactin in humans?

          Prolactin (PRL) is a 23-kDa protein hormone that binds to a single-span membrane receptor, a member of the cytokine receptor superfamily, and exerts its action via several interacting signaling pathways. PRL is a multifunctional hormone that affects multiple reproductive and metabolic functions and is also involved in tumorigenicity. In addition to being a classical pituitary hormone, PRL in humans is produced by many tissues throughout the body where it acts as a cytokine. The objective of this review is to compare and contrast multiple aspects of PRL, from structure to regulation, and from physiology to pathology in rats, mice, and humans. At each juncture, questions are raised whether, or to what extent, data from rodents are relevant to PRL homeostasis in humans. Most current knowledge on PRL has been obtained from studies with rats and, more recently, from the use of transgenic mice. Although this information is indispensable for understanding PRL in human health and disease, there is sufficient disparity in the control of the production, distribution, and physiological functions of PRL among these species to warrant careful and judicial extrapolation to humans.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Place of cabergoline in acromegaly: a meta-analysis.

            Cabergoline is widely considered to be poorly effective in acromegaly. The aim of this study was to obtain a more accurate picture of the efficacy of cabergoline in acromegaly, both alone and in combination with somatostatin analogs. We systematically reviewed all trials of cabergoline therapy for acromegaly published up to 2009 in four databases (PubMed, Pascal, Embase, and Google Scholar). We identified 15 studies (11 prospective) with a total of 237 patients; none were randomized or placebo-controlled. A meta-analysis was conducted on individual data (n = 227). Cabergoline was used alone in nine studies. Fifty-one (34%) of the 149 patients achieved normal IGF-I levels. In multivariate analysis, the decline in IGF-I was related to the baseline IGF-I concentration (β = 1.16; P <0.001), treatment duration (β = 0.28; P < 0.001), and baseline prolactin concentration (β = -0.18; P = 0.01), and with a trend toward a relation with the cabergoline dose (β = 0.38; P =0.07). In five studies, cabergoline was added to ongoing somatostatin analog treatment that had failed to normalize IGF-I. Forty patients (52%) achieved normal IGF-I levels. The change in IGF-I was significantly related to the baseline IGF-I level (β = 0.74; P < 0.001) but not to the dose of cabergoline, the duration of treatment, or the baseline prolactin concentration. This meta-analysis suggests that cabergoline single-agent therapy normalizes IGF-I levels in one third of patients with acromegaly. When a somatostatin analog fails to control acromegaly, cabergoline adjunction normalizes IGF-I in about 50% of cases. This effect may occur even in patients with normoprolactinemia.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Adaptation of islets of Langerhans to pregnancy: beta-cell growth, enhanced insulin secretion and the role of lactogenic hormones.

              Pregnancy is a unique event in the life span of islet beta-cells. Under the influence of pregnancy islet beta-cells undergo major long term up-regulatory structural and functional changes in response to the increased demand for insulin. Adaptive changes that occur in islets during normal pregnancy include: 1) increased glucose-stimulated insulin secretion with a lowered threshold for glucose-stimulated insulin secretion, 2) increased insulin synthesis, 3) increased beta-cell proliferation and islet volume, 4) increased gap-junctional coupling among beta-cells, 5) increased glucose metabolism, and 6) increased c-AMP metabolism. Of the islet changes that occur during pregnancy the increase in beta-cell division and enhanced glucose sensitivity of insulin secretion are most notable. The increase in beta-cell division leads to an increase in islet mass that contributes to the ability of islets to respond to the increased need for insulin. However, the increased glucose sensitivity of beta-cells is likely to be more important. The lowering of the threshold for glucose stimulated insulin secretion is the primary mechanism by which beta-cells can release significantly more insulin under normal blood glucose concentrations. Although the hormonal changes which occur during pregnancy are complex, it appears that lactogenic influences (either placental lactogen and/or prolactin) are sufficient to induce all of the up-regulatory changes that occur in islets during pregnancy. We have demonstrated that rat placental lactogens I and II are the hormones responsible for up-regulating islets during rodent pregnancy. Although most studies have been done using rodent islets, available evidence strongly suggests that human placental lactogen and/or human prolactin are the responsible lactogens for up-regulating islets during human pregnancy. A model for how lactogens up-regulate islets during pregnancy is proposed.
                Bookmark

                Author and article information

                Journal
                JFMS Open Rep
                JFMS Open Rep
                JOR
                spjor
                JFMS Open Reports
                SAGE Publications (Sage UK: London, England )
                2055-1169
                31 May 2021
                Jan-Jun 2021
                : 7
                : 1
                : 20551169211018991
                Affiliations
                [1 ]Endocrinology Unit, Hospital School of Veterinary Medicine, University of Buenos Aires, Buenos Aires, Argentina
                [2 ]Laboratory of Molecular Endocrinology and Signal Transduction, Institute of Experimental Biology and Medicine – CONICET, Buenos Aires, Argentina
                [3 ]Cardiology Unit, Hospital School of Veterinary Medicine, University of Buenos Aires, Buenos Aires, Argentina
                [4 ]Department of Clinical Science and Services, The Royal Veterinary Collage, Hatfield, UK
                [5 ]Veterinary Specialist Consultations, Hilversum, The Netherlands
                Author notes
                [*]Diego D Miceli DVM, PhD, Res-CONICET, Endocrinology Unit, Hospital School of Veterinary Medicine, University of Buenos Aires, Faculty of Veterinary Sciences, Buenos Aires, Argentina, and Laboratory of Molecular Endocrinology and Signal Transduction, Institute of Experimental Biology and Medicine – CONICET, Chorroarin 280, Buenos Aires 1427, Argentina Email: dmiceli@ 123456fvet.uba.ar
                Article
                10.1177_20551169211018991
                10.1177/20551169211018991
                8186120
                f91ea84d-ef35-455c-9f5d-dc81296b15d8
                © The Author(s) 2021

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Categories
                Case Report
                Custom metadata
                January-June 2021
                ts1

                diabetes mellitus remission,hypersomatotropism,acromegaly,cabergoline,insulin resistance

                Comments

                Comment on this article