uu.seUppsala University Publications
Change search
Link to record
Permanent link

Direct link
BETA
Andersson, Arne
Alternative names
Publications (10 of 33) Show all publications
Westermark, G. T., Oskarsson, M., Andersson, A. & Westermark, P. (2015). Eighty years of research on islet amyloidosis in Uppsala. Upsala Journal of Medical Sciences, 120(2), 117-123
Open this publication in new window or tab >>Eighty years of research on islet amyloidosis in Uppsala
2015 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 120, no 2, p. 117-123Article in journal (Refereed) Published
Keywords
Alzheimer's disease, amyloid, IAPP, senile amyloidosis, type 2 diabetes
National Category
Other Medical Sciences not elsewhere specified
Identifiers
urn:nbn:se:uu:diva-255284 (URN)10.3109/03009734.2015.1037032 (DOI)000353920500009 ()25903284 (PubMedID)
Available from: 2015-06-22 Created: 2015-06-15 Last updated: 2017-12-04Bibliographically approved
Andersson, A. & Börjesson, J. L. (2015). Operating in an era of impact factor mania. Upsala Journal of Medical Sciences, 120(2), 124-131
Open this publication in new window or tab >>Operating in an era of impact factor mania
2015 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 120, no 2, p. 124-131Article in journal, Editorial material (Other academic) Published
National Category
Medical and Health Sciences Information Studies
Identifiers
urn:nbn:se:uu:diva-257305 (URN)10.3109/03009734.2015.1034899 (DOI)000353920500010 ()25872663 (PubMedID)
Available from: 2015-07-02 Created: 2015-07-01 Last updated: 2017-12-04Bibliographically approved
Andersson, A. & Ronquist, G. (2012). A substantial increase of the impact factor. Upsala Journal of Medical Sciences, 117(4), 353-354
Open this publication in new window or tab >>A substantial increase of the impact factor
2012 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 117, no 4, p. 353-354Article in journal, Editorial material (Refereed) Published
National Category
Other Medical Sciences not elsewhere specified
Identifiers
urn:nbn:se:uu:diva-220585 (URN)10.3109/03009734.2012.725511 (DOI)23110366 (PubMedID)
Available from: 2014-03-17 Created: 2014-03-17 Last updated: 2017-12-05Bibliographically approved
Westermark, G. T., Davalli, A. M., Secchi, A., Folli, F., Kin, T., Toso, C., . . . Westermark, P. (2012). Further Evidence for Amyloid Deposition in Clinical Pancreatic Islet Grafts. Transplantation, 93(2), 219-223
Open this publication in new window or tab >>Further Evidence for Amyloid Deposition in Clinical Pancreatic Islet Grafts
Show others...
2012 (English)In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 93, no 2, p. 219-223Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The reasons for the long-term complete or partial loss of islet graft function are unknown, but there are obviously other reasons than just pure allogeneic graft rejection. Earlier studies have shown that deposition of islet amyloid polypeptide amyloid in transplanted islets may indicate a mechanism for loss of β cells.

MATERIALS AND METHODS: Sections from liver material from four deceased islet-bearing recipients have been scrutinized for the presence of amyloid. Clinical data and certain aspects of the islet graft pathology of these patients have been published previously.

RESULT: With this extended histological analysis, we demonstrate the occurrence of amyloid deposits in islets transplanted into the liver in three of four patients with type 1 diabetes.

CONCLUSION: The finding adds evidence to the assumption that aggregation of islet amyloid polypeptide might be an important cause of progressing β-cell dysfunction in clinically transplanted islets.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-165755 (URN)10.1097/TP.0b013e31823e46ef (DOI)000299164000019 ()22193043 (PubMedID)
Available from: 2012-01-09 Created: 2012-01-09 Last updated: 2017-12-08Bibliographically approved
Westermark, P., Andersson, A. & Westermark, G. T. (2011). Islet amyloid polypeptide, islet amyloid, and diabetes mellitus. Physiological Reviews, 91(3), 795-826
Open this publication in new window or tab >>Islet amyloid polypeptide, islet amyloid, and diabetes mellitus
2011 (English)In: Physiological Reviews, ISSN 0031-9333, E-ISSN 1522-1210, Vol. 91, no 3, p. 795-826Article, review/survey (Refereed) Published
Abstract [en]

Islet amyloid polypeptide (IAPP, or amylin) is one of the major secretory products of beta-cells of the pancreatic islets of Langerhans. It is a regulatory peptide with putative function both locally in the islets, where it inhibits insulin and glucagon secretion, and at distant targets. It has binding sites in the brain, possibly contributing also to satiety regulation and inhibits gastric emptying. Effects on several other organs have also been described. IAPP was discovered through its ability to aggregate into pancreatic islet amyloid deposits, which are seen particularly in association with type 2 diabetes in humans and with diabetes in a few other mammalian species, especially monkeys and cats. Aggregated IAPP has cytotoxic properties and is believed to be of critical importance for the loss of beta-cells in type 2 diabetes and also in pancreatic islets transplanted into individuals with type 1 diabetes. This review deals both with physiological aspects of IAPP and with the pathophysiological role of aggregated forms of IAPP, including mechanisms whereby human IAPP forms toxic aggregates and amyloid fibrils.

National Category
Endocrinology and Diabetes Physiology
Identifiers
urn:nbn:se:uu:diva-156827 (URN)10.1152/physrev.00042.2009 (DOI)000292724700001 ()21742788 (PubMedID)
Available from: 2011-08-11 Created: 2011-08-09 Last updated: 2018-01-12Bibliographically approved
Andersson, A. (Ed.). (2009). Department of Medical Cell Biology: Annual Report 2008. Uppsala: Institutionen för medicinsk cellbiologi, Uppsala universitet
Open this publication in new window or tab >>Department of Medical Cell Biology: Annual Report 2008
2009 (English)Collection (editor) (Other (popular science, discussion, etc.))
Place, publisher, year, edition, pages
Uppsala: Institutionen för medicinsk cellbiologi, Uppsala universitet, 2009. p. 52
Series
Annual Reports - Department of Medical Cell Biology
Keywords
Annual report
National Category
Cell and Molecular Biology Physiology
Research subject
Medical Cell Biology
Identifiers
urn:nbn:se:uu:diva-186262 (URN)
Available from: 2012-11-29 Created: 2012-11-28 Last updated: 2018-01-12Bibliographically approved
Höglund, E., Mattsson, G., Tyrberg, B., Andersson, A. & Carlsson, C. (2009). Growth Hormone Increases Beta-Cell Proliferation in Transplanted Human and Fetal Rat Islets. Journal of the Pancreas, 10(3), 242-248
Open this publication in new window or tab >>Growth Hormone Increases Beta-Cell Proliferation in Transplanted Human and Fetal Rat Islets
Show others...
2009 (English)In: Journal of the Pancreas, ISSN 1590-8577, E-ISSN 1590-8577, Vol. 10, no 3, p. 242-248Article in journal (Refereed) Published
Abstract [en]

Objective The aim of the study was to increase the number of human islet beta-cells after transplantation with injections of human growth hormone (hGH).

 

Interventions Human islets and fetal rat islets were transplanted under the left kidney capsule and under the right kidney capsule, respectively in nude normoglycemic mice which were then given a daily injection of 200 µg hGH for 1-4 weeks.

 

Main outcome measure Beta-cell proliferation was determined using thymidine incorporation and the beta-cell area was assessed using light microscopy.

 

Results Mice given hGH increased their body weight one week after transplantation and had a more efficient removal of glucose after 3 and 4 weeks. Treatment with hGH resulted in increased beta-cell proliferation in human and fetal rat beta-cells, and the beta-cell area tended to increase. However, serum insulin concentrations and pancreas insulin content remained unchanged.

 

Conclusions hGH increased the proliferation of transplanted human beta-cells as well as improving the glucose tolerance of the transplanted mice.

Keywords
Cell Proliferation; Human Growth Hormone; Insulin-Secreting Cells; Islets of Langerhans; Transplantation
National Category
Endocrinology and Diabetes
Research subject
Medical Cell Biology
Identifiers
urn:nbn:se:uu:diva-102206 (URN)
Available from: 2009-05-05 Created: 2009-05-05 Last updated: 2017-12-13Bibliographically approved
Andersson, A. (Ed.). (2008). Department of Medical Cell Biology: Annual Report 2007. Uppsala: Institutionen för medicinsk cellbiologi, Uppsala universitet
Open this publication in new window or tab >>Department of Medical Cell Biology: Annual Report 2007
2008 (English)Collection (editor) (Other (popular science, discussion, etc.))
Place, publisher, year, edition, pages
Uppsala: Institutionen för medicinsk cellbiologi, Uppsala universitet, 2008. p. 57
Series
Annual Reports - Department of Medical Cell Biology
Keywords
Annual report
National Category
Cell and Molecular Biology Physiology
Research subject
Medical Cell Biology
Identifiers
urn:nbn:se:uu:diva-186263 (URN)
Available from: 2012-11-29 Created: 2012-11-28 Last updated: 2018-01-12Bibliographically approved
Andersson, A., Eriksson, U. ., Jansson, L., Sandler, S., Welsh, M. & Welsh, N. (2007). Claes Hellerström: a friendly islet explorer. Diabetologia, 50(2), 4 p following 496
Open this publication in new window or tab >>Claes Hellerström: a friendly islet explorer
Show others...
2007 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 50, no 2, p. 4 p following 496-Article in journal (Refereed) Published
Keywords
History; 20th Century, History; 21st Century, Humans, Islets of Langerhans/*cytology, Male, Microdissection, Pathology/history, Portraits
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-12006 (URN)17823989 (PubMedID)
Available from: 2007-11-16 Created: 2007-11-16 Last updated: 2017-12-11Bibliographically approved
Lai, E. Y., Persson, A. E., Bodin, B., Källskog, Ö., Andersson, A., Pettersson, U., . . . Jansson, L. (2007). Endothelin-1 and pancreatic islet vasculature: studies in vivo and on isolated, vascularly perfused pancreatic islets. American Journal of Physiology. Endocrinology and Metabolism, 292(6), E1616-E1623
Open this publication in new window or tab >>Endothelin-1 and pancreatic islet vasculature: studies in vivo and on isolated, vascularly perfused pancreatic islets
Show others...
2007 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 292, no 6, p. E1616-E1623Article in journal (Refereed) Published
Abstract [en]

Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor, which also stimulates insulin release. The aim of the present study was to evaluate whether exogenously administered ET-1 affected pancreatic islet blood flow in vivo in rats and the islet arteriolar reactivity in vitro in mice. Furthermore, we aimed to determine the ET-receptor subtype that was involved in such responses. When applying a microsphere technique for measurements of islet blood perfusion in vivo, we found that ET-1 (5 nmol/kg) consistently and markedly decreased total pancreatic and especially islet blood flow, despite having only minor effects on blood pressure. Neither endothelin A (ET(A)) receptor (BQ-123) nor endothelin-B (ET(B)) receptor (BQ-788) antagonists, alone or in combination, could prevent this reduction in blood flow. To avoid confounding interactions in vivo, we also examined the arteriolar vascular reactivity in isolated, perfused mouse islets. In the latter preparation, we demonstrated a dose-dependent constriction in response to ET-1. Administration of BQ-123 prevented this, whereas BQ-788 induced a right shift in the response. In conclusion, the pancreatic islet vasculature is highly sensitive to exogenous ET-1, which mediates its effect mainly through ET(A) receptors.

Keywords
Adrenal Glands/blood supply, Animals, Arterioles/physiology, Blood Glucose/metabolism, Blood Pressure/drug effects, Colon/blood supply, Drug Synergism, Duodenum/blood supply, Endothelin-1/*pharmacology, Insulin/blood, Islets of Langerhans/*blood supply, Male, Mice, Mice; Inbred C57BL, Oligopeptides/pharmacology, Pancreas/blood supply, Peptides; Cyclic/pharmacology, Piperidines/pharmacology, Rats, Rats; Sprague-Dawley, Receptor; Endothelin A/antagonists & inhibitors, Receptor; Endothelin B/antagonists & inhibitors, Regional Blood Flow/drug effects, Vasoconstriction
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-11911 (URN)10.1152/ajpendo.00640.2006 (DOI)000247939100014 ()17284574 (PubMedID)
Available from: 2007-11-06 Created: 2007-11-06 Last updated: 2017-12-11Bibliographically approved
Organisations

Search in DiVA

Show all publications