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Publications (10 of 24) Show all publications
Siraj, E. S., Sjöholm, Å. & Sumner, A. E. (2023). Editorial: Diabetes in Africa in the 21st century: the unique and important challenge of diabetes in Africa, volume II. Frontiers In Public Health, 11, Article ID 1265439.
Open this publication in new window or tab >>Editorial: Diabetes in Africa in the 21st century: the unique and important challenge of diabetes in Africa, volume II
2023 (English)In: Frontiers In Public Health, ISSN 2296-2565, Vol. 11, article id 1265439Article in journal, Editorial material (Refereed) Published
Place, publisher, year, edition, pages
Frontiers, 2023
Keywords
diabetes and malaria; diabetes in Africa; diabetes in underserved; diabetes phenotypes; diabetes risk scores; rural diabetes
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:hig:diva-43015 (URN)10.3389/fpubh.2023.1265439 (DOI)001063363800001 ()37693705 (PubMedID)2-s2.0-85170222517 (Scopus ID)
Available from: 2023-09-15 Created: 2023-09-15 Last updated: 2023-09-29Bibliographically approved
Sjöholm, Å., Corbett, J. A., Leung, P. S. & Portha, B. (2022). Editorial: Understanding the gene expression of β cell dysfunction in diabetes. Frontiers in Endocrinology, 13, Article ID 1069991.
Open this publication in new window or tab >>Editorial: Understanding the gene expression of β cell dysfunction in diabetes
2022 (English)In: Frontiers in Endocrinology, E-ISSN 1664-2392, Vol. 13, article id 1069991Article in journal, Editorial material (Other academic) Published
Place, publisher, year, edition, pages
Frontiers, 2022
National Category
Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-40548 (URN)10.3389/fendo.2022.1069991 (DOI)000890734500001 ()36440197 (PubMedID)2-s2.0-85142644101 (Scopus ID)
Available from: 2022-12-02 Created: 2022-12-02 Last updated: 2024-01-17Bibliographically approved
Sjöholm, Å. (2021). Fulminant diabetes typ 1 – en ny form med snabbt insjuknande. Läkartidningen, 118, Article ID 21004.
Open this publication in new window or tab >>Fulminant diabetes typ 1 – en ny form med snabbt insjuknande
2021 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 118, article id 21004Article in journal (Refereed) Published
National Category
Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-39971 (URN)33788205 (PubMedID)2-s2.0-85103745443 (Scopus ID)
Available from: 2022-09-22 Created: 2022-09-22 Last updated: 2022-09-22Bibliographically approved
Sjöholm, Å. (2021). GAD-65 antibodies in a case of HNF1A-Maturity-Onset Diabetes of the Young: Double diabetes?. Clinical Case Reports, 9(6), Article ID e04151.
Open this publication in new window or tab >>GAD-65 antibodies in a case of HNF1A-Maturity-Onset Diabetes of the Young: Double diabetes?
2021 (English)In: Clinical Case Reports, E-ISSN 2050-0904, Vol. 9, no 6, article id e04151Article in journal (Refereed) Published
Abstract [en]

Diabetes classification is not as defined as it used to be. A patient with one type of diabetes can have diagnostic criteria of another type, which may affect the course of the disease. Clinicians need to consider that when dealing with patients who do not fit the exact description of their diagnosed type of diabetes.

Place, publisher, year, edition, pages
Wiley, 2021
Keywords
autoimmunity, diabetes, GAD-65, MODY
National Category
Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-35796 (URN)10.1002/ccr3.4151 (DOI)000646541600001 ()34194751 (PubMedID)2-s2.0-85105010386 (Scopus ID)
Available from: 2021-05-10 Created: 2021-05-10 Last updated: 2022-03-21Bibliographically approved
Kataja Knight, A., Magnusson, P. & Sjöholm, Å. (2021). Hemiballismus in hyperglycemia. Clinical Case Reports, 9(5), Article ID e04343.
Open this publication in new window or tab >>Hemiballismus in hyperglycemia
2021 (English)In: Clinical Case Reports, E-ISSN 2050-0904, Vol. 9, no 5, article id e04343Article in journal (Refereed) Published
Abstract [en]

Diabetes may cause late complications in the CNS but certain lesions may also occur acutely in hyperglycemia. We describe a case of hyperosmolar non-ketotic syndrome and reversible hemichoreic dyskinesia with morphological changes in basal ganglia. 

Place, publisher, year, edition, pages
Wiley, 2021
Keywords
diabetes, hemiballismus, hemichorea, hyperosmolar non‐ketotic syndrome
National Category
Basic Medicine Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-36039 (URN)10.1002/ccr3.4343 (DOI)000657911400030 ()34084532 (PubMedID)2-s2.0-85107113255 (Scopus ID)
Available from: 2021-06-09 Created: 2021-06-09 Last updated: 2022-03-21Bibliographically approved
Sjöholm, Å. (2021). Potentiellt orsakssamband mellan sars-cov-2 och diabetes. Läkartidningen, 118, Article ID 21039.
Open this publication in new window or tab >>Potentiellt orsakssamband mellan sars-cov-2 och diabetes
2021 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 118, article id 21039Article in journal (Other academic) Published
Place, publisher, year, edition, pages
Läkartidningen, 2021
National Category
Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-35791 (URN)33950514 (PubMedID)2-s2.0-85105457297 (Scopus ID)
Available from: 2021-05-06 Created: 2021-05-06 Last updated: 2022-03-21Bibliographically approved
Sjöholm, Å. (2021). Using adjuvant pharmacotherapy in the treatment of type 1 diabetes.. Expert Opinion on Pharmacotherapy, 22(16), 2143-2148
Open this publication in new window or tab >>Using adjuvant pharmacotherapy in the treatment of type 1 diabetes.
2021 (English)In: Expert Opinion on Pharmacotherapy, ISSN 1465-6566, E-ISSN 1744-7666, Vol. 22, no 16, p. 2143-2148Article in journal (Refereed) Published
Abstract [en]

Introduction: Insulin and its analogues have so far been the only approved treatment for type 1 diabetes in Europe, while in the U.S. the amylin analog pramlintide is approved for adjuvant use with insulin. However, in clinical practice, various drugs against type 2 diabetes have been used off label with insulin for type 1 diabetes. Recently, the EMA approved the SGLT inhibitors dapagliflozin and sotagliflozin as adjuvant treatments to insulin for type 1 diabetes in adults.Areas covered: This article is a survey of adjuvant treatments used against type 1 diabetes, focusing on SGLT inhibitors.Expert opinion: While GLP-1R agonists and metformin may reduce weight gain associated with insulin therapy and possibly also confer non-glycemic benefits, only the SGLT inhibitors dapagliflozin and sotagliflozin have been approved in Europe as adjunctive to insulin for type 1 diabetes. Since these drugs act independently of insulin, they are very valuable additions to the armamentarium against type 1 diabetes. However, they should be used judiciously in select patients to mitigate the risk of diabetic ketoacidosis. Patients should be instructed to avoid risk situations and be taught to measure blood ketones themselves.

Place, publisher, year, edition, pages
Taylor & Francis, 2021
Keywords
GLP-1, SGLT-2 inhibitors, Type 1 diabetes, insulin, metformin, pramlintide
National Category
Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-36392 (URN)10.1080/14656566.2021.1939679 (DOI)000664170800001 ()34132620 (PubMedID)2-s2.0-85108285978 (Scopus ID)
Available from: 2021-06-21 Created: 2021-06-21 Last updated: 2022-03-21Bibliographically approved
Sjöholm, Å., Pereira, M. J., Nilsson, T., Linde, T., Katsogiannos, P., Saaf, J. & Eriksson, J. W. (2020). Type B insulin resistance syndrome in a patient with type 1 diabetes. Endocrinology, diabetes & metabolism case reports, 2020(1), Article ID 190157.
Open this publication in new window or tab >>Type B insulin resistance syndrome in a patient with type 1 diabetes
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2020 (English)In: Endocrinology, diabetes & metabolism case reports, ISSN 2052-0573, Vol. 2020, no 1, article id 190157Article in journal (Refereed) Published
Abstract [en]

Type B insulin resistance syndrome (TBIRS) is a very rare autoimmune disorder with polyclonal autoantibodies against the insulin receptor, resulting in severe and refractory hyperglycemia. Described here is a patient who within a few months after the onset of autoimmune type 1 diabetes increased her insulin requirements more than 20-fold; despite this she had considerable difficulty maintaining a plasma glucose value of <40-60 mmol/L (720-1100 mg/dL). On suspicion of TBIRS, the patient was started on tapering dose of glucocorticoids to overcome the autoimmune insulin receptor blockade, resulting in an immediate and pronounced effect. Within days, insulin requirements decreased by 80-90% and plasma glucose stabilized around 7-8 mmol/L (126-144 mg/dL). The presence of antibodies to the insulin receptor was detected by immunoprecipitation and binding assays. After a 4-month remission on low maintenance dose prednisolone, the patient relapsed, which required repeated plasmaphereses and immune column treatments with temporarily remarkable effect. Mixed and transient results were seen with rituximab, mycophenolic acid and bortezomib, but the glycemic status remained suboptimal. Lack of compliance and recurrent infections may have contributed to this.

Place, publisher, year, edition, pages
Bioscientifica, 2020
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:hig:diva-38217 (URN)10.1530/EDM-19-0157 (DOI)000555811700001 ()32478674 (PubMedID)
Available from: 2022-03-21 Created: 2022-03-21 Last updated: 2022-03-21Bibliographically approved
Kappe, C., Zhang, Q., Nystrom, T. & Sjöholm, Å. (2014). Effects of high-fat diet and the anti-diabetic drug metformin on circulating GLP-1 and the relative number of intestinal L-cells. Diabetology and Metabolic Syndrome, 6, Article ID 70.
Open this publication in new window or tab >>Effects of high-fat diet and the anti-diabetic drug metformin on circulating GLP-1 and the relative number of intestinal L-cells
2014 (English)In: Diabetology and Metabolic Syndrome, ISSN 1758-5996, E-ISSN 1758-5996, Vol. 6, article id 70Article in journal (Refereed) Published
Abstract [en]

Background: Elevated serum free fatty acids (FFAs) contribute to the pathogenesis of type-2-diabetes (T2D), and lipotoxicity is observed in many cell types. We recently showed that simulated hyperlipidemia induces lipoapoptosis also in GLP-1-secreting L-cells in vitro, while metformin confers lipoprotection. The aim of this study was to determine if a high fat diet (HFD) reduces the number of enteroendocrine L-cells and/or GLP-1 plasma levels in a rodent model, and potential effects thereupon of metformin treatment. Methods: C57/Bl6 mice received control/HFD for 12-weeks, and oral administration of metformin/saline for the last 14 days. Blood glucose, glycosylated hemoglobin and plasma insulin and GLP-1 were determined before and after treatment with metformin using ELISAs. GLP-1-immunopositive cells in intestinal tissue sections were quantified using immunohistochemistry. Results: A HFD increased blood glucose, glycosylated hemoglobin, and fasting plasma insulin (33%, 15% and 70% increase, respectively), in conjunction with reduced oral glucose tolerance, indicating the manifestation of insulin resistance. Metformin counteracted these adverse effects, while also reducing prandial plasma FFAs. The number of GLP-1-positive cells was indicated to be reduced (55% reduction of the number of GLP-1-positive cells, p = 0.134), while there was a trend toward increased prandial plasma GLP-1 despite reduced food intake following a HFD. Conclusion: HFD-fed mice rapidly develop insulin resistance. Metformin exerts beneficial glucose lowering effects, and is indicated to improve the incretin response. Albeit no significant effect, a HFD tends to reduce the number of GLP-1-positive cells. However, considering concurrent normal or increased plasma GLP-1, any reduction in the number of GLP-1-positive cells, probably does not contribute to development of the glucose intolerance, but may contribute to progression of the diabetic state through eventual loss of a functional incretin response.

Place, publisher, year, edition, pages
BMC, 2014
Keywords
Metformin, Glucagon-like peptide-1, Insulinotropic, Lipotoxicity, L-cell
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:hig:diva-38207 (URN)10.1186/1758-5996-6-70 (DOI)000338889400001 ()25028601 (PubMedID)
Available from: 2014-08-19 Created: 2022-03-21Bibliographically approved
Fransson, L., Franzén, S., Rosengren, V., Wolbert, P., Sjöholm, Å. & Ortsater, H. (2013). beta-cell adaptation in a mouse model of glucocorticoid-induced metabolic syndrome. Journal of Endocrinology, 219(3), 231-241
Open this publication in new window or tab >>beta-cell adaptation in a mouse model of glucocorticoid-induced metabolic syndrome
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2013 (English)In: Journal of Endocrinology, ISSN 0022-0795, E-ISSN 1479-6805, Vol. 219, no 3, p. 231-241Article in journal (Refereed) Published
Abstract [en]

Glucocorticoids (GCs) are stress hormones primarily responsible for mobilizing glucose to the circulation. Due to this effect, insulin resistance and glucose intolerance are concerns in patients with endogenous overproduction of GCs and in patients prescribed GC-based therapy. In addition, hypercortisolemic conditions share many characteristics with the metabolic syndrome. This study reports on a thorough characterization, in terms of glucose control and lipid handling, of a mouse model where corticosterone is given via the drinking water. C57BL/6J mice were treated with corticosterone (100 or 25 mu g/ml) or vehicle in their drinking water for 5 weeks after which they were subjected to insulin or glucose tolerance tests. GC-treated mice displayed increased food intake, body weight gain, and central fat deposit accumulations. In addition, the GC treatment led to dyslipidemia as well as accumulation of ectopic fat in the liver and skeletal muscle, having a substantial negative effect on insulin sensitivity. Also glucose intolerance and hypertension, both part of the metabolic syndrome, were evident in the GC-treated mice. However, the observed effects of corticosterone were reversed after drug removal. Furthermore, this study reveals insights into beta-cell adaptation to the GC-induced insulin resistance. Increased pancreatic islet volume due to cell proliferation, increased insulin secretion capacity, and increased islet chaperone expression were found in GC-treated animals. This model mimics the human metabolic syndrome. It could be a valuable model for studying the complex mechanisms behind the development of the metabolic syndrome and type 2 diabetes, as well as the multifaceted relations between GC excess and disease.

Place, publisher, year, edition, pages
BioScientifica, 2013
Keywords
glucocorticoid, diabetes, insulin secretion, obesity, islet cells
National Category
Clinical Medicine
Identifiers
urn:nbn:se:hig:diva-38202 (URN)10.1530/JOE-13-0189 (DOI)000327761300005 ()
Available from: 2014-01-07 Created: 2022-03-21Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-5274-9748

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