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Carlsson, Per-Ola
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Publications (10 of 183) Show all publications
Li, W., Zhou, Y., Wang, X., Cai, M., Gao, F., Carlsson, P.-O. & Sun, Z. (2019). A modified in vitro tool for isolation and characterization of rat quiescent islet stellate cells. Experimental Cell Research, 384(1), Article ID 111617.
Open this publication in new window or tab >>A modified in vitro tool for isolation and characterization of rat quiescent islet stellate cells
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2019 (English)In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 384, no 1, article id 111617Article in journal (Refereed) Published
Abstract [en]

Background: Islet stellate cells (ISCs) play a critical role in islet fibrosis, contributing to the progression of pancreatic diseases. Previous studies have focused on fibrosis-associated activated ISCs obtained by standard islet explant techniques. However, in vitro models of quiescent ISCs (qISCs) are lacking. This study aims to develop a method to isolate qISCs and analyze their phenotype during activation.

Methods: Immunofluorescence staining was applied to localize ISCs in normal human, rat, and mouse islets. qISCs were isolated from rat islets using density gradient centrifugation (DGC) method. qRT-PCR, immunoblotting, proliferation, and migration assays were employed for their characterization.

Results: Desmin-positive ISCs were detected in normal human, rat, and mouse islets. Freshly isolated qISCs, obtained by density gradient centrifugation, displayed a polygonal appearance with refringent cytoplasmic lipid droplets and expressed transcriptional markers indicating a low activation/quiescent state. With increasing culture time, the marker expression pattern changed, reflecting ISC activation. qISCs contained more lipid droplets and exhibited lower proliferation and migration abilities compared to spindle-shaped ISCs obtained by traditional explant techniques.

Conclusions: This study describes a new method for efficient isolation of qISCs from rat islets, representing a useful in vitro tool to study the biology of ISCs in more physiological conditions.

Place, publisher, year, edition, pages
ELSEVIER INC, 2019
Keywords
Islet stellate cell, Isolation, Quiescent, Activated, Method
National Category
Cell and Molecular Biology Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-396432 (URN)10.1016/j.yexcr.2019.111617 (DOI)000490031700012 ()31505166 (PubMedID)
Available from: 2019-11-06 Created: 2019-11-06 Last updated: 2019-11-06Bibliographically approved
Singh, K., Martinell, M., Luo, Z., Espes, D., Stålhammar, J., Sandler, S. & Carlsson, P.-O. (2019). Cellular immunological changes in patients with LADA are a mixture of those seen in patients with type 1 and type 2 diabetes. Clinical and Experimental Immunology, 197(1), 64-73
Open this publication in new window or tab >>Cellular immunological changes in patients with LADA are a mixture of those seen in patients with type 1 and type 2 diabetes
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2019 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 197, no 1, p. 64-73Article in journal (Refereed) Published
Abstract [en]

There is currently scarce knowledge of the immunological profile of patients with latent autoimmune diabetes mellitus in the adult (LADA) when compared with healthy controls (HC) and patients with classical type 1 diabetes (T1D) and type 2 diabetes (T2D). The objective of this study was to investigate the cellular immunological profile of LADA patients and compare to HC and patients with T1D and T2D. All patients and age-matched HC were recruited from Uppsala County. Peripheral blood mononuclear cells were isolated from freshly collected blood to determine the proportions of immune cells by flow cytometry. Plasma concentrations of the cytokine interleukin (IL)-35 were measured by enzyme-linked immunosorbent assay (ELISA). The proportion of CD11c(+)CD123(-) antigen-presenting cells (APCs) was lower, while the proportions of CD11c(+)CD123(+) APCs and IL-35(+) tolerogenic APCs were higher in LADA patients than in T1D patients. The proportion of CD3(-)CD56(high)CD16(+) natural killer (NK) cells was higher in LADA patients than in both HC and T2D patients. The frequency of IL-35(+) regulatory T cells and plasma IL-35 concentrations in LADA patients were similar to those in T1D and T2D patients, but lower than in HC. The proportion of regulatory B cells in LADA patients was higher than in healthy controls, T1D and T2D patients, and the frequency of IL-35(+) regulatory B cells was higher than in T1D patients. LADA presents a mixed cellular immunological pattern with features overlapping with both T1D and T2D.

Keywords
Cellular immunology, IL-35, LADA, type 1 diabetes, type 2 diabetes
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:uu:diva-393134 (URN)10.1111/cei.13289 (DOI)000480400100004 ()30843600 (PubMedID)
Funder
Swedish Research Council, 2017-01343Swedish Research Council, 921-2014-7054Swedish Diabetes AssociationSwedish Child Diabetes FoundationEXODIAB - Excellence of Diabetes Research in SwedenNovo Nordisk
Available from: 2019-09-24 Created: 2019-09-24 Last updated: 2019-09-24Bibliographically approved
Ullsten, S., Lau, J. & Carlsson, P.-O. (2019). Decreased beta-Cell Proliferation and Vascular Density in a Subpopulation of Low-Oxygenated Male Rat Islets. Journal of the Endocrine Society, 3(8), 1608-1616
Open this publication in new window or tab >>Decreased beta-Cell Proliferation and Vascular Density in a Subpopulation of Low-Oxygenated Male Rat Islets
2019 (English)In: Journal of the Endocrine Society, E-ISSN 2472-1972, Vol. 3, no 8, p. 1608-1616Article in journal (Refereed) Published
Abstract [en]

Low-oxygenated and dormant islets with a capacity to become activated when neededmay play a crucial role in the complex machinery behind glucose homeostasis. We hypothesized that low-oxygenated islets, when not functionally challenged, do not rapidly cycle between activation and inactivation but are a stable population that remain low-oxygenated. As this was confirmed, we aimed to characterize these islets with regard to cell composition, vascular density, and endocrine cell proliferation. The 2-nitroimidazole low-oxygenation marker pimonidazole was administered as a single or repeated dose to Wistar Furth rats. The stability of oxygen status of islets was evaluated by immunohistochemistry as the number of islets with incorporated pimonidazole adducts after one or repeated pimonidazole injections. Adjacent sections were evaluated for islet cell composition, vascular density, and endocrine cell proliferation. Single and repeated pimonidazole injections over an 8-hour period yielded accumulation of pimonidazole adducts in the same islets. An average of 30% of all islets was in all cases positively stained for pimonidazole adducts. These islets showed a similar endocrine cell composition as other islets but had lower vascular density and beta-cell proliferation. In conclusion, low-oxygenated islets were found to be a stable subpopulation of islets for at least 8 hours. Although they have previously been observed to be less functionally active, their islet cell composition was similar to that of other islets. Consistent with their lower oxygenation, they had fewer blood vessels than other islets. Notably, beta-cell regeneration preferentially occurred in better-oxygenated islets.

Place, publisher, year, edition, pages
Endocrine Society, 2019
Keywords
islet vasculature, pancreatic islets, heterogeneity, beta-cell proliferation
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-330804 (URN)10.1210/js.2019-00101 (DOI)000484384400015 ()31404404 (PubMedID)
Funder
Swedish Research Council, 55X-15043Swedish Child Diabetes FoundationSwedish Diabetes AssociationEXODIAB - Excellence of Diabetes Research in SwedenNovo Nordisk
Note

Title in thesis list of papers: Decreased beta cell proliferation and vascular density in a subpopulation of low-oxygenated rat islets

Available from: 2017-10-04 Created: 2017-10-04 Last updated: 2019-10-17Bibliographically approved
Liljebäck, H., Quach, M., Carlsson, P.-O. & Lau, J. (2019). Fewer Islets Survive from a First Transplant than a Second Transplant: Evaluation of Repeated Intraportal Islet Transplantation in Mice. Cell Transplantation, 28(11), 1455-1460
Open this publication in new window or tab >>Fewer Islets Survive from a First Transplant than a Second Transplant: Evaluation of Repeated Intraportal Islet Transplantation in Mice
2019 (English)In: Cell Transplantation, ISSN 0963-6897, E-ISSN 1555-3892, Vol. 28, no 11, p. 1455-1460Article in journal (Refereed) Published
Abstract [en]

Beta cell replacement is an exciting field where new beta cell sources and alternative sites are widely explored. The liver has been the implantation site of choice in the clinic since the advent of islet transplantation. However, in most cases, repeated islet transplantation is needed to achieve normoglycemia in diabetic recipients. This study aimed to investigate whether there are differences in islet survival and engraftment between a first and a second transplantation, performed 1 week apart, to the liver. C57BL/6 mice were accordingly transplanted twice with an initial infusion of syngeneic islets expressing green fluorescent protein (GFP). The second islet transplant was performed 1 week later and consisted of islets isolated from non-GFP C57BL/6-mice. Animals were sacrificed either 1 day or 1 month after the second transplantation. A control group received a saline infusion instead of GFP-expressing islets, 1 week later obtained a standard non-GFP islet transplant, and was subsequently sacrificed 1 month later. Islet engraftment in the liver was assessed by immunohistochemistry and serum was analyzed for angiogenic factors induced by the first islet transplantation. Almost 70% of islets found in the liver following repeated islet transplantation originated from the second transplantation. The vascular density in the transplanted non-GFP-expressing islets did not differ depending on whether their transplantation was preceded by a primary islet transplantation or saline administration only nor did angiogenic factors in serum prior to the transplantation of non-GFP islets differ between animals that had received a previous islet transplantation or a saline infusion. We conclude that first islet transplantation creates, by unknown mechanisms, favorable conditions for the survival of a second transplant to the liver.

Keywords
GFP, engraftment, islet transplantation, type 1 diabetes
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-398599 (URN)10.1177/0963689719866685 (DOI)000479643300001 ()31359771 (PubMedID)
Funder
Swedish Child Diabetes FoundationSwedish Research Council, 2017-01343EXODIAB - Excellence of Diabetes Research in SwedenSwedish Diabetes Association
Available from: 2019-12-07 Created: 2019-12-07 Last updated: 2020-01-17Bibliographically approved
Drott, C. J., Franzén, P. & Carlsson, P.-O. (2019). Ghrelin in rat pancreatic islets decreases islet blood flow. American Journal of Physiology. Endocrinology and Metabolism, 317(1), E139-E146
Open this publication in new window or tab >>Ghrelin in rat pancreatic islets decreases islet blood flow
2019 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 317, no 1, p. E139-E146Article in journal (Refereed) Published
Abstract [en]

The peptide ghrelin is mainly produced in some of the epithelial cells in the stomach, but also, during starvation, by the epsilon-cells in the endocrine pancreas. Ghrelin, as an endogenous ligand for the growth hormone secretagogue receptor (GHS-R1 alpha). exerts a variety of metabolic functions including stimulation of appetite and weight gain. Its complete role is not yet fully understood, including whether it has any vascular functions. The present study evaluated if ghrelin affects pancreatic and islet blood flow. Ghrelin and the GHS-R1 alpha receptor antagonist GHRP-6 were injected intravenously in rats followed by blood flow measurements using a microsphere technique. Ghrelin decreased, while GHRP-6 in fasted, but not fed, rats selectively increased islet blood flow fourfold. GHS-R1 alpha was identified not only on glucagon-producing cells but also seemed to be present in the islet arterioles. GHRP-6 in fasted rats. only, also improved the peak insulin response to glucose in vivo. thereby substantially blunting the hyperglycemia. GHRP-6 doubled glucose-stimulated insulin release in vitro of both islets obtained from fed and fasted rats. Our results indicate a novel role for endogenous ghrelin acting directly or indirectly as a local vasoconstrictor in the islets during fasting, thereby restricting the insulin response to hyperglycemia. This is to the best of our knowledge the first report that shows this physiological mechanism to restrict insulin delivery from the islets by acting on the vasculature; a mode of action that can be envisaged to complement the previously well-described mechanisms of ghrelin acting directly on the islet endocrine cells.

Keywords
blood flow, ghrelin, pancreatic islets, vascular
National Category
Endocrinology and Diabetes Physiology
Identifiers
urn:nbn:se:uu:diva-390975 (URN)10.1152/ajpendo.00004.2019 (DOI)000475371500005 ()31063397 (PubMedID)
Funder
Swedish Research CouncilEXODIAB - Excellence of Diabetes Research in SwedenSwedish Child Diabetes FoundationSwedish Diabetes AssociationNovo Nordisk
Available from: 2019-08-16 Created: 2019-08-16 Last updated: 2019-08-16Bibliographically approved
Zhou, Y., Li, W., Zhou, J., Chen, J., Wang, X., Cai, M., . . . Sun, Z. (2019). Lipotoxicity reduces beta cell survival through islet stellate cell activation regulated by lipid metabolism-related molecules. Experimental Cell Research, 380(1), 1-8
Open this publication in new window or tab >>Lipotoxicity reduces beta cell survival through islet stellate cell activation regulated by lipid metabolism-related molecules
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2019 (English)In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 380, no 1, p. 1-8Article in journal (Refereed) Published
Abstract [en]

Background: Islet stellate cells (ISCs) activation is mainly associated with islet fibrosis, which contributes to the progression of type 2 diabetes. However, the molecular mechanism underlying this process is not fully understood.

Methods: In order to investigate this process the current study examined ectopic fat accumulation in rats with high-fat diet (HFD) induced obesity. Levels of lipotoxicity-induced ISC activation and islet function were assessed via intraperitoneal glucose and insulin tolerance tests, and immunohistochemistry. The expression of lipid metabolism- and ISC activation-related markers was evaluated in cultured ISCs treated with palmitic acid (PA) using quantitative PCR and western blotting. We also overexpressed sterol regulatory element-binding protein (SREBP)-1c in ISCs by lentiviral transduction, and assessed the effects on insulin release in co-cultures with isolated rat islets.

Results: HFD increased body weight and ectopic fat accumulation in pancreatic islets. Lipotoxicity caused progressive glucose intolerance and insulin resistance, upregulated a-smooth muscle actin, and stimulated the secretion of extracellular matrix. Lipotoxicity reduced the expression of lipid metabolism-related molecules in ISCs treated with PA, especially SREBP-1c. Overexpression of SREBP-1c in ISCs improved islet viability and insulin secretion in co-cultures.

Conclucions: These results indicate that lipotoxicity-induced ISC activation alters islet function via regulation of lipid metabolism, suggesting that therapeutic strategies targeting activated ISC may be an effective treatment for prevention of ISC activation-associated islet dysfunction.

Place, publisher, year, edition, pages
ELSEVIER INC, 2019
Keywords
Islet stellate cell, Lipotoxicity, beta cell, Lipid metabolism, SREBP-1c
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-384985 (URN)10.1016/j.yexcr.2019.04.012 (DOI)000468124700001 ()30998947 (PubMedID)
Available from: 2019-06-14 Created: 2019-06-14 Last updated: 2019-06-14Bibliographically approved
Jansson, L. & Carlsson, P.-O. (2019). Pancreatic Blood Flow with Special Emphasis on Blood Perfusion of the Islets of Langerhans. COMPREHENSIVE PHYSIOLOGY, 9(2), 799-837
Open this publication in new window or tab >>Pancreatic Blood Flow with Special Emphasis on Blood Perfusion of the Islets of Langerhans
2019 (English)In: COMPREHENSIVE PHYSIOLOGY, ISSN 2040-4603, Vol. 9, no 2, p. 799-837Article in journal (Refereed) Published
Abstract [en]

The pancreatic islets are more richly vascularized than the exocrine pancreas, and possess a 5- to 10-fold higher basal and stimulated blood flow, which is separately regulated. This is reflected in the vascular anatomy of the pancreas where islets have separate arterioles. There is also an insulo-acinar portal system, where numerous venules connect each islet to the acinar capillaries. Both islets and acini possess strong metabolic regulation of their blood perfusion. Of particular importance, especially in the islets, is adenosine and ATP/ADP. Basal and stimulated blood flow is modified by local endothelial mediators, the nervous system as well as gastrointestinal hormones. Normally the responses to the nervous system, especially the parasympathetic and sympathetic nerves, are fairly similar in endocrine and exocrine parts. The islets seem to be more sensitive to the effects of endothelial mediators, especially nitric oxide, which is a permissive factor to maintain the high basal islet blood flow. The gastrointestinal hormones with pancreatic effects mainly influence the exocrine pancreatic blood flow, whereas islets are less affected. A notable exception is incretin hormones and adipokines, which preferentially affect islet vasculature. Islet hormones can influence both exocrine and endocrine blood vessels, and these complex effects are discussed. Secondary changes in pancreatic and islet blood flow occur during several conditions. To what extent changes in blood perfusion may affect the pathogenesis of pancreatic diseases is discussed. Both type 2 diabetes mellitus and acute pancreatitis are conditions where we think there is evidence that blood flow may contribute to disease manifestations.

Place, publisher, year, edition, pages
WILEY, 2019
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-406488 (URN)10.1002/cphy.c160050 (DOI)000511301100009 ()30892693 (PubMedID)
Funder
Swedish Research Council, 921-201701343Swedish Child Diabetes FoundationSwedish Diabetes AssociationNovo NordiskErnfors Foundation
Available from: 2020-03-11 Created: 2020-03-11 Last updated: 2020-03-11Bibliographically approved
Liljebäck, H., Espes, D. & Carlsson, P.-O. (2019). Unsurpassed Intrahepatic Islet Engraftment: the Quest for New Sites for Beta Cell Replacement. Cell Medicine, 11, Article ID 2155179019857662.
Open this publication in new window or tab >>Unsurpassed Intrahepatic Islet Engraftment: the Quest for New Sites for Beta Cell Replacement
2019 (English)In: Cell Medicine, ISSN 2155-1790, E-ISSN 2155-1790, Vol. 11, article id 2155179019857662Article in journal, Editorial material (Other academic) Published
Abstract [en]

The liver is currently the site of choice for clinical islet transplantation, even though many alternative implantation sites have lately been proposed as more ideal for graft survival. The suggested sites, for example intramuscular space, omentum, bone marrow, and spleen, are sometimes difficult to compare due to differences in animal model, islet isolation procedure, and islet quality. In addition, the variation in transplanted islet mass is vast. The aim of this commentary is to review alternative implantation sites tested experimentally as well as in clinical islet transplantation. Although many sites have been investigated, none have convincingly proved better suited for clinical islet transplantation than intraportal injection to the liver, regardless of whether it is autologous or allogeneic transplantation. However, in order to fully evaluate upcoming bioengineering techniques, such as scaffolds containing insulin-producing cells derived from stem cells, the need of an alternative site has arisen to enable cellular monitoring, which currently cannot be achieved within the liver.

Place, publisher, year, edition, pages
Sage Publications, 2019
Keywords
intraportal islet transplantation, type 1 diabetes, beta cell replacement
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-390334 (URN)10.1177/2155179019857662 (DOI)000472913100001 ()
Available from: 2019-08-09 Created: 2019-08-09 Last updated: 2019-08-09Bibliographically approved
Grapensparr, L., Christoffersson, G. & Carlsson, P.-O. (2018). Bioengineering with Endothelial Progenitor Cells Improves the Vascular Engraftment of Transplanted Human Islets. Cell Transplantation, 27(6), 948-956
Open this publication in new window or tab >>Bioengineering with Endothelial Progenitor Cells Improves the Vascular Engraftment of Transplanted Human Islets
2018 (English)In: Cell Transplantation, ISSN 0963-6897, E-ISSN 1555-3892, Vol. 27, no 6, p. 948-956Article in journal (Refereed) Published
Abstract [en]

Pancreatic islets isolated for transplantation are disconnected from their vascular supply and need to establish a new functional network posttransplantation. Due to poor revascularization, prevailing hypoxia with correlating increased apoptosis rates in experimental studies can be observed for months posttransplantation. Endothelial progenitor cells (EPCs) are bone marrow-derived cells that promote neovascularization. The present study tested the hypothesis that EPCs, isolated from human umbilical cord blood, could be coated to human islet surfaces and be used to promote islet vascular engraftment. Control or EPC bioengineered human islets were transplanted into the renal subcapsular space of nonobese diabetic/severe combined immunodeficiency mice. Four weeks posttransplantation, graft blood perfusion and oxygen tension were measured using laser Doppler flowmetry and Clark microelectrodes, respectively. Vessel functionality was also assessed by in vivo confocal imaging. The vascular density and the respective contribution of human and recipient endothelium were assessed immunohistochemically by staining for human and mouse CD31. Islet grafts with EPCs had substantially higher blood perfusion and oxygen tension than control transplants. Furthermore, analysis of the vascular network of the grafts revealed that grafts containing EPC bioengineered islets had a superior vascular density compared with control grafts, with functional chimeric blood vessels. We conclude that a simple procedure of surface coating with EPCs provides a possibility to improve the vascular engraftment of transplanted human islets. Established protocols are also easily applicable for intraportal islet transplantation in order to obtain a novel directed cellular therapy at the site of implantation in the liver.

Keywords
endothelial progenitor cells, islet revascularization, neovascularization, islet engraftment
National Category
Surgery Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-361553 (URN)10.1177/0963689718759474 (DOI)000438945100009 ()29862837 (PubMedID)
Funder
Swedish Research CouncilSwedish Child Diabetes FoundationSwedish Diabetes AssociationEXODIAB - Excellence of Diabetes Research in SwedenTorsten Söderbergs stiftelseNovo NordiskStiftelsen Olle Engkvist ByggmästareAFA Insurance
Available from: 2018-10-08 Created: 2018-10-08 Last updated: 2018-10-08Bibliographically approved
Rasouli, B., Ahlqvist, E., Alfredsson, L., Andersson, T., Carlsson, P.-O., Groop, L., . . . Carlsson, S. (2018). Coffee consumption, genetic susceptibility and risk of latent autoimmune diabetes in adults: A population-based case-control study.. Diabetes & Metabolism, 44(4), 354-360, Article ID S1262-3636(18)30087-9.
Open this publication in new window or tab >>Coffee consumption, genetic susceptibility and risk of latent autoimmune diabetes in adults: A population-based case-control study.
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2018 (English)In: Diabetes & Metabolism, ISSN 1262-3636, E-ISSN 1878-1780, Vol. 44, no 4, p. 354-360, article id S1262-3636(18)30087-9Article in journal (Refereed) Published
Abstract [en]

AIM: Coffee consumption is inversely related to risk of type 2 diabetes (T2D). In contrast, an increased risk of latent autoimmune diabetes in adults (LADA) has been reported in heavy coffee consumers, primarily in a subgroup with stronger autoimmune characteristics. Our study aimed to investigate whether coffee consumption interacts with HLA genotypes in relation to risk of LADA.

METHODS: This population-based study comprised incident cases of LADA (n=484) and T2D (n=1609), and also 885 healthy controls. Information on coffee consumption was collected by food frequency questionnaire. Odds ratios (ORs) with 95% CIs of diabetes were calculated and adjusted for age, gender, BMI, education level, smoking and alcohol intake. Potential interactions between coffee consumption and high-risk HLA genotypes were calculated by attributable proportion (AP) due to interaction.

RESULTS: Coffee intake was positively associated with LADA in carriers of high-risk HLA genotypes (OR: 1.14 per cup/day, 95% CI: 1.02-1.28), whereas no association was observed in non-carriers (OR: 1.04, 95% CI: 0.93-1.17). Subjects with both heavy coffee consumption (≥4 cups/day) and high-risk HLA genotypes had an OR of 5.74 (95% CI: 3.34-9.88) with an estimated AP of 0.36 (95% CI: 0.01-0.71; P=0.04370).

CONCLUSION: Our findings suggest that coffee consumption interacts with HLA to promote LADA.

Keywords
Autoimmune diabetes, Coffee consumption, Gene–environmental interaction, LADA, Latent autoimmune diabetes in adults, Type 2 diabetes
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-368173 (URN)10.1016/j.diabet.2018.05.002 (DOI)000447960300007 ()29861145 (PubMedID)
Available from: 2018-12-04 Created: 2018-12-04 Last updated: 2018-12-10Bibliographically approved
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