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Article ; Online: One more piece in the pancreatic chloride puzzle.

Eliasson, Lena

2021 Volume 234, Issue 1, Page(s) e13737

MeSH term(s)	Chlorides ; Pancreas
Chemical Substances	Chlorides
Language	English
Publishing date	2021-11-01
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13737
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Article ; Online: Editorial: Special issue novel aspects of islet peptides.

Eliasson, Lena / Wierup, Nils

Peptides

2022 Volume 157, Page(s) 170879

MeSH term(s)	Peptides
Chemical Substances	Peptides
Language	English
Publishing date	2022-09-21
Publishing country	United States
Document type	Editorial
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2022.170879
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Zs.A 1649: Show issues

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Article ; Online: Pancreatic alpha cells and glucagon secretion: Novel functions and targets in glucose homeostasis.

Wendt, Anna / Eliasson, Lena

Current opinion in pharmacology

2022 Volume 63, Page(s) 102199

Abstract: Diabetes is the result of dysregulation of both insulin and glucagon. Still, insulin has attracted much more attention than glucagon. Glucagon is released from alpha cells in the islets of Langerhans in response to low glucose and certain amino acids. ... ...

Abstract	Diabetes is the result of dysregulation of both insulin and glucagon. Still, insulin has attracted much more attention than glucagon. Glucagon is released from alpha cells in the islets of Langerhans in response to low glucose and certain amino acids. Drugs with the primary aim of targeting glucagon signalling are scarce. However, glucagon is often administered to counteract severe hypoglycaemia, and commonly used diabetes medications such as GLP-1 analogues, sulfonylureas and SGLT2-inhibitors also affect alpha cells. Indeed, there are physiological and developmental similarities between the alpha cell and the insulin-secreting beta cell and new data confirm that alpha cells can be converted into insulin-secreting cells. These aspects and attributes, the need to find novel therapies targeting the alpha cell and more are considered in this review.
MeSH term(s)	Glucagon/metabolism ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Secreting Cells/metabolism ; Glucose/metabolism ; Homeostasis ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Islets of Langerhans/metabolism
Chemical Substances	Insulin ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-03-01
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2022.102199
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Zs.A 5608: Show issues

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Article ; Online: Amino acids and the changing face of the α-cell.

Hamilton, Alexander / Eliasson, Lena / Knudsen, Jakob G

Peptides

2023 Volume 166, Page(s) 171039

Abstract: Glucagon has long been defined by its glucogenic action and as a result α-cells have been characterised based largely on their interaction with glucose. Recent findings have challenged this preconception, bringing to the fore the significant role ... ...

Abstract	Glucagon has long been defined by its glucogenic action and as a result α-cells have been characterised based largely on their interaction with glucose. Recent findings have challenged this preconception, bringing to the fore the significant role glucagon plays in amino acid breakdown and underlining the importance of amino acids in glucagon secretion. The challenge that remains is defining the mechanism that underlie these effects - understanding which amino acids are most important, how they act on the α-cell and how their actions integrate with other fuels such as glucose and fatty acids. This review will describe the current relationship between amino acids and glucagon and how we can use this knowledge to redefine the α-cell.
MeSH term(s)	Amino Acids ; Glucagon/metabolism ; Liver/metabolism ; Glucagon-Secreting Cells/metabolism ; Glucose/metabolism ; Insulin/metabolism
Chemical Substances	Amino Acids ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2) ; Insulin
Language	English
Publishing date	2023-06-07
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2023.171039
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Article ; Online: miRNAs in the Beta Cell-Friends or Foes?

Karagiannopoulos, Alexandros / Cowan, Elaine / Eliasson, Lena

Endocrinology

2023 Volume 164, Issue 5

Abstract: Type 2 diabetes (T2D) develops due to insulin resistance and an inability of the pancreatic β-cells to increase secretion of insulin and reduce elevated blood glucose levels. Diminished β-cell function and mass have been implicated in impaired β-cell ... ...

Abstract	Type 2 diabetes (T2D) develops due to insulin resistance and an inability of the pancreatic β-cells to increase secretion of insulin and reduce elevated blood glucose levels. Diminished β-cell function and mass have been implicated in impaired β-cell secretory capacity and several microRNAs (miRNAs) have been reported to be involved in regulating β-cell processes. We believe miRNAs are nodes in important miRNA-mRNA networks regulating β-cell function and that miRNAs therefore can be targets for the treatment of T2D. MicroRNAs are short (≈19-23 nucleotides [nt]) endogenous noncoding RNAs which regulate gene expression by directly binding to the mRNA of their target genes. Under normal circumstances, miRNAs act as rheostats to keep expression of their gene targets at optimal levels for different β-cell outputs. In T2D, levels of some miRNAs are altered as part of the compensatory mechanism to improve insulin secretion. Other miRNAs are differentially expressed as part of the process of T2D pathogenesis, which results in reduced insulin secretion and increased blood glucose. In this review, we present recent findings concerning miRNAs in islets and in insulin-secreting cells, and their differential expression in diabetes, with a specific focus on miRNAs involved in β-cell apoptosis/proliferation and glucose-stimulated insulin secretion. We present thoughts around miRNA-mRNA networks and miRNAs as both therapeutic targets to improve insulin secretion and as circulating biomarkers of diabetes. Overall, we hope to convince you that miRNAs in β-cells are essential for regulating β-cell function and can in the future be of clinical use in the treatment and/or prevention of diabetes.
MeSH term(s)	Humans ; Insulin-Secreting Cells/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Blood Glucose/metabolism ; Insulin/metabolism ; RNA, Messenger/metabolism ; Glucose/pharmacology ; Glucose/metabolism
Chemical Substances	MicroRNAs ; Blood Glucose ; Insulin ; RNA, Messenger ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-03-04
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqad040
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Article ; Online: The small RNA miR-375 - a pancreatic islet abundant miRNA with multiple roles in endocrine beta cell function.

Eliasson, Lena

Molecular and cellular endocrinology

2017 Volume 456, Page(s) 95–101

Abstract: The pathophysiology of diabetes is complex and recent research put focus on the pancreatic islets of Langerhans and the insulin-secreting beta cells as central in the development of the disease. MicroRNAs (miRNAs), the small non-coding RNAs regulating ... ...

Abstract	The pathophysiology of diabetes is complex and recent research put focus on the pancreatic islets of Langerhans and the insulin-secreting beta cells as central in the development of the disease. MicroRNAs (miRNAs), the small non-coding RNAs regulating post-transcriptional gene expression, are significant regulators of beta cell function. One of the most abundant miRNAs in the islets is miR-375. This review focus on the role of miR-375 in beta cell function, including effects in development and differentiation, proliferation and regulation of insulin secretion. It also discusses the regulation of miR-375 expression, miR-375 as a potential circulating biomarker in type 1 and type 2 diabetes, and the need for the beta cell to keep expression of miR-375 within optimal levels. The summed picture of miR-375 is a miRNA with multiple functions with importance in the formation of beta cell identity, control of beta cell mass and regulation of insulin secretion.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Cell Differentiation ; Cell Proliferation ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Rats ; Signal Transduction
Chemical Substances	Insulin ; MIRN375 microRNA, human ; MicroRNAs
Language	English
Publishing date	2017-02-27
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2017.02.043
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Zs.A 1127: Show issues

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Article: Secretory granule exocytosis and its amplification by cAMP in pancreatic β-cells.

Nagao, Mototsugu / Lagerstedt, Jens O / Eliasson, Lena

Diabetology international

2022 Volume 13, Issue 3, Page(s) 471–479

Abstract: The sequence of events for secreting insulin in response to glucose in pancreatic β-cells is termed " ...

Abstract	The sequence of events for secreting insulin in response to glucose in pancreatic β-cells is termed "
Language	English
Publishing date	2022-04-01
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	2574501-3
ISSN	2190-1686 ; 2190-1678
ISSN (online)	2190-1686
ISSN	2190-1678
DOI	10.1007/s13340-022-00580-3
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Article ; Online: Interleukin-4 reduces insulin secretion in human islets from healthy but not type-2 diabetic donors.

Westholm, Efraim / Edlund, Anna / Karagiannopoulos, Alexandros / Wendt, Anna / Eliasson, Lena

Biochemical and biophysical research communications

2023 Volume 649, Page(s) 87–92

Abstract: Type 2 diabetes (T2D) is associated with low-grade inflammation. Here we investigate if the anti-inflammatory cytokine interleukin-4 (IL-4) affects glucose-stimulated insulin secretion (GSIS) in human islets from non-diabetic (ND) and type-2 diabetic ( ... ...

Abstract	Type 2 diabetes (T2D) is associated with low-grade inflammation. Here we investigate if the anti-inflammatory cytokine interleukin-4 (IL-4) affects glucose-stimulated insulin secretion (GSIS) in human islets from non-diabetic (ND) and type-2 diabetic (T2D) donors. We first confirmed that GSIS is reduced in islets from T2D donors. Treatment with IL-4 for 48 h had no further effect on GSIS in these islets but significantly reduced secretion in ND islets. Acute treatment with IL-4 for 1 h had no effect on GSIS in ND islets which led us to suspect that IL-4 affects a slow cellular mechanism such as gene transcription. IL-4 has been reported to regulate miR-378a-3p and, indeed, we found that this microRNA was increased with IL-4 treatment. However, overexpression of miR-378a-3p in the human beta cell line EndoC-βH1 did not affect GSIS. MiR-378a-3p is transcribed from the same gene as peroxisome proliferator-activated receptor gamma co-activator 1 beta (PCG-1β) and we found that IL-4 treatment showed a clear tendency to increased gene expression of PCG-1β. PCG-1β is a co-activator of peroxisome proliferator-activated receptor gamma (PPARγ) and, the gene expression of PPARγ was also increased with IL-4 treatment. Our data suggests that the protective role of IL-4 on beta cell survival comes at the cost of lowered insulin secretion, presumably involving the PPARγ-pathway.
MeSH term(s)	Humans ; Insulin Secretion ; Diabetes Mellitus, Type 2/metabolism ; Interleukin-4/pharmacology ; Interleukin-4/metabolism ; PPAR gamma/metabolism ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Glucose/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Islets of Langerhans/metabolism
Chemical Substances	Interleukin-4 (207137-56-2) ; PPAR gamma ; Insulin ; Glucose (IY9XDZ35W2) ; MicroRNAs
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.01.092
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Article ; Online: MicroRNAs in Type 2 Diabetes: Focus on MicroRNA Profiling in Islets of Langerhans.

Cowan, Elaine / Karagiannopoulos, Alexandros / Eliasson, Lena

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2592, Page(s) 113–142

Abstract: Differential expression of microRNAs (miRNAs) is observed in many diseases including type 2 diabetes (T2D). Insulin secretion from pancreatic beta cells is central for the regulation of blood glucose levels and failure to release enough insulin results ... ...

Abstract	Differential expression of microRNAs (miRNAs) is observed in many diseases including type 2 diabetes (T2D). Insulin secretion from pancreatic beta cells is central for the regulation of blood glucose levels and failure to release enough insulin results in hyperglycemia and T2D. The importance in T2D pathogenesis of single miRNAs in beta cells has been described; however, to get the full picture, high-throughput miRNA sequencing is necessary. Here we describe a method using small RNA sequencing, from sample preparation to expression analysis using bioinformatic tools. In the end, a tutorial on differential expression analysis is presented in R using publicly available data.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Islets of Langerhans/metabolism ; Insulin-Secreting Cells/metabolism ; Insulin Secretion ; Insulin/metabolism
Chemical Substances	MicroRNAs ; Insulin
Language	English
Publishing date	2022-12-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2807-2_8
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Article ; Online: Selectively bred rodent models for studying the etiology of type 2 diabetes: Goto-Kakizaki rats and Oikawa-Nagao mice.

Nagao, Mototsugu / Asai, Akira / Eliasson, Lena / Oikawa, Shinichi

Endocrine journal

2022 Volume 70, Issue 1, Page(s) 19–30

Abstract: Type 2 diabetes (T2D) is a polygenic disease and studies to understand the etiology of the disease have required selectively bred animal models with polygenic background. In this review, we present two models; the Goto-Kakizaki (GK) rat and the Oikawa- ... ...

Abstract	Type 2 diabetes (T2D) is a polygenic disease and studies to understand the etiology of the disease have required selectively bred animal models with polygenic background. In this review, we present two models; the Goto-Kakizaki (GK) rat and the Oikawa-Nagao Diabetes-Prone (ON-DP) and Diabetes-Resistant (ON-DR) mouse. The GK rat was developed by continuous selective breeding for glucose tolerance from the outbred Wistar rat around 50 years ago. The main cause of spontaneous hyperglycemia in this model is insulin secretion deficiency from pancreatic β-cells and mild insulin resistance in insulin target organs. A disadvantage of the GK rat is that environmental factors have not been considered in the selective breeding. Hence, the GK rat may not be suitable for elucidating predisposition to diabetes under certain environmental conditions, such as a high-fat diet. Therefore, we recently established two mouse lines with different susceptibilities to diet-induced diabetes, which are prone and resistant to the development of diabetes, designated as the ON-DP and ON-DR mouse, respectively. The two ON mouse lines were established by continuous selective breeding for inferior and superior glucose tolerance after high-fat diet feeding in hybrid mice of three inbred strains. Studies of phenotypic differences between ON-DP and ON-DR mice and their underlying molecular mechanisms will shed light on predisposing factors for the development of T2D in the modern obesogenic environment. This review summarizes the background and the phenotypic differences and similarities of GK rats and ON mice and highlights the advantages of using selectively bred rodent models in diabetes research.
MeSH term(s)	Rats ; Mice ; Animals ; Diabetes Mellitus, Type 2/genetics ; Rats, Wistar ; Rodentia ; Glucose Tolerance Test ; Disease Models, Animal ; Insulin ; Glucose ; Causality
Chemical Substances	Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-12-07
Publishing country	Japan
Document type	Review ; Journal Article
ZDB-ID	1151918-6
ISSN	1348-4540 ; 0918-8959
ISSN (online)	1348-4540
ISSN	0918-8959
DOI	10.1507/endocrj.EJ22-0253
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