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Glucagon and type 2 diabetes: the return of the alpha cell

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Standard

Glucagon and type 2 diabetes : the return of the alpha cell. / Lund, Asger; Bagger, Jonatan I; Christensen, Mikkel; Knop, Filip K; Vilsbøll, Tina.

I: Current Diabetes Reports, Bind 14, Nr. 12, 555, 12.2014, s. 1-7.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Lund, A, Bagger, JI, Christensen, M, Knop, FK & Vilsbøll, T 2014, 'Glucagon and type 2 diabetes: the return of the alpha cell', Current Diabetes Reports, bind 14, nr. 12, 555, s. 1-7. https://doi.org/10.1007/s11892-014-0555-4

APA

Lund, A., Bagger, J. I., Christensen, M., Knop, F. K., & Vilsbøll, T. (2014). Glucagon and type 2 diabetes: the return of the alpha cell. Current Diabetes Reports, 14(12), 1-7. [555]. https://doi.org/10.1007/s11892-014-0555-4

Vancouver

Lund A, Bagger JI, Christensen M, Knop FK, Vilsbøll T. Glucagon and type 2 diabetes: the return of the alpha cell. Current Diabetes Reports. 2014 dec;14(12):1-7. 555. https://doi.org/10.1007/s11892-014-0555-4

Author

Lund, Asger ; Bagger, Jonatan I ; Christensen, Mikkel ; Knop, Filip K ; Vilsbøll, Tina. / Glucagon and type 2 diabetes : the return of the alpha cell. I: Current Diabetes Reports. 2014 ; Bind 14, Nr. 12. s. 1-7.

Bibtex

@article{06871eafa0f641c29a42306f443a4c5d,
title = "Glucagon and type 2 diabetes: the return of the alpha cell",
abstract = "In normal physiology, glucagon from pancreatic alpha cells plays an important role in maintaining glucose homeostasis via its regulatory effect on hepatic glucose production. Patients with type 2 diabetes suffer from fasting and postprandial hyperglucagonemia, which stimulate hepatic glucose production and, thus, contribute to the hyperglycemia characterizing these patients. Although this has been known for years, research focusing on alpha cell (patho)physiology has historically been dwarfed by research on beta cells and insulin. Today the mechanisms behind type 2 diabetic hyperglucagonemia are still poorly understood. Preclinical and clinical studies have shown that the gastrointestinal hormone glucose-dependent insulinotropic polypeptide (GIP) might play an important role in this pathophysiological phenomenon. Furthermore, it has become apparent that suppression of glucagon secretion or antagonization of the glucagon receptor constitutes potentially effective treatment strategies for patients with type 2 diabetes. In this review, we focus on the regulation of glucagon secretion by the incretin hormones glucagon-like peptide-1 (GLP-1) and GIP. Furthermore, potential advantages and limitations of suppressing glucagon secretion or antagonizing the glucagon receptor, respectively, in the treatment of patients with type 2 diabetes will be discussed.",
author = "Asger Lund and Bagger, {Jonatan I} and Mikkel Christensen and Knop, {Filip K} and Tina Vilsb{\o}ll",
year = "2014",
month = dec,
doi = "10.1007/s11892-014-0555-4",
language = "English",
volume = "14",
pages = "1--7",
journal = "Current Diabetes Reports",
issn = "1534-4827",
publisher = "Springer Healthcare",
number = "12",

}

RIS

TY - JOUR

T1 - Glucagon and type 2 diabetes

T2 - the return of the alpha cell

AU - Lund, Asger

AU - Bagger, Jonatan I

AU - Christensen, Mikkel

AU - Knop, Filip K

AU - Vilsbøll, Tina

PY - 2014/12

Y1 - 2014/12

N2 - In normal physiology, glucagon from pancreatic alpha cells plays an important role in maintaining glucose homeostasis via its regulatory effect on hepatic glucose production. Patients with type 2 diabetes suffer from fasting and postprandial hyperglucagonemia, which stimulate hepatic glucose production and, thus, contribute to the hyperglycemia characterizing these patients. Although this has been known for years, research focusing on alpha cell (patho)physiology has historically been dwarfed by research on beta cells and insulin. Today the mechanisms behind type 2 diabetic hyperglucagonemia are still poorly understood. Preclinical and clinical studies have shown that the gastrointestinal hormone glucose-dependent insulinotropic polypeptide (GIP) might play an important role in this pathophysiological phenomenon. Furthermore, it has become apparent that suppression of glucagon secretion or antagonization of the glucagon receptor constitutes potentially effective treatment strategies for patients with type 2 diabetes. In this review, we focus on the regulation of glucagon secretion by the incretin hormones glucagon-like peptide-1 (GLP-1) and GIP. Furthermore, potential advantages and limitations of suppressing glucagon secretion or antagonizing the glucagon receptor, respectively, in the treatment of patients with type 2 diabetes will be discussed.

AB - In normal physiology, glucagon from pancreatic alpha cells plays an important role in maintaining glucose homeostasis via its regulatory effect on hepatic glucose production. Patients with type 2 diabetes suffer from fasting and postprandial hyperglucagonemia, which stimulate hepatic glucose production and, thus, contribute to the hyperglycemia characterizing these patients. Although this has been known for years, research focusing on alpha cell (patho)physiology has historically been dwarfed by research on beta cells and insulin. Today the mechanisms behind type 2 diabetic hyperglucagonemia are still poorly understood. Preclinical and clinical studies have shown that the gastrointestinal hormone glucose-dependent insulinotropic polypeptide (GIP) might play an important role in this pathophysiological phenomenon. Furthermore, it has become apparent that suppression of glucagon secretion or antagonization of the glucagon receptor constitutes potentially effective treatment strategies for patients with type 2 diabetes. In this review, we focus on the regulation of glucagon secretion by the incretin hormones glucagon-like peptide-1 (GLP-1) and GIP. Furthermore, potential advantages and limitations of suppressing glucagon secretion or antagonizing the glucagon receptor, respectively, in the treatment of patients with type 2 diabetes will be discussed.

U2 - 10.1007/s11892-014-0555-4

DO - 10.1007/s11892-014-0555-4

M3 - Journal article

C2 - 25344790

VL - 14

SP - 1

EP - 7

JO - Current Diabetes Reports

JF - Current Diabetes Reports

SN - 1534-4827

IS - 12

M1 - 555

ER -

ID: 137512544