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| Journal of Endocrinology and Metabolism, ISSN 1923-2861 print, 1923-287X online, Open Access |
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Editorial
Volume 8, Number 1, February 2018, pages 1-1
Impaired Crosstalk Between Insulin and Glucagon Secretion in Patients With Type 2 Diabetes
Hidekatsu Yanai
Department of Internal Medicine, National Center for Global Health and Medicine Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa, Chiba 272-8516, Japan
Manuscript submitted January 30, 2018, accepted February 14, 2018
Short title: Editorial
doi: https://doi.org/10.14740/jem489w
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In this issue (P6), Morimitsu and Hamasaki report that once-weekly glucagon-like peptide-1 (GLP-1) receptor agonist, dulaglutide ameliorated glycemic control by suppressing fasting and postprandial glucagon secretion in a patient with type 2 diabetes [1]. Their report reminded me a significance of impaired crosstalk between insulin and glucagon secretion in patients with type 2 diabetes.
In normal individuals, serum glucagon falls after carbohydrate ingestion. In diabetic patients, serum glucagon is not suppressed by carbohydrate ingestion despite hyperglycemia [2]. An inverse relationship between insulin and glucagon secretion observed in normal individuals has been lost in patients with type 2 diabetes [3]. Such an impaired crosstalk between insulin and glucagon secretion was also observed in pre-diabetic individuals [4]. Postprandial hyperglucagonemia in type 2 diabetes is likely due to loss of intra-islet postprandial suppression of glucagon secretion by insulin [5]. Therefore, altered insulin-to-glucagon ratio which was used in the report by Morimitsu and Hamasaki should play an important role in the pathophysiology of type 2 diabetes [6].
GLP-1 receptor agonist improved glycemic control by amelioration of insulin-to-glucagon ratio. Effects of other anti-diabetic drugs on insulin-to-glucagon ratio should be studied in the future.
Conflict of Interest
The author declares that he has no conflict of interest concerning this article.
| References | ▴Top |
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- Muller WA, Faloona GR, Aguilar-Parada E, Unger RH. Abnormal alpha-cell function in diabetes. Response to carbohydrate and protein ingestion. N Engl J Med. 1970;283(3):109-115.
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doi pubmed - Meier JJ, Kjems LL, Veldhuis JD, Lefebvre P, Butler PC. Postprandial suppression of glucagon secretion depends on intact pulsatile insulin secretion: further evidence for the intraislet insulin hypothesis. Diabetes. 2006;55(4):1051-1056.
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