Cellular and systemic mechanisms for glucose sensing and homeostasis
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INVITED REVIEW
Cellular and systemic mechanisms for glucose sensing and homeostasis Jong-Woo Sohn 1
&
Won-Kyung Ho 2,3
Received: 30 March 2020 / Revised: 14 August 2020 / Accepted: 14 September 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Glucose is a major source of energy in animals. Maintaining blood glucose levels within a physiological range is important for facilitating glucose uptake by cells, as required for optimal functioning. Glucose homeostasis relies on multiple glucose-sensing cells in the body that constantly monitor blood glucose levels and respond accordingly to adjust its glycemia. These include not only pancreatic β-cells and α-cells that secrete insulin and glucagon, but also central and peripheral neurons regulating pancreatic endocrine function. Different types of cells respond distinctively to changes in blood glucose levels, and the mechanisms involved in glucose sensing are diverse. Notably, recent studies have challenged the currently held views regarding glucosesensing mechanisms. Furthermore, peripheral and central glucose-sensing cells appear to work in concert to control blood glucose level and maintain glucose and energy homeostasis in organisms. In this review, we summarize the established concepts and recent advances in the understanding of cellular and systemic mechanisms that regulate glucose sensing and its homeostasis. Keywords Pancreatic β-cell . Pancreatic α-cell . KATP channel . Trafficking . Endocytosis . Hypothalamus . Hindbrain . Autonomic nervous system
Introduction Under physiological conditions, blood glucose levels are maintained at a range of 80–100 mg/dL or 4.4–5.5 mM [59]. Pancreatic β-cells and α-cells are central to the maintenance of blood glucose homeostasis. Increased blood glucose level after meals stimulates pancreatic β-cells to secrete insulin, which promotes glucose uptake in cells and lowers glucose levels in the blood. Conversely, low blood glucose level
* Jong-Woo Sohn [email protected] * Won-Kyung Ho [email protected] 1
Department of Biological Sciences, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon 34141, South Korea
2
Department of Physiology, Seoul National University College of Medicine, 103 Daehak-ro, Jongro-gu, Seoul 03080, South Korea
3
Department of Brain and Cognitive Sciences, Seoul National University College of Natural Sciences, 1 Gwanak-ro, Gwanak-gu, Seoul 08826, South Korea
between meals stimulates pancreatic α-cells to secrete glucagon, which activates metabolic pathways to raise the blood glucose level. Given the importance of direct glucose sensing by pancreatic endocrine cells, much effort has been made to identify the mechanisms by which these cells monitor blood glucose levels [59]. Glucose is metabolized to ATP when it enters the cells. It is generally accepted that ATP-induced closure of ATPsensitive potassium (KATP) channels, inwardly rectifying K+ channels that consist of pore-forming Kir6.2 and regulatory sulfonylurea receptor 1 (SUR1) subunit
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