Physiology of Glucose: An Updated Review for Healthcare Professionals

Alanazi, Maryam Helal Rasheed; Alanizi, Hamoud Ghayyadh; Almutairi, Amal Khalifah; Al-Rashudi, Khaled Abdul Rahman Suleiman; Alahmari, Khalid Saeed Oudah; Hayjan, Saad Abdulrazaq  Ahmed; Alshehri, Meshal Mahdi Abdulrahman; Alhefdhi, Shatha Ahmed; Bakri, Mohammed Ali Ibrahim; Saleh, Wafa Saadullah; Alhazmi, Anan Homoud; Alajlan, Ali Abdullah Mohammed; Alanazi, Ahmad Asri Awad; Alharbi, Adel Lafi; Alharbi, Bander Nasser; Al-Azmi, Naif Abdulrahman; Ahmed, Ohud Ahmed; Alhajrasi, Hanadi Naji

doi:10.21608/ejchem.2025.405197.12065

Physiology of Glucose: An Updated Review for Healthcare Professionals

Document Type : Review Articles

Authors

¹ Ministry of Defense, Saudi Arabia

² King Khalid University Hospital, Saudi Arabia

³ Ministry of National Guard Health Affairs, Saudi Arabia

⁴ National Guard Prince Mohammad Bin Abdulaziz Hospital, Saudi Arabia

10.21608/ejchem.2025.405197.12065

Abstract

Background: Glucose is the dominant carbohydrate fuel that supports cellular respiration, with availability sustained by coordinated digestion, intestinal absorption, hepatic processing, storage as glycogen, and regulated tissue uptake. Disruption of these processes produces clinically significant dysglycemia.

Aim: To synthesize contemporary physiological concepts of glucose handling across molecular, cellular, and organ-system levels, and to link these mechanisms to diagnostic testing and clinical states relevant to healthcare practice.

Methods: Narrative integration of established mechanisms of glucose metabolism (glycolysis, tricarboxylic acid cycle, oxidative phosphorylation), storage dynamics, transporter biology (SGLT/GLUT families), endocrine regulation (insulin and counter-regulatory hormones), and standard glycemic tests (FBG, RBG, OGTT), with pathophysiologic correlates.

Results: Glucose flux is determined by (1) cellular pathways converting glucose to ATP under anaerobic and aerobic conditions; (2) storage–mobilization cycles governed by insulin–glucagon signaling; (3) tissue-specific transport via SGLTs and GLUT isoforms, notably insulin-responsive GLUT-4; and (4) organ axes—liver, pancreas, adrenal, thyroid, and anterior pituitary—that integrate nutrient and stress cues. Diagnostic assays (FBG, RBG, OGTT) characterize fasting and dynamic regulation, enabling detection of impaired tolerance and diabetes. Perturbations manifest as type 1 diabetes (autoimmune insulin deficiency), type 2 diabetes (insulin resistance with β-cell dysfunction), reactive and fasting hypoglycemia, and metabolic syndrome. Chronic hyperglycemia drives micro- and macrovascular complications; acute crises include hyperosmolar hyperglycemic state, while hypoglycemia endangers neurocognitive function.

Conclusion: Glucose homeostasis emerges from tightly coupled transport, enzymatic, and endocrine controls. Understanding these interactions improves risk stratification, testing choices, and targeted interventions across the dysglycemia spectrum

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