Continuous glucose monitoring
Published in General & Internal Medicine
Continuous glucose monitoring (CGM) emerges as a technology with the potential to provide patients, providers and health care professionals valuable information to achieve a better glycemic control while reducing the disease burden.
CGM devices measure interstitial glucose every 5 to 15 minutes, which highly correlates with blood glucose. They also provide information about trends in blood glucose levels and alert users for hypoglycemia and hyperglycemia. They consist of a glucose sensor placed under the skin, an adherent transmitter over it and a data receiver (either a portable device receiver or a smart phone or smart watch) (1, 2).
CGM provides real-time information about glucose control, allowing individuals to make timely decisions, understand glucose trends and fluctuations and adjust more precisely insulin dosing. It also helps to reduce hypoglycemia and hyperglycemia risks by providing early warnings when glucose levels are dropping or increasing. These benefits and the reduced need to frequent fingerstick tests, help to improve patients’ quality of life and reduce the burden of diabetes management.
There are three main types of CGM devices: real-time CGM, intermittently scanned CGM with and without alarms, and professional CGM (1-3).
Real-time CGM devices measure and store glucose levels continuously and without prompting. They also provide alarms to notify the user that glucose level is approaching or is in the hypoglycemic or hyperglycemic range, as well as arrows that show whether glucose is stable, increasing or decreasing quickly or very quickly.
Intermittently scanned CGM, sometimes called “flash glucose monitors”, measure glucose levels continuously but require scanning for their storage. The second generation of these devices also have alerts for hypoglycemia and hyperglycemia. Professional CGM are placed at the healthcare provider’s office and worn for a period, usually 7 to 14 days. Glucose levels may be blinded or visible for the patient. After this period, the patient returns to the health care office to download and analyze the data.
The use of these devices should always be coupled with patient’s education to adjust medication and change lifestyle behaviors.
CGM devices may be a part of the closed-loop insulin delivery systems, also referred to as the “artificial pancreas”. In these systems, insulin delivery can automatically be adjusted based on CGM data, further improving glucose control (4, 5).
CGM devices costs and concerns related to accuracy and reliability of measurements are some issues that may emerge as barriers to its use. However, CGM technology is in continuous evolution and efforts are being made by the researchers to improve sensor accuracy and to integrate the system with other diabetes management tools (1-3).
The consensus report of ADA and EASD recommended that glycemic control included, in addition with HbA1c, time in range assessment (a CGM-derived indicator) (6, 7). Noteworthy, the use of CGM in diabetic patients at high cardiovascular risk is promising and needs further evaluation according to the Delphi consensus published in Cardiovascular Diabetology (8).
Continuous glucose monitoring technology has revolutionized diabetes management by providing real-time data, glucose trends and hypoglycemia and hyperglycemia alerts, reducing the need to frequent fingerstick tests. These advantages, coupled with education and adequate follow-up, improve glycemic outcomes, reduce the disease burden and significantly improve the quality of life of people with diabetes.
References
- American Diabetes Association Professional Practice C. 7. Diabetes Technology: Standards of Medical Care in Diabetes-2022. Diabetes Care. 2022;45(Suppl 1):S97-S112.
- Sacks DB, Arnold M, Bakris GL, et al. Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus. Diabetes Care. 2023;46(10):e151-e99.
- Simonson GD, Bergenstal RM, Johnson ML, et al. Effect of Professional CGM (pCGM) on Glucose Management in Type 2 Diabetes Patients in Primary Care. J Diabetes Sci Technol. 2021;15(3):539-45.
- Templer S. Closed-Loop Insulin Delivery Systems: Past, Present, and Future Directions. Front Endocrinol (Lausanne). 2022;13:919942.
- Åm, M.K., Teigen, I.A., Riaz, M. et al. The artificial pancreas: two alternative approaches to achieve a fully closed-loop system with optimal glucose control. J Endocrinol Invest. 2023. https://doi.org/10.1007/s40618-023-02193-2
- Davies MJ, Aroda VR, Collins BS, et al. Management of hyperglycaemia in type 2 diabetes, 2022. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetologia. 2022;65(12):1925-1966.
- El-Sayed NA, Aleppo G, Aroda VR, et al. 6. Glycemic Targets: Standards of Care in Diabetes-2023. Diabetes Care. 2023;46(Suppl 1):S97-S110.
- Di Mario C, Genovese S, Lanza GA, et al. Role of continuous glucose monitoring in diabetic patients at high cardiovascular risk: an expert-based multidisciplinary Delphi consensus. Cardiovasc Diabetol. 2022;21(1):164.
Follow the Topic
-
Cardiovascular Diabetology
This journal considers manuscripts on all aspects of the diabetes/cardiovascular interrelationship and the metabolic syndrome; this includes clinical, genetic, experimental, pharmacological, epidemiological and molecular biology research.
Related Collections
With Collections, you can get published faster and increase your visibility.
Vascular Drivers of Cardio-Metabolic Disease: Mechanisms and Clinical Implications
Despite advancements in glycemic control, cardiovascular disease remains the leading cause of morbidity in diabetes. The plateau in clinical outcomes suggests that we may have overlooked a complex, multi-organ communication network—the vasculome. This Collection seeks to move beyond traditional glucocentric frameworks to better understand endothelial biology as a dynamic interface integrating metabolic, immune, neural, and hormonal signals. We focus on the concept of the endothelial interactome, a heterogeneous and spatially diverse regulatory system that contributes to vascular dysfunction, organ-specific complications, and cardiometabolic risk.
The aim of this Collection is to provide a high-impact platform for research that characterizes site-specific endothelial heterogeneity and its interactions with peripheral organ systems in cardiometabolic disease. We particularly encourage studies that identify molecular and cellular “signatures” (e.g., angiokines, inflammatory mediators, and metabolic regulators) that contribute to organ-specific vascular complications. By integrating systems biology approaches with clinical and translational data, we aim to advance understanding of disease mechanisms and identify novel targets for prevention, risk stratification, and precision therapy, including strategies that address persistent vascular dysfunction despite metabolic control.
We welcome original research articles, clinical investigations, observational cohort studies, randomized clinical trials, high-level reviews, and translational perspectives.
Topics of interest include, but are not limited to:
- Neuro-Immune-Vascular Axis: Interactions between autonomic regulation, immune activation, and vascular inflammation in cardiometabolic disease
- Sex as a Biological Variable: Sex-specific mechanisms contributing to vascular complications in diabetes and metabolic disease
- Epigenetic and Immune Memory: Mechanisms of vascular “trained immunity” and potential strategies for reversal or modulation
- Systems Medicine Approaches: Multi-omics, computational modeling, and organ-on-a-chip platforms to study endothelial heterogeneity and inter-organ communication
- Clinical Translation: Biomarkers, imaging approaches, and therapeutic strategies targeting vascular dysfunction and improving cardiovascular outcomes in diabetes and related metabolic disorders
We invite contributions that bridge basic, translational, and clinical research to advance a more integrated understanding of vascular disease in cardiometabolic disorders. Our goal is to translate mechanistic insights into meaningful clinical outcomes that improve prevention, diagnosis, and treatment in metabolic disease.
All submissions in this Collection undergo the journal’s standard peer review process. Similarly, all manuscripts authored by a Guest Editor(s) will be handled by the Editor-in-Chief. As an open access publication, this journal levies an article processing fee (details here). We recognize that many key stakeholders may not have access to such resources and are committed to supporting participation in this issue wherever resources are a barrier. For more information about what support may be available, please visit OA funding and support, or email OAfundingpolicy@springernature.com or the Editor-in-Chief.
Publishing Model: Open Access
Deadline: Jun 09, 2027
Cardiometabolic and Hepatic Interconnections: From Mechanisms to Clinical Implications
Cardiovascular Diabetology features a Collection on "Cardiometabolic and Hepatic Interconnections: From Mechanisms to Clinical Implications". This is a companion Collection with Diabetology & Metabolic Syndrome with the title "MASLD Beyond the Liver: Epidemiology, Pathophysiology, Diagnosis, and Therapeutic Implications in Multisystem Disorders".
Cardiometabolic and liver diseases are no longer viewed as isolated entities. Growing evidence shows that hepatic and cardiovascular dysfunctions are tightly interconnected through shared metabolic, inflammatory, hemodynamic, and hormonal pathways. This crosstalk shapes disease trajectories and opens opportunities for integrated diagnostics and therapies.
Key interconnections include:
- Insulin resistance. The liver is pivotal for glucose and lipid homeostasis. Hepatic insulin resistance drives excess glucose production and dyslipidemia, contributing to the cardiovascular–kidney–metabolic (CKM) syndrome.
- Metabolic dysfunction–associated steatotic liver disease (MASLD). Highly prevalent in obesity and metabolic syndrome, and especially common in type 2 diabetes (T2D), which bears the highest MASLD burden. Progression to steatohepatitis or fibrosis markedly increases atherosclerotic risk.
- Liver-derived factors. Hepatokines (e.g., FGF21) and extracellular vesicles influence cardiac tissue, vascular tone, and systemic metabolism, potentially amplifying inflammation, oxidative stress, and lipotoxicity across organs.
- Systemic inflammation and lipotoxicity. Visceral adipose tissue and the liver release inflammatory cytokines and triglyceride-rich lipids, promoting endothelial dysfunction and perpetuating metabolic disturbances.
- Dyslipidemia. Elevated triglycerides and LDL, with reduced HDL, accelerate atherogenesis and cardiovascular risk.
- Hemodynamic and metabolic stress. Heart failure can cause hepatic congestion and hypoperfusion, while advanced liver disease can precipitate cirrhotic cardiomyopathy and arrhythmias, even in the absence of prior heart failure.
In summary, hepatic and cardiometabolic systems are functionally and pathologically intertwined: liver dysfunction worsens cardiovascular and metabolic health, and cardiometabolic disturbances accelerate hepatic pathology.
This Collection welcomes original research articles, reviews, and meta-analyses focused on this reciprocal relationship. Given the high prevalence of MASLD in T2D, we especially encourage submissions at the T2D–MASLD–cardiovascular interface. Addressing hepatic and cardiometabolic health in parallel is essential for effective risk reduction and patient care.
This Collection supports and amplifies research related to SDG 3, Good Health and Well-Being.
All submissions in this Collection undergo the journal’s standard peer review process. Similarly, all manuscripts authored by a Guest Editor(s) will be handled by the Editor-in-Chief. As an open access publication, this journal levies an article processing fee (details here). We recognize that many key stakeholders may not have access to such resources and are committed to supporting participation in this issue wherever resources are a barrier. For more information about what support may be available, please visit OA funding and support, or email OAfundingpolicy@springernature.com or the Editor-in-Chief.
Publishing Model: Open Access
Deadline: Oct 31, 2026