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Original Article
Diabetes, obesity and metabolism Impact of Carbohydrate Intake Fluctuations on Glucose Profiles: Insights from Continuous Glucose Monitoring-Based Patient Clustering
Keypoint
- Continuous glucose monitoring (CGM) can categorize individuals according to glucose profiles, and greater fluctuations in carbohydrate intake are associated with poorer glycemic control.
- Personalized dietary adjustments, particularly stabilization of carbohydrate intake, may improve glucose management in individuals with high mean glucose levels and a low CGM-derived coefficient of variation.
Hyun Ah Kim1orcid, Kyung Hee Kim2, Young Lee3, Yoon-Ju Song4, Joon Ho Moon2,5, Sung Hee Choi2,5, Tae Jung Oh2,5orcid
Endocrinology and Metabolism 2026;41(1):152-161.
DOI: https://doi.org/10.3803/EnM.2025.2486
Published online: December 12, 2025

1Department of Internal Medicine, Veterans Health Service Medical Center, Seoul, Korea

2Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea

3Veterans Medical Research Institute, Veterans Health Service Medical Center, Seoul, Korea

4Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, Korea

5Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea

Corresponding author: Tae Jung Oh. Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 82 Gumi-ro 173beon-gil, Bundang-gu, Seongnam 13620, Korea Tel: +82-31-787-7078, Fax: +82-31-787-4050, E-mail: ainici5@snu.ac.kr
• Received: June 4, 2025   • Revised: August 10, 2025   • Accepted: September 15, 2025

Copyright © 2026 Korean Endocrine Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Background
    Continuous glucose monitoring (CGM) is widely applied in daily glucose management. However, its potential to categorize individuals based on glucose profiles is not fully established. This study employed CGM-based patient clustering and examined nutritional factors influencing glucose patterns.
  • Methods
    This prospective observational study enrolled 34 individuals with diabetes. Retrospective professional CGM was conducted over 7 days, during which food intake was recorded. K-means clustering was performed using CGM-derived coefficient of variation (CV) and time in range. Macronutrient intake and its fluctuations were compared across clusters.
  • Results
    Participants were grouped into cluster 1 (well-controlled), cluster 2 (highest CV), and cluster 3 (highest mean glucose). Baseline clinical characteristics, daily energy intake (kcal), and macronutrient intake did not differ significantly among clusters. However, carbohydrate intake fluctuations were greater in cluster 3 (CV 41.0%±32.1%, standard deviation [SD] 502.1±363.4 kcal) than in cluster 1 (CV 21.9%±9.0%, SD 260.2±94.1 kcal) and cluster 2 (CV 19.2%±9.1%, SD 250.2±126.1 kcal) (P=0.123 for CV; P=0.024 for SD). The SD (kcal) of carbohydrate intake was positively correlated with mean glucose levels (rho=0.88, P=0.023).
  • Conclusion
    CGM enables categorization of individuals based on glucose profiles, and higher carbohydrate intake fluctuations are associated with poorer glycemic control. Personalized dietary strategies, particularly stabilizing carbohydrate intake, may support better glucose management in individuals with high mean glucose and low CV.
Continuous glucose monitoring (CGM) has become a cornerstone of diabetes management since its introduction more than two decades ago, providing real-time data on glucose levels and fluctuations [1-3]. Unlike hemoglobin A1c (HbA1c), which reflects long-term glycemic control but fails to capture daily variability, CGM records glucose values every 5 minutes, offering granular insights into glycemic dynamics [4]. Key CGM-derived indices—including coefficient of variation (CV), time in range (TIR), time below range (TBR), and time above range (TAR)—allow a comprehensive evaluation of glucose control and guide optimization of therapeutic strategies [5].
Beyond monitoring, CGM data have been applied to classify individuals with diabetes or at risk of the disease by revealing characteristic patterns of metabolic dysfunction [6-8]. For instance, one study demonstrated a progressive shift in CGM indices, documenting increasing glycemic variability and deterioration in glucose homeostasis from healthy individuals to those with prediabetes and subsequently to patients with diabetes [9]. Such classifications aim to enhance early detection and risk stratification of individuals at high risk for diabetes progression, as well as to support personalized treatment approaches [10-12].
Despite these advances, limited research has integrated dietary patterns with CGM-based classification in diabetes. Given the pivotal role of nutrition in shaping glycemic responses, we categorized individuals with diabetes according to CGM-derived clusters and investigated associated nutritional factors. We further evaluated whether CGM-based clustering could predict changes in HbA1c after 3 months compared with baseline. This approach seeks to clarify how real-world dietary patterns affect glucose profiles and long-term glycemic outcomes.
Study participants and study design
This was a prospective, single-center observational study conducted at Seoul National University Bundang Hospital. Eligible participants were adults aged ≥20 years with a diagnosis of diabetes and an HbA1c level of ≥7.0%. Exclusion criteria included acute or active skin lesions unsuitable for CGM placement, current chemotherapy or immunosuppressive therapy, inability to perform fingerstick glucose monitoring, and planned contrast-enhanced computed tomography within 1 week of study initiation.
All participants underwent CGM and were categorized into three clusters according to CGM-derived metrics. The primary aim was to determine how glucose patterns and variability differed across clusters. Glucose variability was evaluated using the CV (%) and standard deviation (SD). The secondary aim was to identify dietary characteristics that distinguished the clusters.
The study was approved by the Institutional Review Board of Seoul National University Bundang Hospital (No. B-1803-459-301), and all participants provided written informed consent. The study adhered to the principles of the Declaration of Helsinki and good clinical practice guidelines.
CGM and clustering
The iPro2 CGM system (Medtronic, Seoul, Korea) was applied to all participants for 7 days. Glucose values were recorded every 5 minutes, and the data were exported into Excel files (Microsoft, Redmond, WA, USA) for analysis. CGM metrics included mean glucose (mg/dL), CV (%), SD (mg/dL), TAR (>250 mg/dL and >180 mg/dL), TIR (70–180 mg/dL), and TBR (<70 mg/dL). K-means clustering was applied to categorize participants into three clusters based on these metrics.
Dietary assessment and day-to-day fluctuations in nutrient intake
During CGM monitoring (days 1–7), dietary intake was recorded using food diaries, with entries organized by meal type (breakfast, lunch, dinner, and snacks). Participants documented detailed descriptions and portion sizes, such as ‘one glass of juice,’ ‘one serving of cooked rice,’ ‘three chopsticks of seasoned bean sprout salad,’ or ‘half an apple.’ All reported food quantities were converted into grams for analysis. Because starting and ending times varied, dietary records from day 1 and day 7 were excluded, leaving days 2–6 for analysis.
Nutrient composition was calculated using the Food and Nutrient Ingredients Database of the Ministry of Food and Drug Safety of South Korea. Data were summarized by meal and macronutrient: carbohydrates (g), proteins (g), fats (g), saturated fats (g), and sodium (g). Analyses included daily energy intake (kcal), energy by meal, energy distribution across meals (% kcal), macronutrient intake (g), and macronutrient ratio (% kcal). All records were reviewed by a registered dietitian at the study hospital.
We also aimed to examine how day-to-day and meal-to-meal energy and nutrient intake fluctuations differed between the three clusters, and to understand potential dietary patterns. Day-to-day fluctuations in energy and macronutrient intake were defined as the CV (%) or SD (kcal) of daily intake from days 2–6. Meal-to-meal fluctuations were assessed as intra-individual CV (%) and SD (kcal) between meals. Intra-individual CV (%) and SD (kcal) were also calculated for CGM metrics. Spearman’s partial correlation was performed while controlling for insulin use.
Other outcomes
Baseline demographic, clinical, and biochemical characteristics were collected, including comorbidities and glucose-lowering therapies. HbA1c was reassessed 3 months after study initiation. Additional outcomes included the proportion of participants achieving HbA1c <7.0% at 3 months, within-cluster changes from baseline, and differences between clusters. These analyses were intended to evaluate whether baseline clustering predicted short-term glycemic improvement.
Statistical analysis
Descriptive data were presented as mean±SD for continuous variables or as frequencies (numbers and percentages) for categorical variables. Comparisons among the three clusters (cluster 1, cluster 2, and cluster 3) were conducted using one-way analysis of variance (ANOVA) for normally distributed continuous variables, the Kruskal-Wallis test for non-normally distributed continuous variables, and the chi-squared test for categorical variables, as appropriate. A P<0.05 was considered statistically significant. For variables with P<0.05, post hoc analyses were performed using the Tukey’s honest significant difference test for ANOVA or the Dunn’s test for non-parametric comparisons. Associations between continuous variables were examined using Spearman’s rank correlation and partial correlation analysis. All statistical analyses were performed with R version 4.1.2 (R Core Team, Vienna, Austria). Figures were created using Graph-Pad Prism version 10.4.0 (GraphPad Software Inc., San Diego, CA, USA).
Study population
A total of 34 participants with type 1 diabetes mellitus (T1DM, n=10) or type 2 diabetes mellitus (T2DM, n=22) and HbA1c levels >7.0% were enrolled between July 2018 and August 2020. Two individuals were excluded: one due to technical failure preventing retrieval of CGM data, and another due to poor adherence to food diary completion. Thus, 32 participants (14 male and 18 female) were included in the final analysis. One additional individual was excluded from the analysis of HbA1c changes at 3 months because a follow-up HbA1c measurement was unavailable.
As shown in Fig. 1, the 32 participants were categorized into three clusters (cluster 1, cluster 2, and cluster 3) using K-means clustering based on CGM data. Multiple clustering trials were conducted using different combinations of CGM metrics, including mean glucose (mg/dL), CV (%), % TAR >250 mg/dL, % TAR >180 mg/dL, % TIR 70–180 mg/dL, and % TBR <70 mg/dL. After evaluating the results, CV (%) and % TIR 70–180 mg/dL were selected as the independent variables that best distinguished glucose profiles across clusters.
Baseline characteristics
Table 1 presents the baseline characteristics of the three clusters: cluster 1 (well-controlled), cluster 2 (high variability), and cluster 3 (high mean glucose). The sex distribution, age, and proportion of participants with T1DM were similar across clusters. The mean duration of diabetes did not differ significantly: cluster 1 (11.8±10.2 years), cluster 2 (12.9±7.1 years), and cluster 3 (14.6±7.5 years). Although body mass index (BMI) and blood pressure were comparable across clusters, obesity prevalence (BMI ≥25 kg/m2) was highest in cluster 3 (87.5%), compared with cluster 1 (40.0%) and cluster 2 (35.7%) (P=0.060).
Baseline fasting plasma glucose, HbA1c, fasting C-peptide, and fasting insulin levels were similar between clusters. However, cluster 3 exhibited significantly higher 2-hour postprandial glucose (286.7±52.0 mg/dL) than cluster 1 (169.1±82.8 mg/dL) and cluster 2 (203.2±71.6 mg/dL) (P=0.023). Triglyceride levels were also significantly higher in cluster 3 (180.6±88.0 mg/dL) than in cluster 1 (110.2±41.8 mg/dL) and cluster 2 (99.4±48.5 mg/dL) (P=0.013).
Other laboratory results, including renal and liver function tests, were comparable across clusters. Comorbidities such as hypertension and dyslipidemia were similarly distributed. Insulin regimens (basal, premixed, or basal bolus) were also used in comparable proportions across the three clusters.
CGM profiles
CGM parameters for each cluster are presented in Table 2 and Fig. 2. Significant differences were observed among clusters for mean glucose (mg/dL), CV (%), SD (mg/dL), % TAR >180 mg/dL, and % TIR 70–180 mg/dL (all P<0.001). Cluster 1 (well-controlled) had the lowest mean glucose (138.1±16.8 mg/dL) and the highest % TIR 70–180 (94.5%±7.0%). Cluster 3 (high mean glucose) showed the highest mean glucose (203.4±40.5 mg/dL) and the lowest % TIR 70–180 (32.6%±18.1%). Cluster 2 (high variability) displayed intermediate mean glucose (168.3±22.6 mg/dL) and TIR (61.2%±14.2%). Post hoc analyses confirmed that both mean glucose and % TIR differed significantly among all three clusters (P<0.05). Cluster 2 exhibited the highest CV (27.3%±5.4%), which was significantly greater than in the other two clusters. Similarly, SD was highest in cluster 2 (46.1±11.5 mg/dL), followed by cluster 3 (35.3±7.4 mg/dL) and cluster 1 (21.0±7.4 mg/dL). Cluster 3 had the highest % TAR >180 mg/dL (51.6%±20.7%), followed by cluster 2 (30.7%±9.8%), while cluster 1 had the lowest (5.5%±7.0%). Post hoc analysis confirmed that the TAR >180 mg/dL in cluster 1 was significantly lower than in clusters 2 and 3.
Nutritional profiles
Table 3 summarizes the energy intake (kcal) of participants in clusters 1, 2, and 3. Total daily energy intake, energy intake by meal, and the distribution of energy (% kcal) across meals did not differ significantly among clusters. Similarly, macronutrient intake (g) and the macronutrient ratio (% kcal) were comparable across groups.
However, significant differences were observed in carbohydrate intake fluctuations. The day-to-day fluctuations of carbohydrate intake (5-day SD) were significantly higher in cluster 3 (high mean glucose) (502.1±363.4 kcal) compared with cluster 1 (well-controlled) (260.2±94.1 kcal) and cluster 2 (high variability) (250.2±126.1 kcal), with a P value of 0.024. In contrast, day-to-day variability in total daily energy intake, protein, and fat did not differ significantly among clusters.
Table 4 presents the Spearman’s partial correlations of intraindividual meal-to-meal fluctuations in total daily energy intake and macronutrient composition with the energy percentage of breakfast, lunch, and dinner, as well as mean energy intake per meal. Both intra-individual meal-to-meal CV (%) and SD (kcal) for total daily energy intake were positively correlated with the energy percentage of lunch meals (rho=0.49, P=0.005; and rho=0.52, P=0.002, respectively).
In addition, both CV (%) and SD (kcal) of total daily energy intake were negatively correlated with mean energy intake per meal. Specifically, carbohydrate CV (%) and SD (kcal) were negatively correlated with mean energy intake per meal (rho=–0.62, P<0.001; and rho=–0.43, P=0.012, respectively). Similarly, fat CV (%) and SD (kcal) also showed negative correlations.
Furthermore, both CV (%) and SD (kcal) of carbohydrate intake were positively correlated with CGM mean glucose levels, with the SD correlation reaching statistical significance (rho=0.88, P=0.023). A sensitivity analysis excluding one visually distant data point from cluster 3 confirmed the robustness of this finding, as the correlation between carbohydrate intake SD and mean glucose remained strong (rho=0.81, P=0.049).
3-Month follow-up
At the 3-month follow-up, HbA1c improved in cluster 1 (well-controlled), decreasing from 8.5%±1.2% at baseline to 7.7%±1.9%. In contrast, no significant change was observed in clusters 2 and 3. HbA1c shifted from 8.7%±0.8% to 8.6%±0.8% in cluster 2 (high variability) and from 8.2%±1.1% to 8.3%±0.8% in cluster 3 (high mean glucose). In cluster 1, the proportion of participants achieving HbA1c <7.0% increased from 0.0% at baseline to 33.3% at follow-up. By comparison, no participants in clusters 2 or 3 achieved or improved to HbA1c <7.0%.
In this study, K-means clustering was performed using standardized CGM metrics derived from ambulatory glucose profile reports—including % TIR, % TBR, mean glucose, SD, and CV—to ensure clinical relevance and comparability across participants [13]. To confirm consistency, clustering analyses were repeated using multiple combinations of validated metrics. % TIR was used to represent overall glycemic control, while CV reflected glycemic variability (%) [14]. Based on these metrics, participants were categorized into three clusters: cluster 1 (well-controlled), cluster 2 (highest CV), and cluster 3 (highest mean glucose).
Cluster 3 (high mean glucose) was characterized by the highest mean glucose level and intermediate glycemic variability, indicating a persistent hyperglycemic profile. This cluster also exhibited the greatest day-to-day fluctuations in carbohydrate intake, suggesting irregular or unbalanced dietary patterns. In contrast, cluster 1 (well-controlled) demonstrated the most favorable glycemic metrics, including both lower mean glucose levels and more consistent carbohydrate intake. Additional analyses showed that higher intra-individual meal-to-meal fluctuations in carbohydrate intake were associated with lower mean energy intake per meal and higher CGM mean glucose levels. Collectively, these findings suggest that in individuals with persistent hyperglycemia and relatively low glycemic variability, inconsistent carbohydrate intake may contribute to suboptimal glycemic control.
The American Diabetes Association’s clinical practice guidelines emphasize lifestyle and behavioral interventions as the foundation of diabetes prevention [15] and highlight the importance of healthy dietary patterns [16]. Dietary approaches such as the Mediterranean diet, intermittent fasting, and low-carbohydrate diets have been associated with improved glycemic control [17-19]. In particular, low-carbohydrate diets have been linked to reduced risk of T2DM [20], improvements in HbA1c, and decreased reliance on glucose-lowering medications [21-23]. These findings underscore that carbohydrate intake patterns play an essential role in diabetes management.
Previous studies have applied CGM-based clustering to identify individuals at risk of diabetes progression and to enhance early risk stratification [9-11]. However, limited work has integrated dietary patterns into CGM-based classification. To our knowledge, this is the first study to suggest that intra-individual fluctuations in energy and macronutrient intake may be linked to distinctive features of glucose profiles.
Our results further imply that dietary patterns characterized by large lunch meals may reflect uneven distribution of carbohydrate or fat intake, consumed in disproportionately high amounts at a single sitting. CGM mean glucose levels were positively correlated with fluctuations in energy and carbohydrate intake, suggesting that carbohydrate-loading dietary patterns may exacerbate hyperglycemia. Thus, dietary patterns involving large, carbohydrate-heavy meals may compromise glucose regulation.
These findings highlight the importance of balanced meal sizes and even nutritional distribution, particularly for individuals with diabetes and high mean glucose levels. Dietary interventions aimed at improving the regularity and balance of carbohydrate consumption may be especially beneficial for those with high mean glucose and low glycemic variability, as observed in cluster 3 (high mean glucose).
Using one week of CGM data, this simplified clustering approach identified individuals more likely to achieve optimal glycemic control in the short term. Cluster 1 (well-controlled), which had favorable baseline CGM profiles, demonstrated HbA1c improvement at 3 months, potentially reflecting greater responsiveness to general lifestyle guidance. In contrast, clusters 2 (high variability) and 3 (high mean glucose) showed no significant improvement, suggesting that these individuals may require more intensive pharmacologic interventions. Overall, the clustering approach demonstrated predictive value for glycemic outcomes over the subsequent 3 months. These findings suggest that early CGM-based clustering could help identify patients more likely to reach short-term glycemic targets and provide prognostic insights useful for clinical decision-making, including determining optimal timing for elective procedures.
However, this study has several limitations. The clustering analysis was exploratory, and the small sample size—with limited numbers of participants in each cluster—reduced the statistical power to detect between-group differences and limited the robustness of subgroup comparisons. Formal power calculations are inherently challenging in unsupervised clustering, as no predefined group structure or effect size exists prior to analysis. Therefore, the findings should be considered hypothesis-generating rather than confirmatory.
In studies with small samples, we acknowledge the potential risk of overfitting. To minimize this, we selected a minimal set of variables for clustering, applied careful parameter selection to avoid over-specification, and interpreted the cluster patterns cautiously. For the one variable that showed a statistically significant difference between clusters—carbohydrate intake variability—we conducted a post hoc power analysis. The observed effect size (Cohen’s f=0.55) corresponded to a statistical power of 76%, suggesting that the finding is reasonably reliable despite the small sample. Nevertheless, confirmation in larger and more homogeneous cohorts is required to validate and generalize these observations.
Our analysis demonstrated that greater variability in carbohydrate intake was associated with higher mean glucose levels. However, given the observational design of this study, the possibility of reverse causation must also be considered. Previous research has indicated that postprandial glucose dips may increase hunger and subsequent energy intake, while irregular meal timing can influence glucose fluctuations. Thus, a bidirectional relationship between glycemic status and dietary behavior is plausible, underscoring the need for further investigation through longitudinal or interventional studies.
CGM data were collected over a 7-day period, but the start time on day 1 and the end time on day 7 varied among participants. To ensure consistency and data quality, only days 2 through 6 were included in the final analysis. Although this monitoring window was relatively short, daily energy and macronutrient intake were similar across all clusters, suggesting that the restriction is unlikely to have introduced substantial dietary bias. Nonetheless, longer monitoring periods would be valuable to determine whether the dietary and glycemic patterns observed here remain consistent over time.
Raw CGM data could have provided additional insights, such as intra-day glucose trends or postprandial excursions. However, these features were excluded due to limited standardization and potential noise. Instead, K-means clustering was performed using standardized CGM metrics derived from ambulatory glucose profile reports, ensuring clinical relevance and comparability across participants.
This study included both T1DM and T2DM patients. The distribution of diabetes type was similar across clusters, and the proportion of participants with T1DM did not differ significantly. Given the small sample, further stratified analyses by diabetes type were not feasible.
All participants received standardized lifestyle education based on Korean Diabetes Association materials, covering balanced meals, regular physical activity, and weight management. However, individual adherence was not formally assessed, and longitudinal behavioral data were not collected, which may have introduced residual confounding.
Alongside carbohydrate intake variability, glycemic variability can be influenced by non-dietary factors such as insulin dosing, physical activity, and hypoglycemic events. Although participants were blinded to CGM data, self-monitored capillary glucose data in insulin users were not considered in this analysis. Moreover, as the study population had a low incidence of hypoglycemia, the findings may not be generalizable to individuals at higher risk for hypoglycemia.
Recognizing the limitation of not accounting for multiple non-dietary influences, we acknowledge that the relationship between carbohydrate intake variability and glycemic variability is likely multifactorial. Nonetheless, this study emphasizes that variability in carbohydrate intake was closely associated with higher mean glucose levels, suggesting that inconsistent dietary intake may contribute to sustained hyperglycemia.
Since this is an observational study, the dietary implications reported here should be regarded as exploratory and hypothesis-generating. This study suggests that CGM can categorize individuals with diabetes according to their glucose profiles, and that such clustering reflects underlying dietary behaviors. High variability in carbohydrate intake was associated with large lunch meals and impaired glycemic control. These findings suggest that, for individuals with a CGM profile of high mean glucose and relatively low CV, dietary strategies emphasizing balanced meal size and distribution of nutrients may be beneficial. Future prospective studies are needed to evaluate whether dietary interventions tailored to CGM-based cluster profiles can improve glycemic outcomes.

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

ACKNOWLEDGMENTS

Tae Jung Oh was supported by an investigator grant from the Seoul National University Bundang Hospital Research Fund (18-2018-0015).

We would like to thank Ms. Nam Yeon Seo, a registered dietitian at the affiliated hospital, for her valuable advice and support during the early phase of this study.

We acknowledge Ji-hyung Kook’s initial efforts in planning the research.

AUTHOR CONTRIBUTIONS

Conception or design: T.J.O. Acquisition, analysis, or interpretation of data: H.A.K., K.H.K., Y.L., Y.J.S., J.H.M., S.H.C., T.J.O. Drafting the work or revising: H.A.K., T.J.O. Final approval of the manuscript: H.A.K., K.H.K., Y.L., Y.J.S., J.H.M., S.H.C., T.J.O.

Fig. 1.
Patient distribution by K-means clustering based on coefficient of variation (CV) and time in range 70–180 mg/dL (TIR).
enm-2025-2486f1.jpg
Fig. 2.
Percentage of time above range (TAR; >180 or >250 mg/dL), time in range (TIR; 70–180 mg/dL), and time below range (TBR; <70 mg/dL) in clusters 1, 2, and 3.
enm-2025-2486f2.jpg
enm-2025-2486f3.jpg
Table 1.
Baseline Clinical Characteristics of Participants Distributed by K-Means Clustering
Characteristic Cluster 1 Cluster 2 Cluster 3 P value
Sex, male:female 3:7 6:8 5:3 0.444
Age, yr 46.2±17.5 50.3±8.8 51.0±14.3 0.693
T1DM, % 30.0 35.7 25.0 >0.999
DM duration, yr 11.8±10.2 14.6±7.5 12.7±9.1 0.728
BMI, kg/m2 25.6±5.7 24.9±6.0 28.1±4.8 0.202
Obesity 4 (40.0) 5 (35.7) 7 (87.5) 0.060
SBP, mm Hg 126.8±11.0 126.9±14.0 135.1±12.6 0.304
DBP, mm Hg 71.9±4.7 71.9±11.6 77.6±9.9 0.354
FPG, mg/dL 123.8±41.6 141.5±47.5 136.4±62.0 0.764
PP2, mg/dL 169.1±82.8 203.2±71.6 286.7±52.0 0.023
HbA1c, % 8.5±1.2 8.7±0.8 8.2±1.1 0.529
C-peptide, ng/mL 2.3±2.2 1.8±2.5 2.4±1.4 0.293
Insulin, μIU/mL 5.3±4.0 6.3±7.1 12.6±18.8 0.167
eGFR MDRD, mL/min/1.73 m2 107.3±52.1 87.5±24.5 90.2±37.4 0.437
AST, IU/L 26.2±5.1 25.4±7.6 26.0±7.5 0.953
ALT, IU/L 22.6±10.4 24.4±9.4 27.6±10.8 0.577
Total cholesterol, mg/dL 193.3±53.6 157.5±55.4 166.5±32.7 0.242
TG, mg/dL 110.2±41.8 99.4±48.5 180.6±88.0 0.013
HDL cholesterol, mg/dL 60.6±10.8 51.5±19.3 48.9±12.9 0.267
LDL cholesterol, mg/dL 119.2±38.9 92.2±33.8 97.8±24.5 0.157
Comorbidities
 Hypertension 5 (50.0) 6 (42.9) 6 (75.0) 0.357
 Dyslipidemia 7 (70.0) 12 (85.7) 7 (87.5) 0.616
Insulin use 0.928
 None 1 (10.0) 1 (7.1) 1 (12.5)
 Basal insulin 0 0 1 (12.5)
 Premixed insulin 3 (30.0) 5 (35.7) 2 (25.0)
 Basal bolus insulin 6 (60.0) 8 (57.1) 4 (50.0)

Values are expressed as mean±standard deviation or number (%). P values represent the results of the one-way analysis of variance (ANOVA), Kruskal-Wallis test, or chi-squared test.

T1DM, type 1 diabetes mellitus; DM, diabetes mellitus; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; PP2, 2-hour postprandial glucose; HbA1c, hemoglobin A1c; eGFR, estimated glomerular filtration rate; MDRD, Modification of Diet in Renal Disease; AST, aspartate transferase; ALT, alkaline transferase; TG, triglyceride; HDL, high density lipoprotein; LDL, low density lipoprotein.

Table 2.
Continuous Glucose Monitoring Profiles of Participants Distributed by K-Means Clustering
Variable Cluster 1 (well-controlled) Cluster 2 (high variability) Cluster 3 (high mean glucose) P value
Mean glucose, mg/dL 138.1±16.8a 168.3±22.6b 203.4±40.5c <0.001
CV, % 15.4±5.6a 27.3±5.4b 17.7±4.3a <0.001
SD, mg/dL 21.0±7.4a 46.1±11.5b 35.3±7.4c <0.001
TAR (>250 mg/dL), % 0.0±0.0 7.0±12.6 15.8±31.7 0.057
TAR (>180 mg/dL), % 5.5±7.0a 30.7±9.8b 51.6±20.7b <0.001
TIR (70–180 mg/dL), % 94.5±7.0a 61.2±14.2b 32.6±18.1c <0.001
TBR (<70 mg/dL), % 0 1 (7.1) 0 0.999

Values are expressed as mean±standard deviation or number (%). P values represent the results of one-way analysis of variance (ANOVA) or the Kruskal-Wallis test.

CV, coefficient of variation; SD, standard deviation; TAR, time above range; TIR, time in range; TBR, time below range.

a,b,c Post hoc analysis was done for variables with P<0.05 by the Tukey’s honest significant difference test or the Dunn’s test.

Table 3.
Nutrient Intake of Participants Distributed by K-Means Clustering
Variable Cluster 1 Cluster 2 Cluster 3 P value
Total daily energy, kcal 2,414.4±316.3 2,525.4±494.1 2,362.9±735.4 0.756
Breakfast, kcal 548.7±175.2 584.9±215.9 596.4±253.0 0.879
Lunch, kcal 812.3±176.5 766.3±210.6 724.9±244.3 0.680
Dinner, kcal 786.7±156.2 841.6±198.5 715.5±199.8 0.325
Snack, kcal 264.7±228.6 332.7±286.3 258.2±236.1 0.764
Breakfast, % kcal 22.4±7.7 23.1±8.1 26.1±10.2 0.458
Lunch, % kcal 35.1±8.3 30.7±7.6 32.1±6.5 0.382
Dinner, % kcal 31.8±5.3 33.7±6.7 33.0±9.0 0.642
Snack, % kcal 10.7±8.2 12.5±9.3 10.8±7.8 0.846
Carbohydrate, g 302.2±52.4 333.4±70.0 337.1±83.8 0.471
Protein, g 112.1±21.3 112.4±34.1 110.1±44.0 0.527
Fat, g 79.0±9.7 87.2±25.8 78.8±41.2 0.178
Carbohydrate, % kcal 51.9±5.0 53.8±8.9 57.4±12.2 0.437
Protein, % kcal 18.5±2.6 17.6±3.9 18.5±3.1 0.757
Fat, % kcal 28.8±4.2 30.6±7.8 28.6±7.3 0.737
Day-to-day fluctuations in energy and nutrient intake, 5-day CV, %
 Total daily energy 27.0±11.5 17.9±7.4 29.5±20.8 0.191
 Carbohydrate 21.9±9.0 19.2±9.1 41.0±32.1 0.123
 Protein 36.3±15.3 32.6±12.4 37.4±29.5 0.849
 Fat 46.5±17.4 37.4±24.4 51.5±35.4 0.310
Day-to-day fluctuations in energy and nutrient intake, 5-day SD, kcal
 Total daily energy 632.2±212.0 436.3±171.5 605.1±239.4 0.052
 Carbohydrate 260.2±94.1 250.2±126.1 502.1±363.4 0.024
 Protein 159.9±65.9 138.0±47.5 154.4±104.0 0.733
 Fat 323.3±104.6 285.8±221.1 374.1±338.4 0.181

Values are expressed as mean±standard deviation. P values within each group represent the results of one-way analysis of variance (ANOVA) or the Kruskal-Wallis test. Day-to-day fluctuations in energy (kcal) and macronutrient intake were defined as the CV (%) or SD (kcal) of daily intake from day 2 to 6 for each individual.

CV, coefficient of variation; SD, standard deviation.

Table 4.
Correlation of Meal-to-Meal Fluctuations in Energy and Nutrient Intake with Meal Types and Mean Energy Intake per Meal
Variable Breakfast, % kcal Lunch, % kcal Dinner, % kcal Mean energy intake per meal
Total daily energy (CV), % –0.17 0.49a –0.10 –0.47a
Carbohydrate (CV), % –0.21 0.21 –0.24 –0.62a
Protein (CV), % 0.18 0.18 –0.24 –0.32
Fat (CV), % 0.21 0.31 –0.32 –0.42a
Total daily energy (SD), kcal –0.36a 0.52a –0.18 –0.17
Carbohydrate (SD), kcal –0.16 0.06 –0.32 –0.43a
Protein (SD), kcal 0.15 0.15 –0.21 0.11
Fat (SD), kcal 0.04 0.39a –0.27 –0.04

Data are presented by Spearman’s partial correlation coefficients after controlling for insulin use. Meal-to-meal fluctuations were defined as intra-personal CV (%) and SD (kcal) between meals.

CV, coefficient of variation; SD, standard deviation.

a P values of statistical significance.

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      Impact of Carbohydrate Intake Fluctuations on Glucose Profiles: Insights from Continuous Glucose Monitoring-Based Patient Clustering
      Endocrinol Metab. 2026;41(1):152-161.   Published online December 12, 2025
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    Impact of Carbohydrate Intake Fluctuations on Glucose Profiles: Insights from Continuous Glucose Monitoring-Based Patient Clustering
    Image Image Image
    Fig. 1. Patient distribution by K-means clustering based on coefficient of variation (CV) and time in range 70–180 mg/dL (TIR).
    Fig. 2. Percentage of time above range (TAR; >180 or >250 mg/dL), time in range (TIR; 70–180 mg/dL), and time below range (TBR; <70 mg/dL) in clusters 1, 2, and 3.
    Graphical abstract
    Impact of Carbohydrate Intake Fluctuations on Glucose Profiles: Insights from Continuous Glucose Monitoring-Based Patient Clustering
    Characteristic Cluster 1 Cluster 2 Cluster 3 P value
    Sex, male:female 3:7 6:8 5:3 0.444
    Age, yr 46.2±17.5 50.3±8.8 51.0±14.3 0.693
    T1DM, % 30.0 35.7 25.0 >0.999
    DM duration, yr 11.8±10.2 14.6±7.5 12.7±9.1 0.728
    BMI, kg/m2 25.6±5.7 24.9±6.0 28.1±4.8 0.202
    Obesity 4 (40.0) 5 (35.7) 7 (87.5) 0.060
    SBP, mm Hg 126.8±11.0 126.9±14.0 135.1±12.6 0.304
    DBP, mm Hg 71.9±4.7 71.9±11.6 77.6±9.9 0.354
    FPG, mg/dL 123.8±41.6 141.5±47.5 136.4±62.0 0.764
    PP2, mg/dL 169.1±82.8 203.2±71.6 286.7±52.0 0.023
    HbA1c, % 8.5±1.2 8.7±0.8 8.2±1.1 0.529
    C-peptide, ng/mL 2.3±2.2 1.8±2.5 2.4±1.4 0.293
    Insulin, μIU/mL 5.3±4.0 6.3±7.1 12.6±18.8 0.167
    eGFR MDRD, mL/min/1.73 m2 107.3±52.1 87.5±24.5 90.2±37.4 0.437
    AST, IU/L 26.2±5.1 25.4±7.6 26.0±7.5 0.953
    ALT, IU/L 22.6±10.4 24.4±9.4 27.6±10.8 0.577
    Total cholesterol, mg/dL 193.3±53.6 157.5±55.4 166.5±32.7 0.242
    TG, mg/dL 110.2±41.8 99.4±48.5 180.6±88.0 0.013
    HDL cholesterol, mg/dL 60.6±10.8 51.5±19.3 48.9±12.9 0.267
    LDL cholesterol, mg/dL 119.2±38.9 92.2±33.8 97.8±24.5 0.157
    Comorbidities
     Hypertension 5 (50.0) 6 (42.9) 6 (75.0) 0.357
     Dyslipidemia 7 (70.0) 12 (85.7) 7 (87.5) 0.616
    Insulin use 0.928
     None 1 (10.0) 1 (7.1) 1 (12.5)
     Basal insulin 0 0 1 (12.5)
     Premixed insulin 3 (30.0) 5 (35.7) 2 (25.0)
     Basal bolus insulin 6 (60.0) 8 (57.1) 4 (50.0)
    Variable Cluster 1 (well-controlled) Cluster 2 (high variability) Cluster 3 (high mean glucose) P value
    Mean glucose, mg/dL 138.1±16.8a 168.3±22.6b 203.4±40.5c <0.001
    CV, % 15.4±5.6a 27.3±5.4b 17.7±4.3a <0.001
    SD, mg/dL 21.0±7.4a 46.1±11.5b 35.3±7.4c <0.001
    TAR (>250 mg/dL), % 0.0±0.0 7.0±12.6 15.8±31.7 0.057
    TAR (>180 mg/dL), % 5.5±7.0a 30.7±9.8b 51.6±20.7b <0.001
    TIR (70–180 mg/dL), % 94.5±7.0a 61.2±14.2b 32.6±18.1c <0.001
    TBR (<70 mg/dL), % 0 1 (7.1) 0 0.999
    Variable Cluster 1 Cluster 2 Cluster 3 P value
    Total daily energy, kcal 2,414.4±316.3 2,525.4±494.1 2,362.9±735.4 0.756
    Breakfast, kcal 548.7±175.2 584.9±215.9 596.4±253.0 0.879
    Lunch, kcal 812.3±176.5 766.3±210.6 724.9±244.3 0.680
    Dinner, kcal 786.7±156.2 841.6±198.5 715.5±199.8 0.325
    Snack, kcal 264.7±228.6 332.7±286.3 258.2±236.1 0.764
    Breakfast, % kcal 22.4±7.7 23.1±8.1 26.1±10.2 0.458
    Lunch, % kcal 35.1±8.3 30.7±7.6 32.1±6.5 0.382
    Dinner, % kcal 31.8±5.3 33.7±6.7 33.0±9.0 0.642
    Snack, % kcal 10.7±8.2 12.5±9.3 10.8±7.8 0.846
    Carbohydrate, g 302.2±52.4 333.4±70.0 337.1±83.8 0.471
    Protein, g 112.1±21.3 112.4±34.1 110.1±44.0 0.527
    Fat, g 79.0±9.7 87.2±25.8 78.8±41.2 0.178
    Carbohydrate, % kcal 51.9±5.0 53.8±8.9 57.4±12.2 0.437
    Protein, % kcal 18.5±2.6 17.6±3.9 18.5±3.1 0.757
    Fat, % kcal 28.8±4.2 30.6±7.8 28.6±7.3 0.737
    Day-to-day fluctuations in energy and nutrient intake, 5-day CV, %
     Total daily energy 27.0±11.5 17.9±7.4 29.5±20.8 0.191
     Carbohydrate 21.9±9.0 19.2±9.1 41.0±32.1 0.123
     Protein 36.3±15.3 32.6±12.4 37.4±29.5 0.849
     Fat 46.5±17.4 37.4±24.4 51.5±35.4 0.310
    Day-to-day fluctuations in energy and nutrient intake, 5-day SD, kcal
     Total daily energy 632.2±212.0 436.3±171.5 605.1±239.4 0.052
     Carbohydrate 260.2±94.1 250.2±126.1 502.1±363.4 0.024
     Protein 159.9±65.9 138.0±47.5 154.4±104.0 0.733
     Fat 323.3±104.6 285.8±221.1 374.1±338.4 0.181
    Variable Breakfast, % kcal Lunch, % kcal Dinner, % kcal Mean energy intake per meal
    Total daily energy (CV), % –0.17 0.49a –0.10 –0.47a
    Carbohydrate (CV), % –0.21 0.21 –0.24 –0.62a
    Protein (CV), % 0.18 0.18 –0.24 –0.32
    Fat (CV), % 0.21 0.31 –0.32 –0.42a
    Total daily energy (SD), kcal –0.36a 0.52a –0.18 –0.17
    Carbohydrate (SD), kcal –0.16 0.06 –0.32 –0.43a
    Protein (SD), kcal 0.15 0.15 –0.21 0.11
    Fat (SD), kcal 0.04 0.39a –0.27 –0.04
    Table 1. Baseline Clinical Characteristics of Participants Distributed by K-Means Clustering

    Values are expressed as mean±standard deviation or number (%). P values represent the results of the one-way analysis of variance (ANOVA), Kruskal-Wallis test, or chi-squared test.

    T1DM, type 1 diabetes mellitus; DM, diabetes mellitus; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; PP2, 2-hour postprandial glucose; HbA1c, hemoglobin A1c; eGFR, estimated glomerular filtration rate; MDRD, Modification of Diet in Renal Disease; AST, aspartate transferase; ALT, alkaline transferase; TG, triglyceride; HDL, high density lipoprotein; LDL, low density lipoprotein.

    Table 2. Continuous Glucose Monitoring Profiles of Participants Distributed by K-Means Clustering

    Values are expressed as mean±standard deviation or number (%). P values represent the results of one-way analysis of variance (ANOVA) or the Kruskal-Wallis test.

    CV, coefficient of variation; SD, standard deviation; TAR, time above range; TIR, time in range; TBR, time below range.

    Post hoc analysis was done for variables with P<0.05 by the Tukey’s honest significant difference test or the Dunn’s test.

    Table 3. Nutrient Intake of Participants Distributed by K-Means Clustering

    Values are expressed as mean±standard deviation. P values within each group represent the results of one-way analysis of variance (ANOVA) or the Kruskal-Wallis test. Day-to-day fluctuations in energy (kcal) and macronutrient intake were defined as the CV (%) or SD (kcal) of daily intake from day 2 to 6 for each individual.

    CV, coefficient of variation; SD, standard deviation.

    Table 4. Correlation of Meal-to-Meal Fluctuations in Energy and Nutrient Intake with Meal Types and Mean Energy Intake per Meal

    Data are presented by Spearman’s partial correlation coefficients after controlling for insulin use. Meal-to-meal fluctuations were defined as intra-personal CV (%) and SD (kcal) between meals.

    CV, coefficient of variation; SD, standard deviation.

    P values of statistical significance.


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