CGM Empowers Obesity and Diabetes Management: Data-Guided Dietary Intervention and Metabolic Function Remodeling

Medical History and Basic Information

Chief Complaint:

A 24-year-old male patient was admitted due to "dry mouth, polydipsia, polyuria, and weight loss for 10 days".

Present History:

Ten days ago, the patient developed dry mouth without obvious inducement, with daily water intake increasing from 1000mL to 3000-3500mL. He also presented with polyuria, increased nocturia, weight loss of approximately 4kg, fatigue, lassitude, and foamy urine. No polyphagia, easy hunger, chest tightness, shortness of breath, blurred vision, nausea, vomiting, or other symptoms were noted. Physical examination at the hospital's Health Check-up Center showed "fasting blood glucose 20.85 mmol/L, glycated hemoglobin 14.5%", and "diabetes mellitus" was considered. The patient was then admitted to our department for further treatment.

Physical Examination:

Blood Pressure (BP): 145/89 mmHg; other vital signs were stable. Body Mass Index (BMI): 32.9 kg/m². No obvious abnormalities were found in the heart, lungs, or abdomen.

Auxiliary Examinations:

Urinalysis: Glucose 2+, Ketone Bodies 4+, Protein 2+; Liver Function: ALT 388 U/L, AST 86 U/L, γGGT 226 U/L, ALP 126 U/L; Renal Function: Uric Acid 588 μmol/L; Blood Lipids: Total Cholesterol 5.65 mmol/L, Triglycerides 4.49 mmol/L, Low-Density Lipoprotein Cholesterol (LDL-C) 3.13 mmol/L; Blood Gas Analysis, Diabetes Autoantibodies, Electrocardiogram, and Chest X-ray showed no obvious abnormalities; Abdominal and Urinary System Color Doppler Ultrasound: Hepatomegaly, Fatty Liver. Random capillary blood glucose after admission: Hi(excessively high).

Admission Diagnosis：

1. Type 2 Diabetes Mellitus (T2DM), Type 2 Diabetic Ketoacidosis, Type 2 Diabetic Nephropathy; 2. Non-alcoholic Steatohepatitis; 3. Obesity; 4. Metabolic Syndrome.

Treatment Regimen Based on Continuous Glucose Monitoring (CGM)

After admission, the patient presented severe hyperglycemia and ketoacidosis. CGM was applied, and insulin pump therapy was initiated for glucose-lowering, rehydration and ketoacidosis correction.

Note: TIR: Time when blood glucose is within the target range (3.9~10.0 mmol/L); TAR: Time when blood glucose is above the target range (>10.0 mmol/L); TBR: Time when blood glucose is below the target range (<3.9 mmol/L)

Through CGM, it was observed that the patient's TIR was 0% for several consecutive days, indicating poor blood glucose control. Considering the severe insulin resistance, drugs not affecting liver function such as Liraglutide and Miglitol were successively added. After confirming no obvious gastrointestinal reactions in the patient, the doses of the drugs were gradually increased to reduce insulin resistance.

Note: TIR: Time when blood glucose is within the target range (3.9~10.0 mmol/L); TAR: Time when blood glucose is above the target range (>10.0 mmol/L); TBR: Time when blood glucose is below the target range (<3.9 mmol/L)

Hepatitis markers were negative, supporting the diagnosis of "non-alcoholic steatohepatitis". After drug treatment, the rechecked liver function gradually improved. Through CGM, it was observed that the patient's blood glucose gradually improved but still did not meet the target. Since the patient had no gastrointestinal reactions, the dose of "Liraglutide" was increased to 1.2mg qn, and "Metformin Hydrochloride Tablets 0.85g qd" was combined to reduce insulin resistance.

Note: TIR: Time when blood glucose is within the target range (3.9~10.0 mmol/L); TAR: Time when blood glucose is above the target range (>10.0 mmol/L); TBR: Time when blood glucose is below the target range (<3.9 mmol/L)

After observing that the patient's blood glucose reached the target through CGM, the insulin pump was withdrawn. The patient was switched to twice-daily premixed insulin injection combined with hypoglycemic drugs such as "Liraglutide, Miglitol, and Metformin". The patient's blood glucose met the target, with daily TIR fluctuating between 95.6% and 100%, and blood glucose control was good, so discharge was arranged.

Note: TIR: Time when blood glucose is within the target range (3.9~10.0 mmol/L); TAR: Time when blood glucose is above the target range (>10.0 mmol/L); TBR: Time when blood glucose is below the target range (<3.9 mmol/L)

Lifestyle Intervention Guided by CGM

After admission, the patient's lifestyle related to diet and exercise was evaluated, and it was found that he had long-term bad eating habits, including long-term and frequent intake of high-sugar, high-GI foods (such as white rice, pasta, sugary drinks, etc.) and refined processed foods. These bad eating habits aggravated insulin resistance and led to large fluctuations in blood glucose.

During CGM monitoring, personalized dietary guidance was provided to the patient based on the food GI value table; at the same time, using the real-time impact of different foods on blood glucose fluctuations displayed by CGM, the patient was helped to intuitively understand the difference in blood glucose impact between low-GI foods (such as whole wheat bread, vegetables, and low-sugar fruits) and high-GI foods (such as white rice and sugary drinks). Through monitoring, the patient found that high-GI foods caused a rapid rise in blood glucose, with obvious blood glucose spikes in CGM data, while the intake of low-GI foods made blood glucose more stable and avoided sharp fluctuations.

Through these data feedback, the patient was motivated to correct bad eating habits, began to strictly follow the low-GI diet principle, gradually reduced the intake of high-sugar foods, and significantly improved postprandial blood glucose fluctuations.

Follow-up Status

The patient was followed up regularly after discharge. With the relief of hyperglycemic toxicity, the patient's islet function gradually recovered. Insulin was gradually reduced to withdrawal, the doses of oral hypoglycemic drugs and "Liraglutide" remained unchanged, and the patient insisted on following the low-GI diet.

Three weeks after discharge, the patient rechecked liver function at the outpatient clinic of our department, which was normal. Considering that the hyperglycemic toxic effect was gradually relieved and islet function was gradually recovered, while the patient was obese, long-term use of insulin was not conducive to weight loss. Therefore, the hypoglycemic regimen was adjusted to: Liraglutide Injection 1.8mg qn + Metformin Hydrochloride Tablets 0.85g bid + Miglitol Tablets 50mg tid. The patient felt that capillary blood glucose monitoring was troublesome and requested CGM again. During CGM, the patient's blood glucose was well controlled, with TAR 0.00% and TIR 100%.

Note: TIR: Time when blood glucose is within the target range (3.9~10.0 mmol/L); TAR: Time when blood glucose is above the target range (>10.0 mmol/L); TBR: Time when blood glucose is below the target range (<3.9 mmol/L)

Case Summary

In this case, CGM was used to accurately guide treatment and lifestyle intervention, achieving comprehensive benefits including rapid blood glucose control, insulin reduction and withdrawal, weight management, and liver function recovery. Rational use of GLP-1 receptor agonists, α-glucosidase inhibitors, and Metformin avoided excessive dependence on insulin, while taking into account hypoglycemia and metabolic improvement, ultimately successfully achieving the goal of personalized treatment. In addition, by intuitively presenting the real-time impact of different foods on blood glucose fluctuations, the patient's understanding of diabetic diet was deepened, helping the patient restore a healthy lifestyle.