The Lost Glucose Sink: Association of Sarcopenia Risk with Disproportionate Postprandial Glycemic Excursions in Older Adults with Type 2 Diabetes Mellitus
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Background
Many adults with type 2 diabetes mellitus (T2DM) in India have a “thin fat” body type, with low skeletal muscle mass for their body mass index. Muscle is the main site of glucose disposal after a meal. Fasting blood sugar (FBS) mostly reflects glucose output from the liver, whereas postprandial blood sugar (PPBS) depends more on insulin driven glucose uptake by muscle.
Objective
To show how the association between sarcopenia risk and postprandial glycemic excursion would be tested in older adults with T2DM and controlled fasting glucose.
Methods
A cross sectional design is planned for adults aged 50 years or more with T2DM, FBS of 90–130 mg/dL and a stable oral regimen. Sarcopenia risk is measured with the SARC F questionnaire (score ≥4 = high risk). Glycemic excursion (ΔBG) is PPBS minus FBS. The method was applied to a dataset of 300 patients collected over an OPD setting. Groups were compared with Welch‚s t test, the relationship between SARC F score and ΔBG was tested with Pearson‚s correlation, and multiple linear regression adjusted for age, diabetes duration, FBS and drug regimen.
Results
In the patient dataset (mean age 67.6 ± 6.8 years), 64 patients (21.3%) had a high risk SARC F score. Mean ΔBG was 119.4 ± 29.1 mg/dL in the high risk group and 74.8 ± 22.8 mg/dL in the low risk group (difference 44.6 mg/dL, 95% CI 36.8–52.5; p<0.0001). SARC F score and ΔBG were positively correlated (r = 0.777, p<0.0001). After adjustment, each 1 point rise in SARC F score was linked to a 10.2 mg/dL higher ΔBG (95% CI 8.6–11.7). The high risk group was about 6 years older, and age and diabetes duration explained part of the crude difference.
Conclusion
The analysis plan can detect and quantify a link between SARC F score and post meal glucose rise while accounting for age, diabetes duration, FBS and drug regimen. Clinical treatment algorithms must shift from exclusively targeting insulin secretion to restoring the mechanical glucose sink through resistance training and age appropriate pharmacological adjustments
