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Glucose effectiveness and its components in relation to body mass index
Micaela Morettini1, Francesco Di Nardo1, Laura Ingrillini1
1Department of Information Engineering, Università Politecnica delle Marche, Ancona, Italy.
Obesity impairs glucose effectiveness (SG), the insulin-independent component of glucose tolerance. This decline begins in overweight individuals and does not worsen with increasing BMI above 30 kg m-2.
Area of Science:
- Metabolic Physiology
- Endocrinology
- Obesity Research
Background:
- Obesity is linked to reduced insulin sensitivity (SI), affecting glucose tolerance.
- The impact of obesity on glucose effectiveness (SG), the insulin-independent component, is less understood.
- This study investigates SG and its components across different body mass index (BMI) categories.
Purpose of the Study:
- To analyze glucose effectiveness (SG) and its components in lean, overweight, and obese individuals.
- To determine how BMI categories influence the insulin-independent aspects of glucose metabolism.
- To assess the relationship between BMI and SG and its sub-components (GEZI, BIE).
Main Methods:
- Cross-sectional study involving three BMI groups: Lean (LE), Overweight (OW), and Obese (OB).
- Subjects underwent a 3-hour frequently sampled intravenous glucose tolerance test (FSIGT).
- Minimal model analysis was used to calculate SG, glucose effectiveness at zero insulin (GEZI), and basal insulin effect (BIE).
Main Results:
- Glucose effectiveness (SG) was significantly reduced in overweight and obese individuals compared to lean individuals.
- SG showed a significant inverse correlation with BMI (r = -0.3, P < 0.0001).
- No significant difference in SG was observed between obese and overweight groups, or between Obese I and Morbidly Obese subgroups. Glucose effectiveness at zero insulin (GEZI) followed similar trends, while basal insulin effect (BIE) did not differ significantly across groups.
Conclusions:
- Glucose effectiveness (SG) and its primary component, GEZI, deteriorate in overweight individuals compared to those with normal BMI.
- Further increases in BMI beyond 30 kg m-2 do not lead to a significant additional decline in SG.
- The findings highlight that the impairment of insulin-independent glucose disposal begins at lower BMI thresholds.
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