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High-Fat Diet-Induced Obesity Enhances Small Intestinal Glucose and NaCl Absorption Through Selective Transporter
Balasubramanian Palaniappan1, Niraj Nepal1,2, John Crutchley3
1Department of Biomedical Sciences, Joan C Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.
International Journal of Molecular Sciences
|May 13, 2026
Summary
Diet-induced obesity enhances intestinal glucose absorption by increasing sodium-dependent glucose co-transporter 1 (SGLT1) affinity. It also upregulates chloride/bicarbonate exchangers (DRA/PAT1) transcription, potentially contributing to metabolic dysfunction.
Area of Science:
- Physiology
- Metabolism
- Gastroenterology
Background:
- Metabolic dysfunction in diet-induced obesity (DIO) is linked to altered intestinal nutrient and electrolyte transport.
- Mechanisms driving obesity-associated functional changes in intestinal transporters are not fully understood.
Purpose of the Study:
- To investigate the impact of high-fat diet (HFD)-induced obesity on key intestinal absorptive transporters in mice.
- To examine effects on sodium-dependent glucose co-transporter 1 (SGLT1), Na+/H+ exchanger 3 (NHE3), and Cl-/HCO3- exchangers (DRA/PAT1).
Main Methods:
- Assessed transporter activity in intact villus cells and brush border membrane vesicles (BBMV) from HFD-fed mice.
- Performed kinetic analysis (Km, Vmax) to determine changes in transporter function.
- Quantified transporter mRNA, protein expression, and brush border membrane localization.
Main Results:
- SGLT1 activity increased due to enhanced affinity (reduced Km), with no change in expression or Vmax.
- DRA/PAT1 activity and transport capacity (elevated Vmax) increased, accompanied by upregulated mRNA, total protein, and BBM expression.
- NHE3 activity and expression remained unchanged in HFD-fed mice.
Conclusions:
- DIO enhances intestinal glucose absorption by increasing SGLT1 affinity.
- DIO upregulates DRA/PAT1 transcription, increasing chloride absorption capacity.
- These transporter alterations may amplify nutrient absorption and contribute to metabolic dysregulation in obesity.
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