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Intestinal nutrient transport in genetically obese mice
1Department of Physiology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103-2714, USA.
The American Journal of Clinical Nutrition
|September 1, 1995
Summary
Genetic obesity in mice leads to increased small intestine growth, enhancing nutrient absorption proportionally to metabolic mass. This adaptation ensures nutrient supply matches increased metabolic demands without altering efficiency ratios.
Area of Science:
- Physiology
- Metabolism
- Gastroenterology
Background:
- Obese animals possess a significantly larger metabolic mass compared to lean counterparts.
- The small intestine's role in nutrient supply to this increased mass requires adaptive mechanisms.
Purpose of the Study:
- To investigate the adaptive mechanisms of the small intestine in genetically obese mice.
- To compare nutrient uptake, transporter density, and mucosal permeability between obese and lean mice.
Main Methods:
- Isolated everted intestinal sleeves from obese (C57BL/6J ob/ob) and lean male mice were used.
- D-glucose and five amino acid uptakes, transporter site density, and mucosal permeability were measured.
- Uptake rates were analyzed per milligram of tissue and per centimeter of intestine.
Main Results:
- Nutrient uptake per milligram of intestinal tissue was similar between obese and lean mice.
- Intestinal D-glucose transporter density and mucosal permeability were also comparable.
- However, nutrient uptake per centimeter of intestine was approximately 40% greater in obese mice, correlating with increased intestinal weight.
Conclusions:
- Genetic obesity in mice is associated with significant intestinal growth.
- This increased intestinal mass augments the absorption of all nutrients, proportionally to metabolic mass.
- The ratio of intestinal absorptive capacity to metabolic mass remains constant, indicating proportional adaptation.