Symposium 10: Adipose tissue
DOI:
https://doi.org/10.47196/diab.v54i3Sup.312Keywords:
adipose tissue, diabetesAbstract
Symposium 10: Insulin resistance: from pathophysiology to treatment
Adipose tissue
The adipocyte uptakes the glucose stimulated by the insulin, and this function becomes resistant in obesity and type 2 diabetes (T2D). However, the adipose tissue (AT) is not a meaningful place of quantity of glucose stimulated by insulin attraction. It represents a 5% of the oral glucose load in humans.
In spite of this, the organ-specific GLUT-4 deletion in the AT of mice shows as a result insulin resistance in the liver and the skeletal muscle that aims to indirect and physiologically meaningful effects as a consequence of the insulin resistance in the uptake of glucose in the AT.
References
- Schwartz SS, Epstein S, Corkey BE, et al. The time is right for a New Classification System for Diabetes: Rationale and Implications of the B-Cell-Centric Classification Schema. Diabetes Care 2016;39:179-186.
- Shulman GI. Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease. N Engl J Med 2014;371:1131-41.
- Petersen MC, Shulman GI. Mechanisms of Insulin Action and Insulin Resistance. Physiol Rev 2018; 98:2133-2223.
- Lumeng CN, Saltiel AR. Inflammatory links between obesity and metabolic disease. The Journal of Clinical Investigation. 2011;121(6):2111-2117.
- Archer E, Lavie CJ, Hill JO. The Contributions of “Diet”, “Genes” and Physical Activity to the Etiology of Obesity: Contrary Evidence and Consilience Progress in Cardiovascular Diseases 2018; 61(2):89-102.
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