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Physiopathology of Insulin Resistance
Insulin resistance is a condition where the body’s cells become resistant to the effects of insulin, which is a hormone produced by the pancreas that regulates glucose metabolism. Insulin resistance can lead to high blood glucose levels, which can contribute to the development of type 2 diabetes and other metabolic disorders. The physiopathology of insulin resistance involves several complex mechanisms, including:
1-Dysregulation of lipid metabolism: In insulin-resistant individuals, there is an increase in the release of free fatty acids (FFAs) from adipose tissue, which can lead to an accumulation of FFAs in non-adipose tissues, such as the liver, muscle, and pancreas. This accumulation of FFAs can interfere with insulin signalling and contribute to insulin resistance.
2-Chronic inflammation: Inflammation can play a significant role in the development of insulin resistance. It can disrupt insulin signalling pathways and promote the release of pro-inflammatory cytokines, which can further contribute to insulin resistance.
3-Mitochondrial dysfunction: Mitochondria are the cellular organelles that produce energy. In insulin-resistant individuals, mitochondrial dysfunction can lead to impaired glucose uptake and utilization, contributing to insulin resistance.
4-Oxidative stress: Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them. Increased oxidative stress can cause damage to cells and tissues, leading to insulin resistance.
5-Genetic factors: There are several genetic factors that can contribute to insulin resistance. These include mutations in genes involved in insulin signalling, glucose metabolism, and adipocyte differentiation.
6-Lifestyle factors: Sedentary lifestyles, poor diets, and being overweight or obese can contribute to insulin resistance. These factors can increase the release of FFAs and cause chronic inflammation, mitochondrial dysfunction, and oxidative stress.
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