Have you ever felt trapped in a cycle of continuous hunger and food cravings and never feeling satiated? Many of us live through this feeling every day when the more nutrients we consume, the more we crave and never feel quite satisfied. What are the underlying mechanisms and implications of this state of the metabolic system? Well this might seem like a detour but stay tuned with me! I am going to bring it around full circle and try to simplify the complex scenario involving insulin resistance.
Insulin resistance itself is quite simple to understand. It is the condition where our body cells are not responding to the insulin produced by our pancreas. The underlying biological mechanism leading to the condition of insulin resistance appears to be inflammation which can be modulated by the fatty acid composition of the diet. The human body has numerous checks and balances in place to provide optimal blood glucose levels and avoid unnecessary upheavals. These days we have excess nutrients and insulin has the difficult task of defending the body against potential damage from excessive nutrient intake. All nutrients are however naturally inflammatory since their metabolism into other compounds can lead to increased inflammation. Cellular inflammation can disrupt and deactivate insulin’s action by disturbing signaling mechanisms within the cell.
Insulin resistance can be modulated by the fatty acid composition in our food. Omega-6 and saturated fatty acids (such as palmitic acid) are the pro-inflammatory molecules, whereas omega-3 fatty acids are anti-inflammatory molecules. Consuming omega-3 fatty acids can decrease and even reverse inflammation within the hypothalamus. Saturated fats can cause inflammation in the hypothalamus of the brain disrupting the signaling pathways mediated by the hormones insulin and leptin that make us feel ‘full and satisfied’. As a result, our brain continues to send hunger signals to our stomach and unfortunately the vicious cycle of inflammation and insulin resistance continues. As a result, there is accumulation of excess calories which are stored as fat in the adipose tissue.
Excess weight however, is not the cause of insulin resistance. The origin of insulin resistance may start with inflammation in the hypothalamus that disrupt satiety signals, increase hunger and food intake starting an orchestra of events that go downhill. When there is excess fat in the body, that is not necessarily a problem if the fat can be safely stored in healthy fat cells that are responsive to insulin. However, fat cells do not have an unlimited capacity to expand. When they expand uncontrollably, it results in inflammation of the fat cell. With ongoing inflammation in the fat cell, high levels of free fatty acids can leave the fat cell to enter the general circulation where they can be taken up by other organs, such as liver and skeletal muscles. These organs also eventually develop insulin resistance. The liver in fact, cannot safely store large amounts of fat which can lead to fatty liver disease.
Skeletal muscle is a very important tissue for uptake of glucose and for storing energy. Physical activity can reduce insulin resistance in skeletal muscles and also increases the uptake of glucose without requiring insulin. The amount and composition of fatty acids in the diet can have a significant role in the modulation of insulin resistance. Last but not the least, monitoring thyroid function can optimize metabolism and prevent the development of insulin resistance.