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Receptors in the magnesium / therapeutic use cell nucleus that are involved in triggering the effects of insulin (peroxisome proliferator activating receptors, PPAR) may fail and thus lead to insulin resistance, inflammation of the liver, and scarring of the liver. Finally, magnesium / therapeutic use recent research suggests magnesium / therapeutic use that leptin resistance may contribute to the development of NASH. Think of this theory as analogous to the process of insulin resistance. Leptin is a very small hormone that is secreted by the brain, fat, and stomach cells in response to eating. Its main effect is to curb the appetite. Patients with NASH have abnormally elevated levels of leptin but experience no loss of appetite. That is, they are resistant to the appetite-curbing effect of leptin. The leptin also helps control the processes of inflammation and scarring within the liver cells. Furthermore, interestingly enough, leptin also increases insulin sensitivity. But the fact that patients with NASH are insulin resistant supports the idea that the leptin receptors are malfunctioning.
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