Figure 1: Matabolic pathway for fatty acid metabolism
Fat metabolism and glucose homeostasis are interconnected. According to Savage et al. (2007), fatty acid metabolism contributes to the pathogenesis of insulin resistance (IR) and type II diabetes. IR is a condition that the normal insulin amount is insufficient to produce a normal insulin response form fat, liver nd muscle. It reduces the effect of insulin and causes hydrolysis of triglycerides and hence, the free fatty acids in blood plasma increases. the increase of fatty acids in blood plasma reduces the glucose uptake in muscle (stored as glycogen) and elevates the liver glucose production, which contribute to the high glucose level in blood plasma and thus, lead to type II diabetes (Wikipedia, 2009). However, abnormal glucoase homeostasis and hyperglycemia still remain as the main factors of type II diabetes.
The free fatty acids in blood plasma are supposed to be taken up by the muscle and liver to be stored as triglygerides through motichomdrial beta-oxidation pathway (Figure 1). A variety of fatty acids metobolic are built up withing the insulin target cells when the system becomes imbalance and results IR. However, not all fatty acids cause IR. The polysaturated fatty acids have a little or no effect on insulin signaling while omega-3 might increase the insulin sensitivity. Cao at al' (2008) found that palmitoleate (free fatty acid produced by adipocytes) increases the insulin sensitivity by inhibiting the expression of SCD-1 in muscle and liver. By this. the stearosis (excess fat deposition in liver) is decreased and the insulin signaling is improved. High-fat diet supresses the de novo biosynthesis of fatty acid in adipose tisues, leads to decrease in palmitoleate and contributes to IR.
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Hue Lu Choh
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References:
- Olefsky, J. M. (2008). Fat Talks, Liver and Muscle Listen. Cell, Vol 134, Issue 6, Pages 914-916
- Insulin Sensiticity, retrieved 20th April 2009, from Wikipedia, the free encyclopedia, http://en.wikipedia.org/wiki/Insulin_sensivity