Cholesterol dietary changes affecting

The other major lipid component of cell membranes that may affect their electrical properties is cholesterol. The cholesterol content of the red cell membranes of subjects with SCD has not been studied as extensively as the phospholipid content. However, it is possible that variations in the cholesterol content of the cell membranes of subjects with SCD, due either to dietary or metabolic limitations, could contribute to the changes in phase angle we observed in the children with SCD in the present study. 

Beher et al. (23,24) concluded that pituitary hormones act on sterol and bile acid elimination rather than on bile acid synthesis. They supported this argument by studies using cholestyramine (23,26), a bile acid sequestering anion exchanger, and psyllium hydrocolloid (27), which provides dietary bulk and lowers tissue cholesterol. Both of these agents decreased the /1/2 and increased the synthesis and excretion of the bile acids in hypophysectomized rats but did not affect bile acid pool size. Thus the faster bile acid synthesis and excretion rates in MK-135 [cholestyramine] treated animals are due to an increased rate of elimination of bile acids from their pools. Since bile acid pool size did not change in the hypophysectomized rats, they concluded that the defect in sterol metabolism in these animals [hypophysectomized] is concerned not with the conversion of liver sterols to bile acids but with the rate of elimination of bile acids from their pools. (23)... 

Recent studies in humans and animal models have revealed that modulation of stearoyl-CoA desaturase-1 (SCDl) activity by dietary intervention or genetic manipulation strongly influences several facets of energy metabolism to affect the susceptibility to obesity, insulin resistance, diabetes and hyperlipidaemia (Flowers and Ntambi, 2008, 2009 Paton and Ntambi, 2008). SCDl catalyzes the DO-di desaturation of a range of fatty acyl-CoA substrates. The preferred substrate is stearoyl-CoA, which produces OA from stearic acid (18 0). The major product of SCDl, OA (18 ln-9), is the key substrate for the formation of complex lipids such as phospholipids, TAG, cholesterol esters, wax esters and alkyl-2,3-diacylglycerols. Reduced OA synthesis is associated with several metabolic changes that elicit protection from obesity, cellular Upid accumulation and insulin resistance (Miyazaki et al., 2000 Ntambi et al., 2002 Sampath et al., 2007). 

Fig. 1 illustrates the excretion routes for cholesterol. The liver synthesizes cholesterol and secretes it into the biliary tract as cholesterol or bile acids. This amounts to somewhat less than 1 g/day. Minor losses occur in the urine as steroid hormones and via the skin as sebum and desquanmated epithelial cells. An important question addressed in Fig. 2 is how does the cholesterol absorbed from the diet affect these synthetic and excretory pathways There are 4 possibilities. First, as a patient changes from a cholesterol-free to a cholesterol-containing diet his hepatic cholesterol synthesis may decrease to compensate for the added exogenous load. Or the liver may simply re-excrete all of this dietary load plus the endogenously synthesized cholesterol and bile acids. Unfortunately, there are 2 remaining possibilities, namely. 

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