![]() ![]() melanogaster apparently does not occur via ADH. Under these dietary conditions most of the glycerol was converted into the glycerol entity of the triacylglycerols, and the fatty acyl groups were derived from ethanol Since the flux of -glycerol into lipid was as rapid in ADH-deficient larvae as wild-type larvae, glycerol metabolism in D. However, instead of three fatty acids attached as in. Ethanol was found to be an efficient inhibitor of the flux of -glycerol into lipid in third-instar larvae. Like fats, they are comprised of fatty acid chains attached to a glycerol or sphingosine backbone. For 6% dietary glycerol a significant degree of induction occurred within 4 h for GPDH but only after 16 h for ADH. Maximum inductions of ADH and GPDH by 6% glycerol were reached in about 24 h, and higher concentrations of dietary glycerol did not result in greater levels of ADH or GPDH induction in that time frame. As little as 1.5% dietary glycerol was found to induce both ADH activity and GPDH activity in third-instar larvae. Because of these apparent linkages, we examined some of the metabolic effects of dietary glycerol and dietary glycerol with ethanol on D. Sphingolipids have a similar structure to glycerophospholipidsbut instead of glycerol, they contain a sphingosine backbone in addition to the typical polar head group and nonpolar fatty acid tail. sn-Glycerol-3-phosphate dehydrogenase (GPDH) provides the glycerol backbone for lipid synthesis, and GPDH is induced by dietary ethanol in D. Instead of a single phosphate head group, these contain a glycerol backbone that forms ester linkages to two fatty acids and a polar head group. Most of the ethanol is metabolized by the pathway initiated by alcohol dehydrogenase (ADH), and much of it is converted to nontoxic lipid. Drosophila melanogaster is very tolerant of the toxic efects of ethanol and is able to use low to moderate levels of ethanol as a nutrient. ![]()
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