de Novo Lipogenesis and Carbohydrates

Weight gain and obesity are serious problems in Western nations, mainly because of the health costs involved in treating obesity related diseases. Mainstream advice for losing excess weight is to reduce energy intake and increase energy expenditure in an effort to produce a negative energy balance (despite the long-term benefits of this strategy being questionable). One of the popular methods of achieving a reduction in energy intake is to reduce fat levels, because fat contains the most energy of all of the macronutrients. In response, food manufacturers have taken advantage of the demand for low fat foods and created a range of virtually fat free products. Many people consume these foods under the false impression that they will aid in weight loss. However, few people realise that the liver is able to convert carbohydrate into fatty acids in a process called de novo lipogenesis.

Research shows that plasma triglyceride levels rise after consumption of both high carbohydrate and high fat meals. Dietary triglycerides are digested to monoglycerides and fatty acids and absorbed into the enterocytes of the small intestine, where they are reformed into triglycerides and packaged into chylomicrons. These chylomicrons then enter circulation via the lymphatic circulation. After consuming a carbohydrate meal, circulating triglycerides can also increase as the digested glucose is converted in the liver to fatty acids. This process causes increases in the amounts of malonyl-CoA, which in turn inhibits fatty acid transport into the mitochondria and therefore fatty acid oxidation. Under conditions of high circulating insulin, the newly formed fatty acids are esterified to glycerol and packaged into very low density lipoproteins (VLDL). These then enter the circulation and contribute to the postprandial plasma triglyceride levels. After a high carbohydrate mixed meal, plasma rise significantly significantly.

Research1 has investigated the effects of feeding a high carbohydrates mixed meal on the rate of de novo lipogenesis in human subjects. Healthy individuals were fed a liquid meal containing 54% carbohydrate, 32% fat and 14% protein, after a 12 hour fast. The results showed that the eight subjects all responded in a similar way to the meal. Postprandially, de novo lipogenesis increased significantly compared to the fasting state, and peaked 4.2 hours after the meal. The peak rate of de novo lipogenesis correlated with peak insulin levels, as expected. Acute stimulation of de novo lipogenesis therefore accounts for some of the elevation in circulating triglycerides after a mixed meal, and this is very likely controlled by insulin and therefore a result of carbohydrate ingestion. Because insulin increases malonyl-CoA levels, fatty acid oxidation is also reduced by inhibition of the carnitine shuttle.

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1Timlin, M. T. and Parks, E. J. 2005. Temporal pattern of de novo lipogenesis in the postprandial state in healthy men. American Journal of Clinical Nutrition. 81: 35-4

About Robert Barrington

Robert Barrington is a writer, nutritionist, lecturer and philosopher.
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