Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet.

Hudgins, Lisa C.; Hellerstein, M. K.; Seidman, Cynthia; Neese, Richard A.; Diakun, J; Hirsch, Jules

doi:10.1172/jci118645

Cited by 328 publications

(276 citation statements)

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“…Results from both MIDA Hudgins et al, 1996;Neese et al, 1995;Faix et al, 1993;Hellerstein, 1995) and 2 H 2 O incorporation (Leitch & Jones, 1993;Jones et al, 1995) agree that hepatic DNL is a quantitatively minor pathway in men under conditions of a normal Western (high fat) diet. Calculated synthesis rate of palmitate or total non-essential FA based on¯ux through the circulating VLDL-TG pool is`1 ± 2 gad, a small amount compared to the 50 ± 150 g fat in the diet each day.…”

Section: Regulation Of Dnl In Humansmentioning

confidence: 88%

“…Nor do static changes in FA composition provide information about¯uxes through pathways; for example, DNLafat oxidation cycling could occur at a very high or a very low rate and remain consistent with these observations. Nevertheless, a similar principle (dilution of the essential FA linoleate in circulating lipids) has been used recently as a method for estimating rates of DNL (Petrek et al, 1997;Hudgins et al, 1996;see below).…”

Section: Comparison Of Fatty Acid (Fa) Composition In Adipose Tissue mentioning

confidence: 99%

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De novo lipogenesis in humans: metabolic and regulatory aspects

1999

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The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO. Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO oxidation to increase and match CHO intake. Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute signi®cantly to the wholebody energy economy. It is concluded that DNL is not the pathway of ®rst resort for added dietary CHO, in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO and fat in humans are discussed, but require further investigation. IntroductionIn this review, I will address the fate of surplus dietary carbohydrate (CHO) in humans. More speci®cally, the focus will be on conversion of CHO to fat, or de novo lipogenesis (DNL), with the question framed in quantitative terms: to what extent is surplus dietary CHO energy converted to fat? The various ways in which CHO content of the diet can be increased will be considered: increased CHO that replaces dietary fat (high-CHO low-fat, eucaloric diets); CHO added to a mixed diet, where CHO energy is less than total energy expenditure (TEE) but total energy intake exceeds TEE; and CHO consumption in excess of TEE. This review will therefore focus on the upper limits and consequences of increased CHO intake rather than on the lower limits and consequences of insuf®cient fat intake. Background and historical review

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Section: Regulation Of Dnl In Humansmentioning

confidence: 88%

Section: Comparison Of Fatty Acid (Fa) Composition In Adipose Tissue mentioning

confidence: 99%

De novo lipogenesis in humans: metabolic and regulatory aspects

1999

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“…Human clinical investigations have demonstrated that a diet low in fat and rich in carbohydrates (closely resembling the HCD used in our mouse study), even when administered for short periods of time, for example, 5 or 25 days, can lead to occurrence of uncomplicated fatty liver [12][13][14][15]. Thus, this mouse model is a highly relevant means of investigating mechanisms of hepatic steatosis.…”

Section: Introductionmentioning

confidence: 91%

Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

et al. 2007

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“…After a single carbohydrate-rich meal only 1 ± 2% of the palmitate of the verylow-density-lipoprotein (VLDL) triacylglycerol-bound fatty acids (TGFAs) is derived from de novo synthesis (Hellerstein et al, 1991a,b). When eucaloric high-carbohydrate, low-fat diets are ingested, de novo lipogenesis is stimulated in human adults, but the rate of conversion of glucose to fatty acids remains low, in the order of 12 g triacylglycerol palmitate synthesized per day (Hudgins et al, 1996). It is of interest that fatty acid synthesis is less stimulated when starch or complex carbohydrates are substituted for simple sugars or short-chain glucose polymers (Hudgins, 1995).…”

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confidence: 99%

“…The effects of a high-CHO, lowfat diet on plasma lipid concentration (increased fasting plasma triacylglycerol, and decreased HDL-cholesterol concentrations) appear to be mainly mediated by increased sucrose and fructose intake (Coulston et al, 1983;Hudgins et al, 1995). The fatty acid preferentially formed by mammalian fatty acid synthase is the saturated fatty acid palmitate (16:0) (Hudgins et al, 1996). Therefore, when de novo lipogenesis is stimulated following ingestion of a high carbohydrate diet rich in sucrose and fructose, it would be important to know whether increased de novo synthesis of saturated fat contributes to the fatty acid patterns associated with an increased risk of cardiovascular disease.…”

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confidence: 99%

Response to and range of acceptable fat intake in adults

Jéquier

1999

Eur J Clin Nutr

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Cellular energy metabolism depends on two main energy substrates: glucose and fatty acids. The major determinants of the fuel mix oxidized are glucose availability and insulin secretion that both promote glucose oxidation. Fatty acid oxidation occurs mainly when glucose availability is reduced, for instance during the postabsorptive period, or when energy expenditure is increased, for instance during exercise of long duration. When eucaloric diets with high carbohydrate and low fat content are ingested, de novo lipogenesis is stimulated in adults, but the rate of conversion of glucose to fatty acids is low, which means that carbohydrate intake does not have much in¯uence on fat requirements. The lower limit of fat intake depends on three factors: the fat requirement to meet energy needs, the need for essential fatty acids, and the amount of fat in the diet that is necessary to absorb fat-soluble vitamins. The lower limit of fat intake to meet the energy needs of adults is assumed to be between 10 and 15% of dietary energy, provided that enough carbohydrates are available. For adults, the requirement for essential fatty acids is in the range of 3 ± 5% of dietary energy for linoleic acid, and 0.5 ± 1.0% of dietary energy for linolenic acid. Fat energy should not be below 10% of total energy intake in order to ensure an unrestricted absorption of fat-soluble vitamins, particularly vitamins A and E. The recommendations on upper limits of fat intake for adults must take into account the degree of physical activity. International recommendations indicate that active individuals in energy balance may consume up to 35% of their total energy intake as dietary fat, whereas sedentary individuals should not consume more than 30% of their energy from fat. Saturated fatty acids should not exceed 10% of the energy intake. IntroductionWhile protein and energy requirements have been studied extensively in humans (Scrimshaw et al, 1972), the relative contribution of carbohydrates and fats to cover energy needs has received less attention. In many rural communities of developing countries, carbohydrates contribute between 70 and 75% to total energy intake, while fat intake contributes only 12 ± 15% (FAOUN, 1970). By contrast, the traditional adult Eskimo diet in the last century contained about 7% carbohydrate and 50% fat energy (Bang et al, 1980). A range of fat intake between 12 and 50% of total energy intake appears to be compatible with a normal body composition and the maintenance of good health in individuals who are adapted to these types of diets and to their environment. This does not imply, however, that these extreme values of fat and carbohydrate intakes can be recommended for adults of developed countries with a sedentary lifestyle. Lower limit of fat intake in adultsThe lower limit of fat intake depends on three factors: the fat requirement to meet energy needs, the need for essential fatty acids, and the amount of fat in the diet that is necessary to absorb the fat soluble vitamins.Fat requirement to meet energy nee...

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Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet.

Cited by 328 publications

References 42 publications

De novo lipogenesis in humans: metabolic and regulatory aspects

De novo lipogenesis in humans: metabolic and regulatory aspects

Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

Response to and range of acceptable fat intake in adults

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