Fractional hepatic de novo lipogenesis in healthy subjects during near-continuous oral nutrition and bed rest: a comparison with published data in artificially fed, critically ill patients

Minehira, Kaori; Tappy, Luc; Chioléro, René; Vladimirova, V P; Berger, Mette M.; Revelly, Jean-Pierre; Schwarz, Jean-Marc

doi:10.1054/clnu.2002.0559

Cited by 6 publications

(3 citation statements)

References 18 publications

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“…35 ▪ Critically ill, insulin-resistant patients fed enteral or parenteral diets varying in carbohydrate content had increased hepatic DNL. [36][37][38][39] These studies demonstrated that in patients with insulin-resistance, fasting DNL is increased even under circumstances in which carbohydrate intake is limited, suggesting that hyperinsulinemia per se stimulates DNL. This finding was confirmed by a molecular study in rodents.…”

Section: Hyperinsulinemia Nafld and Fasting Hepatic Dnlmentioning

confidence: 99%

“…In an outpatient study 13 Importantly, these same participants had a 56% decrease in DNL during feeding (n=40). 13 Although the children in this study were not selected for the Hepatic de novo lipogenesis (DNL) measured after an overnight fast in lean and obese patients with normoinsulinemia compared with obese, 11 critically ill, [36][37][38][39] and HIV-positive 35 patients with hyperinsulinemia. Levels of DNL were significantly higher in patients with hyperinsulinemia.…”

Section: Study In Childrenmentioning

confidence: 99%

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Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?

Schwarz¹,

Clearfield²,

Mulligan³

2017

Journal of Osteopathic Medicine

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Epidemiologic studies suggest a link between excess sugar consumption and obesity, fatty liver disease, metabolic syndrome, and type 2 diabetes mellitus. One important pathway that may link these metabolic diseases to sugar consumption is hepatic conversion of sugar to fat, a process known as de novo lipogenesis (DNL). Mechanistic studies have shown that diets high in simple sugars increase both DNL and liver fat. Importantly, removal of sugar from diets of children with obesity for only 9 days consistently reduced DNL and liver fat and improved glucose and lipid metabolism. Although the sugar and beverage industries continue to question the scientific evidence linking high-sugar diets to metabolic diseases, major health organizations now make evidence-based recommendations to limit consumption of simple sugars to no more than 5% to 10% of daily intake. Clear recommendation about moderating sugar intake to patients may be an important nonpharmacologic tool to include in clinical practice.

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Section: Hyperinsulinemia Nafld and Fasting Hepatic Dnlmentioning

confidence: 99%

Section: Study In Childrenmentioning

confidence: 99%

Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?

Schwarz¹,

Clearfield²,

Mulligan³

2017

Journal of Osteopathic Medicine

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“…In addition, it is minimally affected by CHO intakes, while when considered over periods of weeks, months or years, total fat balance is rather closely related to energy balance [4][5][6][7]. Even under extreme conditions (high CHO surplus) de novo lipogenesis flux represents a small fraction of both the surplus CHO energy ingested and of the total fat stored in the body [5].…”

Section: Endogenous Fa Synthesismentioning

confidence: 99%

Origin of fatty acids in the body: endogenous synthesis versus dietary intakes

Galli

Risé

2006

Eur. J. Lipid Sci. Technol.

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Origin of fatty acids in the body: endogenous synthesis versus dietary intakesFats, as fatty acids (FA), together with carbohydrates, represent a major substrate group for energy production. In contrast to carbohydrates FA are less efficiently used for energy and more easily stored in tissues. A major issue, still not completely solved, concerns the origin of FA in the organism. The two theoretical alternatives are a) endogenous de novo lipogenesis from carbohydrates, and b) supply through the diet. Various pieces of evidence indicate that the first option, while well-documented in simple biological systems, plays a minimal role in vivo. The exogenous origin therefore represents the preferred, major route of FA supply to the body. This is also supported by the observation that only the enzymes involved in the production of long-chain polyunsaturated FA from their precursors, and not those involved in the synthesis of the FA that are abundant in the diet, are operating in vivo. Finally, as a consequence of the load of fats in our diets, competition for esterification, and reciprocal replacements, of the unsaturated FA and FA classes, that are most abundantly provided by the diet, take place in plasma lipids.

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Metabolic effects of parenteral nutrition enriched with n-3 polyunsaturated fatty acids in critically ill patients

et al. 2006

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Fractional hepatic de novo lipogenesis in healthy subjects during near-continuous oral nutrition and bed rest: a comparison with published data in artificially fed, critically ill patients

Cited by 6 publications

References 18 publications

Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?

Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?

Origin of fatty acids in the body: endogenous synthesis versus dietary intakes

Metabolic effects of parenteral nutrition enriched with n-3 polyunsaturated fatty acids in critically ill patients

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