Experimental evidence has suggested that in high-carbohydrate PN administration, excess acetyl-CoA generated from glucose oxidation provides substrate for upregulation fat synthesis within the liver or hepatic de novo lipogenesis ( 11, 12). Red text indicates the cellular processes mediating each conversion.Ĭaloric requirements can be met with parenteral carbohydrates and protein alone however, high-carbohydrate PN or PN devoid of fat calories can result in EFAD, with the development of hepatic steatosis in both animal models ( 7, 8) and patients ( 9, 10). Nonbold black text indicates the important macronutrient metabolites. Intake of insufficient amounts of fat can result in EFAD.Īcetyl-CoA is a common intermediate of protein, carbohydrate, and fat metabolism, facilitating the conversion of excess protein and carbohydrate calories to fat, which is the densest form of energy storage. FAs synthesized endogenously in the setting of nutrient excess are packaged as TGs, which accumulate in adipocytes and the liver, and can lead to nonalcoholic fatty liver disease. Consumption of excess fat or carbohydrate that can be converted to fat results in increased de novo lipogenesis in which fat is produced from acetyl-CoA molecules that are common intermediates of protein and carbohydrate metabolism ( Figure 1). Maintaining fat intake within an appropriate range to meet physiologic demands is important. In children 1–10 y of age parenteral fat doses are typically 2–2.5 g ⋅ kg −1 ⋅ d −1 and decrease to 1–2 g ⋅ kg −1 ⋅ d −1 in adolescents ( 6). For parenterally fed infants, recommended intravenous fat doses range from 2.5 to 3 g ⋅ kg −1 ⋅ d −1. Average enteral fat requirements decrease with increasing age but remain substantial at 30–40% of total energy for 2- to 4 y-old children, 25–35% for up to 18-y-old adolescents ( 3, 4), and 20–30% for adults ( 5). However, they are also components of cell membranes, second messengers in cellular signaling cascades, precursors of modulators of inflammation and platelet function, and serve as substrate for de novo biosynthesis of cholesterol and endogenous steroids.Īdequate fat intake for enterally fed infants up to 2 y old is considered ∼30 g/d ( 3). They serve primarily as a dense source of cellular energy. In the present day, these products continue to evolve with the goal of achieving optimal nutrition via the intravenous route.įats serve many purposes in the body that render them biologically vital. Lipid emulsions for intravenous administration became available in the United States in the 1970s to supply appropriate fat requirements to patients with intestinal failure who require PN for long-term nutritional support. Early on, when intravenous delivery of fat was still in its infancy and the first intravenous lipid emulsions were not yet approved for use in the United States, plasma, blood products, and topical oils were often used to provide essential FAs (EFAs) ( 2). However, patients sustained on fat-free PN in the long term developed essential FA deficiency (EFAD), characterized by growth impairment, developmental delay, dermatitis, and renal and pulmonary abnormalities. These initial formulations allowed infants to survive and even meet certain growth markers over a finite period of PN dependence ( 1). In the 1960s, PN formulations were designed to provide intravenous carbohydrates, amino acids, electrolytes, and minerals to meet nutritional needs. For patients with intestinal failure who are unable to absorb sufficient nutrients via the enteral route, parenteral nutrition (PN) 7 is a lifesaving therapy.
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