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Regulation of Cholesterol Metabolism in Liver: Link to NAFLD and Impact of n-3 PUFAs.

Bae JS, Oh AR, Cha JY - J Lifestyle Med (2013)

Bottom Line: Several pharmaceutical approaches to NAFLD management have been examined, but no particular treatment has been considered both safe and highly effective.Growing evidence reveal that supplemental fish oil, seal oil and purified n-3 fatty acids can reduce hepatic lipid content in NAFLD through extensive regulation by inhibiting lipogenesis, promoting fatty acid oxidation and suppressing inflammatory responses.This article introduces the n-3 PUFAs, and addresses the evidence and mechanisms by which endogenously synthesized n-3 PUFAs or increased dietary n-3 PUFAs may ameliorate NAFLD.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cell Metabolism and Gene Regulation, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Korea.

ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease that affects one-third of adults in westernized countries. NAFLD represents a wide spectrum of hepatic alterations, ranging from simple triglyceride accumulation in the liver to steatohepatitis. Several pharmaceutical approaches to NAFLD management have been examined, but no particular treatment has been considered both safe and highly effective. Growing evidence reveal that supplemental fish oil, seal oil and purified n-3 fatty acids can reduce hepatic lipid content in NAFLD through extensive regulation by inhibiting lipogenesis, promoting fatty acid oxidation and suppressing inflammatory responses. Recently, the fat-1 transgenic mice capable of converting n-6 to n-3 polyunsaturated fatty acids (PUFAs) have been used to examine the effects of endogenous n-3 PUFAs on NAFLD. The increased n-3 PUFAs in fat-1 transgenic mice reduced diet-induced hyperlipidemia and fatty liver through induction of CYP7A1 expression and activation of cholesterol catabolism to bile acid. This article introduces the n-3 PUFAs, and addresses the evidence and mechanisms by which endogenously synthesized n-3 PUFAs or increased dietary n-3 PUFAs may ameliorate NAFLD.

No MeSH data available.


Related in: MedlinePlus

Metabolism of n-3 and n-6 polyunsaturated fatty acids (PUFAs). Linolenic acid (LA) and alpha-linolenic acid (ALA) are the parent PUFAs for n-6 and n-3, respectively. The fat-1 gene encodes an n-3 desaturase that converts n-6 to n-3 fatty acid.
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f1-jlm-03-19: Metabolism of n-3 and n-6 polyunsaturated fatty acids (PUFAs). Linolenic acid (LA) and alpha-linolenic acid (ALA) are the parent PUFAs for n-6 and n-3, respectively. The fat-1 gene encodes an n-3 desaturase that converts n-6 to n-3 fatty acid.

Mentions: Fatty acids, essential components of all cell membranes, play a number of key roles in metabolism such as being a major metabolic fuel (storage and transport energy), and the ligands for transcription factors. Although animals can synthesize saturated fatty acids and some monounsaturated fatty acids from carbon groups in carbohydrates and proteins, they lack the enzymes, desaturases, which are necessary to insert a cis double bond at the n-6 or the n-3 position of a fatty acid. Consequently, linoleic acid (LA, C18:2; n-6) and alpha-linolenic acid (ALA, C18:3; n-3) are essential nutrients that must be taken from food [8]. Human can synthesize long-chain n-6 PUFAs, such as arachidonic acid (AA; C20:4;n-6) from LA and long-chain n-3 PUFAs, such as eicosapentaenoic acid (EPA; C20:5; n-3) and docosahexaenoic acid (DHA; C22:6; n-3) from ALA (Fig. 1). However, EPA and DHA have to be obtained from diet because mammals inefficiently convert ALA to EPA and DHA [9]. n-3 PUFAs are enriched in fish oil, flaxseed and some nuts whereas n-6 PUFAs are found predominantly in grain and vegetable oil. It has been estimated that the ratio of n-6 to n-3 PUFAs in the diet of early humans was 1:1 [10], but the ratio in the typical Western diet is now almost 10:1 due to increased use of vegetable oils rich in LA as well as reduced fish consumption [11]. A lower intake in dietary sources of n-3 PUFAs seems to be associated with NAFLD [4,12]. In fact, patients with hepatic steatosis present a lower n-3/n-6 PUFA ratio in liver tissue biopsies, namely in phospholipids subfractions, and in red blood cells [5,6].


Regulation of Cholesterol Metabolism in Liver: Link to NAFLD and Impact of n-3 PUFAs.

Bae JS, Oh AR, Cha JY - J Lifestyle Med (2013)

Metabolism of n-3 and n-6 polyunsaturated fatty acids (PUFAs). Linolenic acid (LA) and alpha-linolenic acid (ALA) are the parent PUFAs for n-6 and n-3, respectively. The fat-1 gene encodes an n-3 desaturase that converts n-6 to n-3 fatty acid.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4390754&req=5

f1-jlm-03-19: Metabolism of n-3 and n-6 polyunsaturated fatty acids (PUFAs). Linolenic acid (LA) and alpha-linolenic acid (ALA) are the parent PUFAs for n-6 and n-3, respectively. The fat-1 gene encodes an n-3 desaturase that converts n-6 to n-3 fatty acid.
Mentions: Fatty acids, essential components of all cell membranes, play a number of key roles in metabolism such as being a major metabolic fuel (storage and transport energy), and the ligands for transcription factors. Although animals can synthesize saturated fatty acids and some monounsaturated fatty acids from carbon groups in carbohydrates and proteins, they lack the enzymes, desaturases, which are necessary to insert a cis double bond at the n-6 or the n-3 position of a fatty acid. Consequently, linoleic acid (LA, C18:2; n-6) and alpha-linolenic acid (ALA, C18:3; n-3) are essential nutrients that must be taken from food [8]. Human can synthesize long-chain n-6 PUFAs, such as arachidonic acid (AA; C20:4;n-6) from LA and long-chain n-3 PUFAs, such as eicosapentaenoic acid (EPA; C20:5; n-3) and docosahexaenoic acid (DHA; C22:6; n-3) from ALA (Fig. 1). However, EPA and DHA have to be obtained from diet because mammals inefficiently convert ALA to EPA and DHA [9]. n-3 PUFAs are enriched in fish oil, flaxseed and some nuts whereas n-6 PUFAs are found predominantly in grain and vegetable oil. It has been estimated that the ratio of n-6 to n-3 PUFAs in the diet of early humans was 1:1 [10], but the ratio in the typical Western diet is now almost 10:1 due to increased use of vegetable oils rich in LA as well as reduced fish consumption [11]. A lower intake in dietary sources of n-3 PUFAs seems to be associated with NAFLD [4,12]. In fact, patients with hepatic steatosis present a lower n-3/n-6 PUFA ratio in liver tissue biopsies, namely in phospholipids subfractions, and in red blood cells [5,6].

Bottom Line: Several pharmaceutical approaches to NAFLD management have been examined, but no particular treatment has been considered both safe and highly effective.Growing evidence reveal that supplemental fish oil, seal oil and purified n-3 fatty acids can reduce hepatic lipid content in NAFLD through extensive regulation by inhibiting lipogenesis, promoting fatty acid oxidation and suppressing inflammatory responses.This article introduces the n-3 PUFAs, and addresses the evidence and mechanisms by which endogenously synthesized n-3 PUFAs or increased dietary n-3 PUFAs may ameliorate NAFLD.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cell Metabolism and Gene Regulation, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Korea.

ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease that affects one-third of adults in westernized countries. NAFLD represents a wide spectrum of hepatic alterations, ranging from simple triglyceride accumulation in the liver to steatohepatitis. Several pharmaceutical approaches to NAFLD management have been examined, but no particular treatment has been considered both safe and highly effective. Growing evidence reveal that supplemental fish oil, seal oil and purified n-3 fatty acids can reduce hepatic lipid content in NAFLD through extensive regulation by inhibiting lipogenesis, promoting fatty acid oxidation and suppressing inflammatory responses. Recently, the fat-1 transgenic mice capable of converting n-6 to n-3 polyunsaturated fatty acids (PUFAs) have been used to examine the effects of endogenous n-3 PUFAs on NAFLD. The increased n-3 PUFAs in fat-1 transgenic mice reduced diet-induced hyperlipidemia and fatty liver through induction of CYP7A1 expression and activation of cholesterol catabolism to bile acid. This article introduces the n-3 PUFAs, and addresses the evidence and mechanisms by which endogenously synthesized n-3 PUFAs or increased dietary n-3 PUFAs may ameliorate NAFLD.

No MeSH data available.


Related in: MedlinePlus