High oleic peanuts improve parameters leading to fatty liver development and change the microbiota in mice intestine

AbstractStudies on animal models have demonstrated that feeding a low-arginine diet inhibits triacylglycerol (TAG) secretion from the liver, resulting in marked fatty liver development in rats. Here, we first showed that culturing hepatocytes in the medium mimicking the serum amino acid profile of low-arginine diet-fed rats induced TAG accumulation in the cells, indicating that the specific amino acid profile caused TAG accumulation in hepatocytes. Dietary adenine supplementation completely recovered hepatic TAG secretion and abolished hepatic TAG accumulation in rats. A comprehensive non-linear analysis revealed that inhibition of hepatic TAG accumulation by dietary adenine supplementation could be predicted using only serum amino acid concentration data. Comparison of serum amino acid concentrations indicated that histidine, methionine, and branched-chain amino acid (BCAA) concentrations were altered by adenine supplementation. Furthermore, when the serum amino acid profiles of low-arginine diet-fed rats were altered by modifying methionine or BCAA concentrations in their diets, their hepatic TAG accumulation was abolished. Altogether, these results suggest that an increase in methionine and BCAA levels in the serum in response to dietary arginine deficiency is a key causative factor for hepatic TAG accumulation, and dietary adenine supplementation could disrupt this phenomenon by altering serum amino acid profiles.

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Influence of Fatty Liver Development and Recurrence of Primary Disease on Nutritional Status after Pancreaticoduodenectomy

Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) ◽

10.3919/jjsa.76.671 ◽

2015 ◽

Vol 76 (4) ◽

pp. 671-676

Author(s):

Masaaki KATAOKA ◽

Shigeru YOSHIOKA ◽

Masayuki SHIOBARA ◽

Kazuo WAKATSUKI ◽

Syuuka ARAI ◽

...

Keyword(s):

Nutritional Status ◽

Fatty Liver ◽

Liver Development ◽

Primary Disease

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Improving Shelf Life of Roasted and Salted Inshell Peanuts Using High Oleic Fatty Acid Chemistry

Peanut Science ◽

10.3146/pnut.31.1.0009 ◽

2004 ◽

Vol 31 (1) ◽

pp. 40-45 ◽

Cited By ~ 29

Author(s):

R. W. Mozingo ◽

S. F. O'Keefe ◽

T. H. Sanders ◽

K. W. Hendrix

Keyword(s):

Fatty Acid ◽

Shelf Life ◽

Oxygen Barrier ◽

Consumer Complaint ◽

High Oleic ◽

A Value ◽

Arachis Hypogaea L ◽

Shelf Life Stability ◽

High Oleic Peanuts ◽

Life Evaluations

Abstract Major markets for the large-seeded virginia-type peanut (Arachis hypogaea L.) include roasted inshell and salted inshell products with short shelf life being a common consumer complaint. Unlike many other peanut products, it is not economically possible to package these inshell peanuts in nitrogen flushed, oxygen barrier bags. A number of studies have shown that roasted runner-type peanuts with high contents of oleic fatty acid have improved oxidative stability and longer shelf life. A large-seeded, virginia-type peanut cultivar (AgraTech VC-2) with the high oleic trait has been released but no information is available on its shelf life stability. Therefore, this high oleic cultivar and the normal oleic cultivar VA 98R from the 2000 and 2001 crop were used for shelf life evaluations. Peanuts were sized into the fancy inshell grade for roasted inshell and salted inshell products. Peroxide value (PV) results for the roasted inshell peanuts indicated that normal oleic fatty acid (50% range) peanuts reached a PV of 20 meq/kg by the end of 4 wk of storage. On the other hand, the high oleic fatty acid (80% range) peanuts did not reach a value of 20 meq/kg until approximately 32 wk. When salted inshell the normal oleic peanuts exceed a PV of 20 meq/kg before the 2nd wk, whereas the high oleic peanuts still had not reached a PV of 20 meq/kg after 40 wk of storage. These results show a significant advantage of high oleic peanuts for extending shelf life of large-seeded, virginia-type peanuts for either roasted or salted inshell processing.

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Inhibition of Dexamethasone-induced Fatty Liver Development by Reducing miR-17-5p Levels

Molecular Therapy ◽

10.1038/mt.2015.64 ◽

2015 ◽

Vol 23 (7) ◽

pp. 1222-1233 ◽

Cited By ~ 15

Author(s):

William W Du ◽

Fengqiong Liu ◽

Sze Wan Shan ◽

Xindi Cindy Ma ◽

Shaan Gupta ◽

...

Keyword(s):

Fatty Liver ◽

Liver Development

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Investigating the role of cortisol and growth hormone in fatty liver development: fatty liver index in patients with pituitary adenomas

Pituitary ◽

10.1007/s11102-016-0726-1 ◽

2016 ◽

Vol 19 (5) ◽

pp. 461-471 ◽

Cited By ~ 4

Author(s):

Matthias K. Auer ◽

Günter K. Stalla ◽

Mareike R. Stieg

Keyword(s):

Growth Hormone ◽

Fatty Liver ◽

Pituitary Adenomas ◽

Liver Development ◽

Liver Index ◽

Fatty Liver Index

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Molecular cloning of the goose ACSL3 and ACSL5 coding domain sequences and their expression characteristics during goose fatty liver development

Molecular Biology Reports ◽

10.1007/s11033-014-3053-5 ◽

2014 ◽

Vol 41 (4) ◽

pp. 2045-2053 ◽

Cited By ~ 6

Author(s):

H. He ◽

H. H. Liu ◽

J. W. Wang ◽

J. Lv ◽

L. Li ◽

...

Keyword(s):

Fatty Liver ◽

Molecular Cloning ◽

Liver Development ◽

Expression Characteristics

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A High-Fat Diet Attenuates Amp-Activated Protein Kinase α1 in Adipocytes to Induce Exosome Shedding and Nonalcoholic Fatty Liver Development in Vivo

10.2337/figshare.13259768 ◽

2020 ◽

Author(s):

Ada Admin ◽

Chenghui Yan ◽

Xiaoxiang Tian ◽

Jiayin Li ◽

Dan Liu ◽

...

Keyword(s):

Adipose Tissue ◽

Protein Kinase ◽

Fatty Liver ◽

Lipid Accumulation ◽

High Fat Diet ◽

Liver Development ◽

High Fat ◽

Tissue Specific ◽

Nonalcoholic Fatty Liver ◽

Amp Activated Protein Kinase

Exosomes are important for intercellular communication, but the role of exosomes in the communication between adipose tissue (<a>AT</a>) and the liver remains unknown. The aim of this study is to determine the contribution of AT-derived exosomes in nonalcoholic fatty liver disease (<a>NAFLD</a>). Exosome components, liver fat content, and liver function were monitored in AT in mice fed a <a>high-fat diet </a>(<a>HFD</a>) or treated with metformin- or GW4869 and with AMP-activated protein kinase (AMPKα1) floxed (Prkaα1fl/fl/WT), <a>Prkaα1-/-</a>, liver tissue-specific Prkaα1-/-, or AT-specific Prkaα1-/- modification. In cultured adipocytes and white adipose tissue (WAT), the absence of <a>AMPKα1</a> increased exosome release and exosomal proteins by elevating <a>tumor susceptibility gene 101 (TSG101</a>)-mediated exosome biogenesis. In adipocytes treated with palmitic acid, TSG101 facilitated scavenger receptor class B (CD36) sorting into exosomes. CD36-containing exosomes were then endocytosed by hepatocytes to induce lipid accumulation and inflammation. Consistently, an HFD induced more severe lipid accumulation and cell death in <a>Prkaα1-/- </a>and adipose tissue-specific Prkaα1-/- mice than in WT and liver-specific Prkaα1-/- mice. AMPK activation by metformin reduced adipocyte-mediated exosome release and mitigated fatty liver development in WT and liver specific Prkaα1-/- mice. Moreover, administration of the exosome inhibitor GW4869 blocked exosome secretion and alleviated HFD-induced fatty livers in Prkaα1-/- and adipocyte-specific Prkaα1-/- mice. We conclude that HFD-mediated AMPKα1 inhibition promotes NAFLD by increasing numbers of AT C<a>D36</a>-containing exosomes.

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