The problem of establishing relationships between hepatic steatosis and hepatic insulin resistance

doi:10.1016/j.cmet.2012.03.004

. 2012 May 2;15(5):570-3.

doi: 10.1016/j.cmet.2012.03.004.

The problem of establishing relationships between hepatic steatosis and hepatic insulin resistance

Robert V Farese Jr¹, Rudolf Zechner, Christopher B Newgard, Tobias C Walther

Affiliations

PMID: 22560209
PMCID: PMC3767424
DOI: 10.1016/j.cmet.2012.03.004

The problem of establishing relationships between hepatic steatosis and hepatic insulin resistance

Robert V Farese Jr et al. Cell Metab. 2012.

. 2012 May 2;15(5):570-3.

doi: 10.1016/j.cmet.2012.03.004.

Authors

Robert V Farese Jr¹, Rudolf Zechner, Christopher B Newgard, Tobias C Walther

Affiliation

¹ Gladstone Institute of Cardiovascular Disease, Department of Medicine, University of California, San Francisco, CA 94158, USA. bfarese@gladstone.ucsf.edu

PMID: 22560209
PMCID: PMC3767424
DOI: 10.1016/j.cmet.2012.03.004

Abstract

Excessive deposition of fat in the liver (hepatic steatosis) is frequently accompanied by hepatic insulin resistance. Whether this correlation is due to a causal relationship between the conditions has been the subject of considerable debate, and the literature abounds with conflicting data and theories. Here we provide a perspective by defining the problem and its challenges, analyzing the possible causative relationships, and drawing some conclusions.

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References

1. Biddinger S, Hernandez-Ono A, Rask-Madsen C, Haas J, Alemán J, Suzuki R, Scapa E, Agarwal C, Carey M, Stephanopoulos G, et al. Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis. Cell Metab. 2008;7:125–135. - PMC - PubMed
1. Boni L, Rando R. The nature of protein kinase C activation by physically defined phospholipid vesicles and diacylglycerols. J Biol Chem. 1985;260:10819–10825. - PubMed
1. Brown J, Betters J, Lord C, Ma Y, Han X, Yang K, Alger H, Melchior J, Sawyer J, Shah R, et al. CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance. J Lipid Res. 2010;51:3306–3315. - PMC - PubMed
1. Brown M, Goldstein J. Selective versus total insulin resistance: a pathogenic paradox. Cell Metab. 2008;7:95–96. - PubMed
1. Chakravarthy M, Pan Z, Zhu Y, Tordjman K, Schneider J, Coleman T, Turk J, Semenkovich C. “New” hepatic fat activates PPARalpha to maintain glucose, lipid, and cholesterol homeostasis. Cell Metab. 2005;1:309–322. - PubMed

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[1] Biddinger S, Hernandez-Ono A, Rask-Madsen C, Haas J, Alemán J, Suzuki R, Scapa E, Agarwal C, Carey M, Stephanopoulos G, et al. Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis. Cell Metab. 2008;7:125–135. - PMC - PubMed

[2] Biddinger S, Hernandez-Ono A, Rask-Madsen C, Haas J, Alemán J, Suzuki R, Scapa E, Agarwal C, Carey M, Stephanopoulos G, et al. Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis. Cell Metab. 2008;7:125–135. - PMC - PubMed

[3] Boni L, Rando R. The nature of protein kinase C activation by physically defined phospholipid vesicles and diacylglycerols. J Biol Chem. 1985;260:10819–10825. - PubMed

[4] Boni L, Rando R. The nature of protein kinase C activation by physically defined phospholipid vesicles and diacylglycerols. J Biol Chem. 1985;260:10819–10825. - PubMed

[5] Brown J, Betters J, Lord C, Ma Y, Han X, Yang K, Alger H, Melchior J, Sawyer J, Shah R, et al. CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance. J Lipid Res. 2010;51:3306–3315. - PMC - PubMed

[6] Brown J, Betters J, Lord C, Ma Y, Han X, Yang K, Alger H, Melchior J, Sawyer J, Shah R, et al. CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance. J Lipid Res. 2010;51:3306–3315. - PMC - PubMed

[7] Brown M, Goldstein J. Selective versus total insulin resistance: a pathogenic paradox. Cell Metab. 2008;7:95–96. - PubMed

[8] Brown M, Goldstein J. Selective versus total insulin resistance: a pathogenic paradox. Cell Metab. 2008;7:95–96. - PubMed

[9] Chakravarthy M, Pan Z, Zhu Y, Tordjman K, Schneider J, Coleman T, Turk J, Semenkovich C. “New” hepatic fat activates PPARalpha to maintain glucose, lipid, and cholesterol homeostasis. Cell Metab. 2005;1:309–322. - PubMed

[10] Chakravarthy M, Pan Z, Zhu Y, Tordjman K, Schneider J, Coleman T, Turk J, Semenkovich C. “New” hepatic fat activates PPARalpha to maintain glucose, lipid, and cholesterol homeostasis. Cell Metab. 2005;1:309–322. - PubMed

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The problem of establishing relationships between hepatic steatosis and hepatic insulin resistance

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The problem of establishing relationships between hepatic steatosis and hepatic insulin resistance

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