Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome

Yki‐Järvinen, Hannele

doi:10.1016/s2213-8587(14)70032-4

Cited by 1,040 publications

(874 citation statements)

References 112 publications

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“…Thus, while IR development increases triglyceride accumulation in the liver (Samuel et al 2010, Samuel & Shulman 2012, fatty liver produces an excess of glucose and triglycerides, which are key components in IR and MetS (Anstee et al 2013, Yki-Jarvinen 2014. Consistently, other studies have shown that decreased hepatic steatosis, induced by lipase (ATGL) overproduction is accompanied by improved insulin sensitivity and insulin-signalling (Turpin et al 2011).…”

Section: Discussionmentioning

confidence: 70%

“…Albeit the precise mechanisms linking characteristics of the MetS and NAFLD are not completely known, a complex relationship exists between the two (Marchesini & Marzocchi 2007, Mitsutake et al 2011. In this sense, an excess of glucose and triglycerides, which are key components in the MetS, is produced by fatty liver (Anstee et al 2013, Yki-Jarvinen 2014. On the other hand, IR development, which alters carbohydrate and lipid metabolism, increases triglyceride accumulation in the liver (Samuel et al 2010, Samuel & Shulman 2012.…”

Section: Introductionmentioning

confidence: 99%

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Hepatic lipase deficiency produces glucose intolerance, inflammation and hepatic steatosis

Andrés‐Blasco¹,

Herrero-Cervera²,

Vinué³

et al. 2015

Journal of Endocrinology

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Metabolic syndrome and type 2 diabetes mellitus constitute a major problem to global health, and their incidence is increasing at an alarming rate. Non-alcoholic fatty liver disease, which affects up to 90% of obese people and nearly 70% of the overweight, is commonly associated with MetS characteristics such as obesity, insulin resistance, hypertension and dyslipidemia. In the present study, we demonstrate that hepatic lipase (HL)-inactivation in mice fed with a high-fat, high-cholesterol diet produced dyslipidemia including hypercholesterolemia, hypertriglyceridemia and increased non-esterified fatty acid levels. These changes were accompanied by glucose intolerance, pancreatic and hepatic inflammation and steatosis. In addition, compared with WT mice, HL K/K mice exhibited enhanced circulating MCP1 levels, monocytosis and higher percentage of CD4CTh17C cells. Consistent with increased inflammation, livers from HL K/K mice had augmented activation of the stress SAPK/JNK-and p38-pathways compared with the activation levels of the kinases in livers from WT mice. Analysis of HL K/K and WT mice fed regular chow diet showed dyslipidemia and glucose intolerance in HL K/K mice without any other changes in inflammation or hepatic steatosis. Altogether, these results indicate that dyslipidemia induced by HL-deficiency in combination with a high-fat, high-cholesterol diet promotes hepatic steatosis and inflammation in mice which are, at least in part, mediated by the activation of the stress SAPK/JNK-and p38-pathways. Future studies are warranted to asses the viability of therapeutic strategies based on the modulation of these kinases to reduce hepatic steatosis associated to lipase dysfunction.

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Hepatic lipase deficiency produces glucose intolerance, inflammation and hepatic steatosis

Andrés‐Blasco¹,

Herrero-Cervera²,

Vinué³

et al. 2015

Journal of Endocrinology

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“…For several years fatty liver was considered as a 'silent bystander', but now the matter of debate is if fatty liver disease is a cause or a consequence of the clinical features of MS [9][10][11][12][13].…”

Section: Nalfd: the Liver At The Centermentioning

confidence: 99%

Nonalcoholic fatty liver disease as trigger of cardiovascular and metabolic complication in metabolic syndrome

et al. 2015

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“…Inzwischen ist geklärt, dass sie als Folge der Insulinresistenz die hepatische Manifestation des metabolischen Syndroms darstellt [9,10] und die Entwicklung zum Typ-2-Diabetes mellitus in erheblichem Maße fördert [6,7,11]. Außerdem weisen immer mehr Studien darauf hin, dass die NAFLD ein von allen bekannten Risikofaktoren unabhängiges Risiko für Herz-Kreislaufkrankheiten darstellt [12].…”

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“…Die NAFLD ist die Folge modernen Lebensstils [10,13]. Zu viel Nahrungsenergie und zu wenig Bewegung gelten als besonders relevante Risikofaktoren.…”

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Schützt moderater Weinkonsum vor nichtalkoholischer Fettleber?

Worm¹

2015

38th World Congress of Vine and Wine (Part 2)

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Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome

Cited by 1,040 publications

References 112 publications

Hepatic lipase deficiency produces glucose intolerance, inflammation and hepatic steatosis

Hepatic lipase deficiency produces glucose intolerance, inflammation and hepatic steatosis

Nonalcoholic fatty liver disease as trigger of cardiovascular and metabolic complication in metabolic syndrome

Schützt moderater Weinkonsum vor nichtalkoholischer Fettleber?

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