The blind men 'see' the elephant-the many faces of fatty liver disease

Sanal, Madhusudana Girija

doi:10.3748/wjg.14.831

Cited by 41 publications

(21 citation statements)

References 139 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, disturbances in the cytokine network, including alterations in the tumor necrosis factor-a (TNF-a) [27] level, were shown to be involved in ethanol-induced steatosis. These pivotal factors, however, appear to be common in the pathogenesis of both NAFLD [28][29][30] and AFLD. Therefore, the inverse association between FL and alcohol consumption cannot be explained by these alterations alone.…”

Section: Discussionmentioning

confidence: 78%

Alcohol drinking patterns and the risk of fatty liver in Japanese men

et al. 2010

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 78%

Alcohol drinking patterns and the risk of fatty liver in Japanese men

et al. 2010

View full text Add to dashboard Cite

show abstract

“…An upregulated PTP1B activity activates lipogenic mechanisms, involving the activation of SREBP-1c and of its target gene, FAS, as was shown originally for rats fed fructoseenriched diets (14)(15)(16)(17). Moreover, PTP1B expression is a valuable indicator for the diagnosis of nonalcoholic-fatty-liver-disease, a disorder closely related to hepatic insulin resistance and metabolic syndrome (72)(73)(74). However, the manipulation of PTP1B by dietary Se powerfully influences liver lipid metabolism.…”

Section: Discussionmentioning

confidence: 92%

Redox Regulation of Protein Tyrosine Phosphatase 1B by Manipulation of Dietary Selenium Affects the Triglyceride Concentration in Rat Liver

Mueller

Klomann

Wolf

et al. 2008

The Journal of Nutrition

View full text Add to dashboard Cite

Protein tyrosine phosphatase 1B (PTP1B) is a key enzyme in the counter-regulation of insulin signaling and in the stimulation of fatty acid synthesis. Selenium (Se), via the activities of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), is involved in the removal of H(2)O(2) and organic peroxides, which are critical compounds in the modulation of PTP1B activity via glutathionylation. Our study with growing rats investigated how the manipulation of dietary Se concentration influences the regulation of PTP1B and lipogenic effects mediated by PTP1B. Weanling albino rats were divided into 3 groups of 10. The negative control group (NC) was fed a Se-deficient diet for 8 wk. Rats in groups Se75 and Se150 received diets supplemented with 75 or 150 microg Se/kg. Se supplementation of the rats strongly influenced expression and activity of the selenoenzymes cytosolic GPx, plasma GPx, phospholipidhydroperoxide GPx, and cytosolic TrxR, and liver PTP1B. Liver PTP1B activity was significantly higher in groups Se75 and Se150 than in the NC group and this was attributed to a lowered inhibition of the enzyme by glutathionylation. The increased liver PTP1B activity in groups Se75 and Se150 resulted in 1.1- and 1.4-fold higher liver triglyceride concentrations than in the NC rats. The upregulation of the sterol regulatory element binding protein-1c and of fatty acid synthase, 2 PTP1B targets, provided a possible explanation for the lipogenic effect of PTP1B due to the manipulation of dietary Se. We therefore conclude that redox-regulated proteins, such as PTP1B, represent important interfaces between dietary antioxidants such as Se and the regulation of metabolic processes.

show abstract

“…Recent evidence suggests that FFA exposure and overload may be potentially more hazardous to hepatocytes and can lead to a dysfunctional unfolded protein response and diminished capacity for the endoplasmic reticular (ER) pathway to prevent apoptosis (21,22,27). Hepatic flux or lipid equilibrium is maintained by four interrelated mechanisms: uptake of FFA, de novo lipogenesis, secretion of VLDL, and ␤-oxidation (12,35,46). A defect in any one of these mechanisms leads to aberrant storage of lipid and potential exposure to FFA (33,35).…”

Section: Discussionmentioning

confidence: 97%

“…Hepatic flux or lipid equilibrium is maintained by four interrelated mechanisms: uptake of FFA, de novo lipogenesis, secretion of VLDL, and ␤-oxidation (12,35,46). A defect in any one of these mechanisms leads to aberrant storage of lipid and potential exposure to FFA (33,35).…”

Section: Discussionmentioning

confidence: 99%

Glp-1 analog, liraglutide, ameliorates hepatic steatosis and cardiac hypertrophy in C57BL/6J mice fed a Western diet

Mells

Pingping

Sharma

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

184

154

View full text Add to dashboard Cite

The aims of this study were designed to determine whether liraglutide, a long-acting glucagon-like peptide, could reverse the adverse effects of a diet high in fat that also contained trans-fat and high-fructose corn syrup (ALIOS diet). Specifically, we examined whether treatment with liraglutide could reduce hepatic insulin resistance and steatosis as well as improve cardiac function. Male C57BL/6J mice were pair fed or fed ad libitum either standard chow or the ALIOS diet. After 8 wk the mice were further subdivided and received daily injections of either liraglutide or saline for 4 wk. Hyperinsulinemic-euglycemic clamp studies were performed after 6 wk, revealing hepatic insulin resistance. Glucose tolerance and insulin resistance tests were performed at 8 and 12 wk prior to and following liraglutide treatment. Liver pathology, cardiac measurements, blood chemistry, and RNA and protein analyses were performed. Clamp studies revealed hepatic insulin resistance after 6 wk of ALIOS diet. Liraglutide reduced visceral adiposity and liver weight (P < 0.001). As expected, liraglutide improved glucose and insulin tolerance. Liraglutide improved hypertension (P < 0.05) and reduced cardiac hypertrophy. Surprisingly, liver from liraglutide-treated mice had significantly higher levels of fatty acid binding protein, acyl-CoA oxidase II, very long-chain acyl-CoA dehydrogenase, and microsomal triglyceride transfer protein. We conclude that liraglutide reduces the harmful effects of an ALIOS diet by improving insulin sensitivity and by reducing lipid accumulation in liver through multiple mechanisms including, transport, and increase β-oxidation.

show abstract

The blind men 'see' the elephant-the many faces of fatty liver disease

Abstract: Sanal MG. The blind men 'see' the elephant-the many faces of fatty liver disease. World

Cited by 41 publications

References 139 publications

Alcohol drinking patterns and the risk of fatty liver in Japanese men

Alcohol drinking patterns and the risk of fatty liver in Japanese men

Redox Regulation of Protein Tyrosine Phosphatase 1B by Manipulation of Dietary Selenium Affects the Triglyceride Concentration in Rat Liver

Glp-1 analog, liraglutide, ameliorates hepatic steatosis and cardiac hypertrophy in C57BL/6J mice fed a Western diet

Contact Info

Product

Resources

About