Insulin resistance in patients with cirrhosis and portal hypertension

Erice, Eva; Llop, Elba; Berzigotti, Annalisa; Abraldes, Juan G.; Conget, Ignacio; Seijó, Susana; Reverter, Enric; Albillos, Agustı́n; Bosch, Jackie; García‐Pagán, Juan Carlos

doi:10.1152/ajpgi.00389.2011

Cited by 28 publications

(26 citation statements)

References 48 publications

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“…The relationship between HOMA-2 index and portal hypertension was reported previously in a cohort of cirrhotic patients with mixed etiology [18] and it was shown that the HOMA index significantly predicts the presence of esophageal varices in CHC-related cirrhotic patients irrespective of the presence of diabetes [19]. The pathophysiological link between portal hypertension and IR could be potentially explained by the fact that insulin can modulate the endothelial synthesis of nitric oxide and endothelin [28,29], to induce tumor necrosis factor alpha secretion, and to stimulate hepatic stellate cells [19,30,31].…”

Section: Discussionsupporting

confidence: 67%

“…Eighty percent of the patients had alcohol consumption more than 80 g/day. The median MELD score was 15 [9][10][11][12][13][14][15][16][17][18][19][20][21] and 26% of the patients had compensated (Child-Pugh score A) cirrhosis. The median HOMA-2 index value was 2 (1.2-3.1) in our population of ALD cirrhotic patients.…”

Section: Patient Characteristicsmentioning

confidence: 99%

“…In addition, IR may be related to portal hypertension. The hepatic venous pressure gradient (HVPG) has been correlated to the homeostasis model assessment (HOMA) index, a strong surrogate of IR in patients with nonalcoholic steatohepatitis [17], but also in cirrhotic patients with mixed etiology [18]. The HOMA index has also been reported to be a predictor of the presence of gastroesophageal varices in CHC patients [19].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Insulin resistance is associated with esophageal varices in alcoholic liver disease patients

Degré

Gustot

Gerkens

et al. 2016

European Journal of Gastroenterology &Amp; Hepatology

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Section: Discussionsupporting

confidence: 67%

Section: Patient Characteristicsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Insulin resistance is associated with esophageal varices in alcoholic liver disease patients

Degré

Gustot

Gerkens

et al. 2016

European Journal of Gastroenterology &Amp; Hepatology

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“…In tissue from human liver diseases associated with hepatic insulin resistance (eg NAFLD, ALD and NASH (14)) and elevated VAP-1 expression, we have demonstrated modifications in GLUT expression compared to normal livers (Fig 2). Human studies have linked insulin resistance to altered expression of GLUT isoforms by granulosa cells (28)and adipose tissue (33) and rodent livers demonstrate increased GLUT-1 and decreased GLUT-2 expression when insulin resistance is induced by high fat diet (54) or alcohol exposure (48).…”

Section: Discussionmentioning

confidence: 78%

Dysregulated hepatic expression of glucose transporters in chronic disease: contribution of semicarbazide-sensitive amine oxidase to hepatic glucose uptake

Karim

Liaskou

Fear

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Insulin resistance is common in patients with chronic liver disease (CLD). Serum levels of soluble vascular adhesion protein-1 (VAP-1) are also increased in these patients. The amine oxidase activity of VAP-1 stimulates glucose uptake via translocation of transporters to the cell membrane in adipocytes and smooth muscle cells. We aimed to document human hepatocellular expression of glucose transporters (GLUTs) and to determine if VAP-1 activity influences receptor expression and hepatic glucose uptake. Quantitative PCR and immunocytochemistry were used to study human liver tissue and cultured cells. We also used tissue slices from humans and VAP-1-deficient mice to assay glucose uptake and measure hepatocellular responses to stimulation. We report upregulation of GLUT1, -3, -5, -6, -7, -8, -9, -10, -11, -12, and -13 in CLD. VAP-1 expression and enzyme activity increased in disease, and provision of substrate to hepatic VAP-1 drives hepatic glucose uptake. This effect was sensitive to inhibition of VAP-1 and could be recapitulated by H2O2. VAP-1 activity also altered expression and subcellular localization of GLUT2, -4, -9, -10, and -13. Therefore, we show, for the first time, alterations in hepatocellular expression of glucose and fructose transporters in CLD and provide evidence that the semicarbazide-sensitive amine oxidase activity of VAP-1 modifies hepatic glucose homeostasis and may contribute to patterns of GLUT expression in chronic disease.

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“…23 No 4: 397-403 reduced insulin clearance secondary to hepatic insu ciency and porto-systemic shunting [10]. It was also demonstrated that insulin resistance is positively correlated with portal hypertension (PHT) evaluated directly by hepatic venous pressure gradient (HVPG) measurement [11] or indirectly as the presence of esophageal varices (EV) [12]. Furthermore, obesity and diabetes represent independent risk factors for development of hepatocellular carcinoma in patients with NASH [13].…”

Section: Introductionmentioning

confidence: 99%

The Metabolic Syndrome Is Not Correlated with the Short-term Risk of Decompensation in Patients with Cirrhosis

Procopeţ

Farcau

Balagel

et al. 2014

JGLD

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Background & Aims: Obesity proved to favor clinical decompensation in patients with cirrhosis. Our aim was to investigate if metabolic syndrome (MS) in cirrhotic patients represents a risk factor for decompensation.Methods: 704 cirrhotics, included in a MS prevalence study were considered for evaluation; 121 patients were excluded because they did not complete the follow-up and 303 because they were decompensated at the start of the study. The remaining 280 were followed-up for a median period of 28.1±18 months. Patients were censored at the end of follow-up or at occurrence of a liver related event (LRE). Liver related events were considered the following: decompensation (ascites, variceal bleeding, hepatorenal syndrome, jaundice, encephalopathy), hepatocellular carcinoma, portal vein thrombosis and infections.Results: All MS criteria except the abdominal circumference were significantly different between decompensated and compensated patients. HDL-cholesterol levels were lower in decompensated patients. Among the 280 patients who completed the follow-up, 85 (30%) presented LREs. Ascites was the most frequent event. In the univariate analysis of the MS criteria we found a trend to significance of an inverse correlation between MS and LREs. There was no significant difference between patients with or without MS regarding survival free of LREs, 76.7% and 66.5%, respectively. None of the MS criteria reached the level of significance in discriminating patients with and without LREs.Conclusions: In short term, presence of MS was not a risk factor for LREs. In short term, liver function and lower nutritional status influenced the prognosis. In decompensated patients, the MS defining criteria are not applicable.Abbreviations: BMI: body mass index; EV: esophageal varices; HR: hazard ration; HVPG: hepatic venous pressure gradient; LRE: liver related event; MS: metabolic syndrome; PHT: portal hypertension; WC: waist circumference.

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Insulin resistance in patients with cirrhosis and portal hypertension

Abstract: Erice E, Llop E, Berzigotti A, Abraldes JG, Conget I, Seijo S, Reverter E, Albillos A, Bosch J, García-Pagán JC. Insulin resistance in patients with cirrhosis and portal hypertension.

Cited by 28 publications

References 48 publications

Insulin resistance is associated with esophageal varices in alcoholic liver disease patients

Insulin resistance is associated with esophageal varices in alcoholic liver disease patients

Dysregulated hepatic expression of glucose transporters in chronic disease: contribution of semicarbazide-sensitive amine oxidase to hepatic glucose uptake

The Metabolic Syndrome Is Not Correlated with the Short-term Risk of Decompensation in Patients with Cirrhosis

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