Serum HCV RNA levels and HCV genotype do not affect insulin resistance in nondiabetic patients with chronic hepatitis C: a multicentre study

Tsochatzis, Emmanuel; Manolakopoulos, Spilios; Papatheodoridis, George V.; Hadziyannis, Emilia; Triantos, Christos; Zisimopoulos, Konstantinos; Goulis, Ioannis; Tzourmakliotis, Dimitrios; Akriviadis, Evangelos; Manesis, Emanuel K.; Archimandritis, Athanasios

doi:10.1111/j.1365-2036.2009.04094.x

Cited by 23 publications

(14 citation statements)

References 29 publications

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“…In addition, similar to other HCV studies, increasing age, higher BMI, lower HDL levels, and the presence of metabolic syndrome were positively associated with IR. (9, 27) Interestingly, although generally there is a higher prevalence of diabetes among males(30), in this study, female gender was associated with higher IR. It is possible that varying muscle mass and levels of physical activity may account for these gender differences, though these were not assessed.…”

Section: Discussioncontrasting

confidence: 45%

“…(9, 27) The viral factors examined here, including HCV duration of infection, viral load, and genotype, did not appear to have much impact on IR, with small estimates that were in the biologically implausible direction. Evidence against any substantial impact, however, was not strong for genotype 1, because the confidence interval extended to a potentially important 19-point increase.…”

Section: Discussionmentioning

confidence: 81%

“…This rate is lower than those observed in studies of HCV-infected non-diabetic patients with similar patient selection criteria that utilized the surrogate measurement of IR, HOMA-IR, with reported rates ranging from 32 to 54%. (9, 26, 27) The difference in observed rates is likely due to use of low HOMA-IR cut-off values (mainly >2 or >3) to define insulin resistance that have been shown to have high misclassification rates, as well as the limited reliability of this surrogate estimate that can be influenced by degrees of obesity and ethnicity. (12, 13) The three prior studies to date utilizing the hyperinsulinemic-euglycemic clamp did not specifically assess the distribution of insulin resistance in the HCV population and were limited by small sample sizes and a lack of heterogeneity with respect to gender and race/ethnicity.…”

Section: Discussionmentioning

confidence: 99%

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Insulin Sensitivity and Variability in Hepatitis C Virus Infection Using Direct Measurement

et al. 2012

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Background & Aims Studies investigating insulin resistance (IR) in chronic hepatitis C virus (HCV) infection have used surrogate measures of IR that have limited reliability. We aimed to describe the distribution and risk factors associated with IR and its change over time in HCV using direct measurement. Methods One hundred and two non-cirrhotic, non-diabetic, HCV-infected subjects underwent clinical, histologic, and metabolic evaluation, and 27 completed repeat evaluation at 6 months. Insulin-mediated glucose uptake was measured by steady-state plasma glucose (SSPG) concentration during the insulin suppression test. Results Three subjects with diabetes were excluded and 95 completed all testing. SSPG ranged from 39 to 328 mg/dL (mean 135 mg/dL) and was stable over time (mean SSPG change -0.3 mg/dL). SSPG was associated with Latino ethnicity (Coef 67, 95%CI 37-96), BMI (Coef 19 per 5 kg/m2, 95%CI 5-32), ferritin (Coef 1.4 per 10 ng/ml, 95%CI 0.2-2.5), male gender (Coef -48, 95%CI -80 to -16), and HDL (Coef -16, 95%CI -28 to -5 mg/dL). Current tobacco use (Coef 55, 95%CI 19-90), steatosis (Coef -44, 95%CI -86 to -3), and increases in BMI (Coef 30 per 5 kg/m2, 95%CI 6-53) and triglyceride (Coef 3.5 per 10 mg/dL, 95%CI 0.3-6.7) predicted change in SSPG. Conclusions There was a wide spectrum of insulin resistance in our HCV population. Host factors, rather than viral factors, appeared to more greatly influence insulin action and its change in HCV.

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Section: Discussioncontrasting

confidence: 45%

Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

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Insulin Sensitivity and Variability in Hepatitis C Virus Infection Using Direct Measurement

et al. 2012

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“…Finally, we observed an association between serum hepcidin and IR. IR is a viral effect of CHC, developing in early stages, and is further exacerbated by metabolic abnormalities [30,31]. In our cohort of mildly overweight patients, a dual viral and metabolic cause of IR is very likely.…”

Section: Discussionmentioning

confidence: 99%

Serum hepcidin levels are related to the severity of liver histological lesions in chronic hepatitis C

Tsochatzis

Papatheodoridis

Koliaraki

et al. 2009

Journal of Viral Hepatitis

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Hepcidin is synthesized in the liver and has a crucial role in iron homoeostasis. Its synthesis is up-regulated in chronic inflammation and iron excess. We examined the determinants of serum hepcidin and liver hepcidin mRNA levels and their association with histological lesions in patients with chronic hepatitis C (CHC) and healthy controls. We studied 96 patients with CHC and 30 controls. Serum hepcidin levels were measured by an in-house competitive ELISA. Hepcidin mRNA levels were determined by a one-step qRT-PCR in total RNA extracted from liver biopsy specimens of 27 patients with CHC and six disease controls. Histological lesions were evaluated according to Ishak's classification. Serum hepcidin was significantly lower in patients with CHC than healthy controls (14.6 ± 7.3 vs 34.6 ± 17.3 ng/mL, P < 0.001). In patients with CHC, serum hepcidin correlated positively with aspartate aminotransferase (r = 0.334, P = 0.001) and insulin resistance (r = 0.27, P = 0.016) and had a trend for correlation with alanine aminotransferase (r = 0.197, P = 0.057) and serum haemoglobin (r = 0.188, P = 0.067) but not with ferritin. A significant positive correlation was also found between serum hepcidin levels and both necroinflammation (r = 0.259, P = 0.011) and fibrosis (r = 0.214, P = 0.036). Serum hepcidin was among others an independent predictor of cirrhosis (odds ratio: 1.145, P = 0.039). Liver hepcidin mRNA levels did not differ between patients and controls and were relatively lower in patients with than without cirrhosis (19.3 ± 21.7 vs 38.3 ± 26.0, P = 0.067). Patients with CHC have reduced serum hepcidin levels, which correlate with worse necroinflammation and fibrosis. The previously mentioned observations suggest a viral effect on hepatic hepcidin production, but might also support its involvement in the inflammatory process.

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“…Studies have shown that HOMA-IR levels are higher in patients with genotypes 1 and 4 [19], and that patients with genotype 3 are those in whom HOMA-IR levels are the lowest [17]. In a study from Greece, HOMA-IR levels were comparable across viral genotypes [124], and these results suggest that the severe steatosis observed in genotype 3 may not result in increased IR. It is noteworthy that SREBP-1c not only influences production of enzymes regulating lipogenesis and reducing fatty acid β-oxidation, but is a protein interfering in intracellular insulin signaling.…”

Section: Relationship Between Insulin Resistance and Steatosis In Hcvmentioning

confidence: 99%

Review article Insulin resistance and its consequences in chronic hepatitis C

Kukla¹,

Piotrowski²,

Waluga³

et al. 2015

ceh

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Chronic hepatitis C (CHC) is generally a slowly progressive disease, but some factors associated with rapid progression have been identified. Hepatitis C virus (HCV) may contribute to a broad spectrum of metabolic disturbances – namely, steatosis, insulin resistance (IR), increased prevalence of impaired glucose tolerance, type 2 diabetes mellitus (T2DM), lipid metabolism abnormalities and atherosclerosis.HCV can directly or indirectly cause both IR and steatosis, but it is still not resolved whether this viral impact bears the same prognostic value as the metabolic counterparts. As the population exposed to HCV ages, the morbidity due to this disease is increasing. The rising epidemic of obesity contributes to higher prevalence of IR and T2DM. Our understanding of the mutual association between both disease states continues to grow, but is still far from complete. This review briefly discusses the most probable mechanisms involved in IR development in the course of CHC. Molecular mechanisms for the direct and indirect influence of HCV on intracellular insulin signaling are described. Subsequently, the consequences of IR/T2DM for disease progression and management are summarized.

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Serum HCV RNA levels and HCV genotype do not affect insulin resistance in nondiabetic patients with chronic hepatitis C: a multicentre study

Abstract: SUMMARY BackgroundChronic hepatitis C (CHC) induces insulin resistance (IR) and subsequently diabetes.

Cited by 23 publications

References 29 publications

Insulin Sensitivity and Variability in Hepatitis C Virus Infection Using Direct Measurement

Insulin Sensitivity and Variability in Hepatitis C Virus Infection Using Direct Measurement

Serum hepcidin levels are related to the severity of liver histological lesions in chronic hepatitis C

Review article Insulin resistance and its consequences in chronic hepatitis C

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