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Insulin resistance, adipokine profile and hepatic expression of SOCS-3 gene in chronic hepatitis C.

ABSTRACT: AIM:To analyze adipokine concentrations, insulin resistance and hepatic expression of suppressor of cytokine signaling 3 (SOCS-3) in patients with chronic hepatitis C genotype 1 with normal body weight, glucose and lipid profile. METHODS:The study group consisted of 31 patients with chronic hepatitis C and 9 healthy subjects. Total levels of adiponectin, leptin, resistin, visfatin, omentin, osteopontin and insulin were measured using an ELISA kit. The hepatic expression of SOCS-3 was determined by the use of the reverse transcription polymerase chain reaction method. RESULTS:Homeostasis model assessment for insulin resistance (HOMA-IR) values were significantly higher in hepatitis C virus (HCV) infected patients without metabolic disorders compared to healthy controls (2.24 vs 0.59, P = 0.0003). Hepatic steatosis was observed in 32.2% of patients with HCV infection and was found in patients with increased HOMA-IR index (2.81 vs 1.99, P = 0.05) and reduced adiponectin level (5.96 vs 8.37, P = 0.04). Inflammatory activity (G ? 2) was related to increased osteopontin concentration (34.04 vs 23.35, P = 0.03). Advanced liver fibrosis (S ? 2) was associated with increased levels of omentin and osteopontin (436.94 vs 360.09, P = 0.03 and 32.84 vs 20.29, P = 0.03) and reduced resistin concentration (1.40 vs 1.74, P = 0.047). No correlations were reported between adipokine profile, HOMA-IR values and hepatic expression of the SOCS-3 gene. CONCLUSION:We speculated that no relationship between adipokines and HOMA-IR values may indicate that HCV can induce insulin resistance itself. Some adipokines appear to be biochemical markers of steatosis, inflammation and fibrosis in patients with chronic HCV infection. © 2014 Baishideng Publishing Group Inc. All rights reserved.

SUBMITTER: Wojcik K

PROVIDER: S-EPMC4130852 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Insulin resistance, adipokine profile and hepatic expression of SOCS-3 gene in chronic hepatitis C.

Wójcik Kamila K Jabłonowska Elżbieta E Omulecka Aleksandra A Piekarska Anna A

World journal of gastroenterology 20140801 30

<h4>Aim</h4>To analyze adipokine concentrations, insulin resistance and hepatic expression of suppressor of cytokine signaling 3 (SOCS-3) in patients with chronic hepatitis C genotype 1 with normal body weight, glucose and lipid profile.<h4>Methods</h4>The study group consisted of 31 patients with chronic hepatitis C and 9 healthy subjects. Total levels of adiponectin, leptin, resistin, visfatin, omentin, osteopontin and insulin were measured using an ELISA kit. The hepatic expression of SOCS-3 ...[more]

PMID: 25132761

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Project description:BackgroundInsulin resistance (IR) is a risk factor for ischaemic heart disease and myocardial infarction (MI). IR often manifests in MI and is regarded as an independent predictor of in-hospital mortality, which can provide early risk stratification for recurrent acute coronary events.MethodsThe study enrolled 200 patients (130 males and 70 females aged 61.4 ± 1.12 years) diagnosed with ST elevation MI. At days 1 and 12 from the MI onset, IR levels and lipid profiles, as well as serum glucose, insulin, adipokine and ghrelin levels, were measured.ResultsFree fatty acid (FFA) levels had the most pronounced changes: IR patients had a 9-fold increase in FFA levels at day 1, and patients without IR had a 6-fold increase. Leptin levels at days 1 and 12, in IR patients were, on average, 1.5- and 2-fold higher compared to the controls and patients with no IR (р < 0.05). Leptin levels in IR patients were increased throughout the entire hospital stay. Resistin levels in IR patients were, on average, 1.4-fold higher throughout the entire hospital stay, while in non-IR patients, resistin levels were similar to the controls. Adiponectin levels in IR patients were decreased compared to the controls, while in patients with IR, they were similar to the controls. Both IR and non-IR MI patients had 3-fold and 3.7-fold lower ghrelin levels at day 1, respectively, compared to the controls. The correlation analysis showed a negative correlation between ghrelin and FFA (r = -0.48 р = 0.007), ghrelin and leptin (r = -0.4 р = 0.003), ghrelin and insulin (r = -0.54 р = 0.002), and ghrelin and glucose (r = -0.31 р = 0.002) in MI patients.ConclusionDyslipidaemia, along with insulinaemia and glycaemia, is one of the most significant IR risk factors in the acute and early recovery phases of MI. Dyslipidaemia is characterised by a high FFA level; an imbalance of leptin, resistin, and adiponectin; and a deficiency of ghrelin in the acute and early recovery periods of MI. FFA and ghrelin can be used as promising molecular markers to stratify the risk of recurrent acute coronary events and diabetes mellitus in MI patients.

Project description:Prematurity and overfeeding in infants are associated with insulin resistance in childhood and may increase the risk of adult disease. Total parenteral nutrition (TPN) is a major source of infant nutritional support and may influence neonatal metabolic function. Our aim was to test the hypothesis that TPN induces increased adiposity and insulin resistance compared with enteral nutrition (EN) in neonatal pigs. Neonatal pigs were either fed enteral formula orally or i.v. administered a TPN mixture for 17 d; macronutrient intake was similar in both groups. During the 17-d period, we measured body composition by dual-energy X-ray absorptiometry scanning; fasting i.v. glucose tolerance tests (IVGTT) and hyperinsulinemic-euglycemic clamps (CLAMP) were performed to quantify insulin resistance. On d 17, tissue was collected after 1-h, low-dose CLAMP for tissue insulin signaling assays. TPN pigs gained less lean and more body fat and developed hepatic steatosis compared with EN pigs. After 7 and 13 d, IVGTT showed evidence of insulin resistance in the TPN compared with the EN group. Fasting plasma glucose and insulin also were higher in TPN pigs. CLAMP showed that insulin sensitivity was markedly lower in TPN pigs than in EN pigs. TPN also reduced the abundance of the insulin receptor, insulin receptor substrate 1, and phosphatidylinositol 3 kinase in skeletal muscle and liver and the proliferation of total pancreatic cells and ?-cells. Hepatic proinflammatory genes as well as c-Jun-N-terminal kinase 1 phosphorylation, plasma interleukin 6, and tumor necrosis factor-? were all higher in TPN pigs than in EN pigs. The results demonstrate that chronic TPN induces a hepatic inflammatory response that is associated with significant insulin resistance, hepatic steatosis, and fat deposition compared with EN in neonatal pigs. Further studies are warranted to establish the mechanism of TPN-induced insulin resistance and hepatic metabolic dysfunction and whether there are persistent metabolic consequences of this lifesaving form of infant nutritional support.

Dataset Information

Insulin resistance, adipokine profile and hepatic expression of SOCS-3 gene in chronic hepatitis C.

Publications

Insulin resistance, adipokine profile and hepatic expression of SOCS-3 gene in chronic hepatitis C.

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