Elevated serum tumor necrosis factor alpha and ferritin may contribute to the insulin resistance found in HCV positive Egyptian patients

Elsammak, Mohamed; Refai, Wael; Elsawaf, Amani; Abdelfattah, Ihab; Elatti, E. Abd; Ghazal, Abeer

doi:10.1185/030079905x38141

Cited by 30 publications

(22 citation statements)

References 35 publications

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“…However, in their study, these levels correlated to the degree of alanine transaminase elevation as a marker of hepatic injury, which does not agree with our results. In partial agreement with our results were those of El-Sammak et al, 14 in 2005, who reported significantly higher levels of TNF in patients with HCV infection HCV and those with HCV infection and diabetes compared with patients with diabetes alone and control subjects, without any significant difference between patients with HCV infection and those with HCV infection and diabetes. El-Zayadi et al 15 had demonstrated a significant difference between HCV-infected individuals and healthy blood donors within the Egyptian groups.…”

Section: Discussionsupporting

confidence: 94%

Evaluation of Serum Level of Tumor Necrosis Factor Receptor II in Hepatitis C Virus (Genotype 4)-Infected Middle-Aged Men with and without Diabetes and Its Complications in Egypt: A Pilot Study

Said

Husseiny

Mosaad

2011

Journal of Investigative Medicine

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BackgroundTumor necrosis factor α (TNF-α) is a type of cytokine produced by macrophages and other cell types in response to various stimuli. Many studies have shown that TNF-α is involved in the development of diabetes. It also has a pivotal role in the inflammatory process of chronic hepatitis C.ObjectivesThis study aimed to examine the hypothesis that TNF is increased in patients infected with hepatitis C virus (HCV) and with diabetes rather than in patients infected with HCV or with diabetes alone.MethodsPatients were divided into 5 groups: patients with diabetes without complications and without HCV infection (group 1), patients with diabetes and complications but without HCV infection (group 2), patients without diabetes but with HCV infection (group 3), patients with diabetes without complications but with HCV infection (group 4), and patients with diabetes and complications and with HCV infection (group 5).ResultsResults revealed an activation of the TNF axis in all tested patients when compared with the level of healthy Egyptians done in previous studies. However, although there was a gradual escalation in the activation of the TNF axis in these groups, the increase did not amount to a statistical difference between them (P > 0.05). However, the trend was toward the higher values in HCV infection with diabetes and its complications. The number of studied patients may be a limitation of this research. There was no correlation between the level of TNF receptor II and the levels of transaminases, albumin, and creatinine in the different groups or the degree of microalbuminuria in the groups of patients with diabetic complications. Also, there was no relation between the hepatic or splenic size and the level of TNF receptor II.ConclusionsThe presence of diabetes and its complications in patients with HCV infection could not be attributed only to the activation of the TNF system at least in Egyptian patients.

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Section: Discussionsupporting

confidence: 94%

Evaluation of Serum Level of Tumor Necrosis Factor Receptor II in Hepatitis C Virus (Genotype 4)-Infected Middle-Aged Men with and without Diabetes and Its Complications in Egypt: A Pilot Study

Said

Husseiny

Mosaad

2011

Journal of Investigative Medicine

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“…Elsammak et al 25 have demonstrated increased levels of serum TNF-α in 27 Egyptian patients with HCV infection, which showed significant positive correlation with the HCV RNA viral load. In addition, Talaat 26 has reported elevation of TNF-α levels in 82 patients with HCV infection (20 patients with mild cirrhosis, 20 patients with moderate cirrhosis, 20 patients with severe cirrhosis, and 22 patients with hepatocellular carcinoma) at different stages of disease.…”

Section: Discussionmentioning

confidence: 97%

RANTES, TNF-α, Oxidative Stress, and Hematological Abnormalities in Hepatitis C Virus Infection

Tawadrous

Aziz²,

Amin³

et al. 2012

Journal of Investigative Medicine

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“…Most importantly, we report the novel finding that C10 is effective at blocking palmitate and LPS-induced activation of IL6 and iNos-producing inflammatory pathways in both 3T3L1 adipocytes and RAW 264.7 macrophages without blocking insulin-stimulated AKT signaling, suggesting that C10 may be efficacious as a novel therapeutic agent for the treatment of obesity/inflammation-induced insulin resistance. Furthermore, since C10 inhibits LPS and palmitate induction of iNos expression in both adipocytes and macrophages, it might also be beneficial in correcting the stress-induced hyperglycemia observed in acute inflammatory processes such as infection/sepsis (Berstein 2005, De Souza et al 2005, Elsammak et al 2005. It is clear, however, that additional studies into the effects of C10 on FFA-induced insulin resistance (i.e.…”

Section: Discussionmentioning

confidence: 99%

Phenylmethimazole blocks palmitate-mediated induction of inflammatory cytokine pathways in 3T3L1 adipocytes and RAW 264.7 macrophages

McCall¹,

Holliday²,

Dickerson³

et al. 2010

Journal of Endocrinology

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Visceral adipocytes and associated macrophages produce and release excessive amounts of biologically active inflammatory cytokines via the portal and systemic vascular system, which induce insulin resistance in insulin target tissues such as fat, liver, and muscle. Free fatty acids (FFAs) absorbed via the portal system or released from adipocytes also induce insulin resistance. In this report, we show that phenylmethimazole (C10) blocks basal IL6 and leptin production as well as basal Socs-3 expression in fully differentiated 3T3L1 cells (3T3L1 adipocytes) without affecting insulin-stimulated AKT signaling. In addition, C10 inhibits palmitate-induced IL6 and iNos up-regulation in both 3T3L1 adipocytes and RAW 264.7 macrophages, LPS-induced NF-kB and IFN-b activation in 3T3L1 cells, and LPS-induced iNos, Ifn-b, Il1b, Cxcl10, and Il6 expression in RAW 264.7 macrophages. C10 also blocks palmitate-induced Socs-3 up-regulation and insulin receptor substrate-1 (IRS-1) serine 307 phosphorylation in 3T3L1 adipocytes. Additionally, we show for the first time that although palmitate increases IRS-1 serine 307 phosphorylation in 3T3L1 adipocytes, AKT serine 473 phosphorylation is enhanced, not reduced, by palmitate. These results suggest that through inhibition of FFA-mediated signaling in adipocytes and associated macrophages, as well as possibly other insulin target cells/tissues (i.e. non-immune cells), C10 might be efficacious to prevent or reverse cytokine-induced insulin resistance seen in obesity-related insulin resistance and type 2 diabetes mellitus.

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Elevated serum tumor necrosis factor alpha and ferritin may contribute to the insulin resistance found in HCV positive Egyptian patients

Abstract: Patients with HCV infection had a significantly higher level of TNFalpha and ferritin which may explain their insulin resistance. HOMA index and serum TNFalpha levels correlated positively with the HCV load.

Cited by 30 publications

References 35 publications

Evaluation of Serum Level of Tumor Necrosis Factor Receptor II in Hepatitis C Virus (Genotype 4)-Infected Middle-Aged Men with and without Diabetes and Its Complications in Egypt: A Pilot Study

Evaluation of Serum Level of Tumor Necrosis Factor Receptor II in Hepatitis C Virus (Genotype 4)-Infected Middle-Aged Men with and without Diabetes and Its Complications in Egypt: A Pilot Study

RANTES, TNF-α, Oxidative Stress, and Hematological Abnormalities in Hepatitis C Virus Infection

Phenylmethimazole blocks palmitate-mediated induction of inflammatory cytokine pathways in 3T3L1 adipocytes and RAW 264.7 macrophages

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