Metabolic Response to Infection

Beisel, William R.

doi:10.1146/annurev.me.26.020175.000301

Cited by 281 publications

(122 citation statements)

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“…23,24 Our findings, that reduced HDL level was positively associated with hepatitis C infection and inversely associated with hepatitis B infection (albeit nonsignificantly), have two possible explanations. First, this may be due to proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor (TNF) that are well documented to be positively associated with MS. By relating blood profiles to circulating cytokines in patients with chronic viral hepatitis due to HBV or HCV infection, Fabris et al 25 found that the differences between HBV and HCV in terms of the mechanism of liver damage and viral clearance manifested by the levels of circulating cytokines were related to differences in blood lipids profiles such as HDL.…”

Section: Dyslipidaemiamentioning

confidence: 73%

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

et al. 2006

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Objectives: We aimed to assess the association between metabolic syndrome (MS) and hepatitis B/C virus infection using a large population-based study. Design and methods: A population-based cross-sectional study design was adopted with a total of 53 528 subjects being enrolled from the integrated multiple diseases screening program in Keelung, Taiwan. Evidence of past hepatitis B/C infection, acquired during childhood or as a young adult, was identified during the two-stage liver cancer screening part of the process. Information on biochemical markers and anthropometric measures related to MS, such as fasting blood sugar, triglyceride and high-density lipoprotein (HDL), abdominal circumference and blood pressure (BP), were collected routinely while screening for hypertension, type 2 diabetes, and hyperlipidemia. Logistic regression was used to estimate odds ratios and related 95% confidence intervals for the associations between MS and hepatitis B/C infection. Results: High blood pressure (SBPX135 mmHg or DBPX85 mmHg) (adjusted odd ratio: 0.89 (0.83-0.94)) and high triglyceride (X150 mg/dl) (adjusted odds ratio: 0.65 (0.60-0.69)) were, after adjusting for gender and age, inversely associated with being HBsAg positive (Po0.05). The likelihood of developing MS was lower in the HBsAg positive than the HBsAg negative (adjusted odds ratio: 0.84 (0.76-0.93)). A positive association between being anti-HCV positive and having low serum HDL (male o40 mg/dl, female o50 mg/dl) was also noted (adjusted odds ratio: 1.61 (1.37-1.88) after controlling for gender and age). High triglyceride was inversely associated with being anti-HCV positive (adjusted odds ratio: 0.63 (0.55-0.71). Conclusions: There is an inverse association between MS and hepatitis B virus infection whereas the association was heterogeneous for HCV infection with a positive association with abnormal serum HDL but an inverse association with hypertriglyceridemia.

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Section: Dyslipidaemiamentioning

confidence: 73%

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

et al. 2006

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“…In evaluating the significance of these observations to the systemic actions of TNF, it is useful to consider the integrative role that TNF plays in promoting the acute-phase response (53) to infections and invasive stimuli, such as cancers. During the acute-phase response accelerated net breakdown of skeletal muscle and fat occurs with a concomitant shift to anabolic metabolism in the liver, to support the synthesis of acute-phase reactant proteins, as well as to bone marrow and wounds, for cellular proliferation within the immune system and for healing of injured tissue (53)(54)(55)(56)(57)(58)(59). These metabolic alterations represent a reprioritization of carbon and energy utilization in the injured or septic animal for survival.…”

Section: Discussionmentioning

confidence: 99%

A phosphatidylinositol 3-kinase/Akt/mTOR pathway mediates and PTEN antagonizes tumor necrosis factor inhibition of insulin signaling through insulin receptor substrate-1

Özeş

Akça

Mayo

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

357

270

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Tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) by the insulin receptor permits this docking protein to interact with signaling proteins that promote insulin action. Serine phosphorylation uncouples IRS-1 from the insulin receptor, thereby inhibiting its tyrosine phosphorylation and insulin signaling. For this reason, there is great interest in identifying serine͞threonine kinases for which IRS-1 is a substrate. Tumor necrosis factor (TNF) inhibited insulin-promoted tyrosine phosphorylation of IRS-1 and activated the Akt͞protein kinase B serine-threonine kinase, a downstream target for phosphatidylinositol 3-kinase (PI 3-kinase). The effect of TNF on insulin-promoted tyrosine phosphorylation of IRS-1 was blocked by inhibition of PI 3-kinase and the PTEN tumor suppessor, which dephosphorylates the lipids that mediate PI 3-kinase functions, whereas constitutively active Akt impaired insulin-promoted IRS-1 tyrosine phosphorylation. Conversely, TNF inhibition of IRS-1 tyrosine phosphorylation was blocked by kinase dead Akt. Inhibition of IRS-1 tyrosine phosphorylation by TNF was blocked by rapamycin, an inhibitor of the mammalian target of rapamycin (mTOR), a downstream target of Akt. mTOR induced the serine phosphorylation of IRS-1 (Ser-636͞639), and such phosphorylation was inhibited by rapamycin. These results suggest that TNF impairs insulin signaling through IRS-1 by activation of a PI 3-kinase͞Akt͞ mTOR pathway, which is antagonized by PTEN.

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“…One of the biochemical derangements that frequently is noted in infected m a m m a l s is a decrease in the ability of insulin to promote glucose uptake and to stimulate anabolic processes (1,2). A compensatory hyperinsulinemia results.…”

mentioning

confidence: 99%

Studies of insulin resistance in adipocytes induced by macrophage mediator.

Pekala¹,

Kawakami²,

Vine³

et al. 1983

The Journal of Experimental Medicine

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An apparent insulin resistance is noted in 3T3-L1 adipocytes after the addition of an endotoxin-induced mediator from macrophages. Examination at the level of the insulin receptor has revealed that the mediator does not effect either the functional ability of the cells to bind insulin or the ability of insulin to stimulate the uptake of glucose. The resistance appears to reflect a post-receptor interference with the insulin-induced biosynthesis of the anabolic enzymes, acetyl Co-A carboxylase and fatty acid synthetase, which are required for the conversion of glucose into storage lipid. These studies offer a new in vitro model for investigating the molecular basis of insulin resistance.

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Metabolic Response to Infection

Cited by 281 publications

References 0 publications

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

A phosphatidylinositol 3-kinase/Akt/mTOR pathway mediates and PTEN antagonizes tumor necrosis factor inhibition of insulin signaling through insulin receptor substrate-1

Studies of insulin resistance in adipocytes induced by macrophage mediator.

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