Diet‐induced adiposity alters the serum profile of inflammation in C57BL/6N mice as measured by antibody array

Fenton, Jenifer I.; Núñez, Nomelí P.; Yakar, Shoshana; Perkins, Susan N.; Hord, Norman G.; Hursting, Stephen D.

doi:10.1111/j.1463-1326.2008.00974.x

Cited by 74 publications

(77 citation statements)

References 39 publications

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“…Immune response alterations and carcinogenesis ILP molecules have been reported to play a crucial role in altered inflammatory responses to infectious challenge commonly observed in insulin resistance-related metabolic disorders (Fenton et al 2009, Bitar & Al-Mulla 2012.…”

Section: Insulin Resistance Immune Response Alterations and Cancer:mentioning

confidence: 99%

Insulin resistance and cancer: the role of insulin and IGFs

Djiogue¹,

Kamdje²,

Vecchio³

et al. 2012

Endocrine-Related Cancer

223

188

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Insulin, IGF1, and IGF2 are the most studied insulin-like peptides (ILPs). These are evolutionary conserved factors well known as key regulators of energy metabolism and growth, with crucial roles in insulin resistance-related metabolic disorders such as obesity, diseases like type 2 diabetes mellitus, as well as associated immune deregulations. A growing body of evidence suggests that insulin and IGF1 receptors mediate their effects on regulating cell proliferation, differentiation, apoptosis, glucose transport, and energy metabolism by signaling downstream through insulin receptor substrate molecules and thus play a pivotal role in cell fate determination. Despite the emerging evidence from epidemiological studies on the possible relationship between insulin resistance and cancer, our understanding on the cellular and molecular mechanisms that might account for this relationship remains incompletely understood. The involvement of IGFs in carcinogenesis is attributed to their role in linking high energy intake, increased cell proliferation, and suppression of apoptosis to cancer risks, which has been proposed as the key mechanism bridging insulin resistance and cancer. The present review summarizes and discusses evidence highlighting recent advances in our understanding on the role of ILPs as the link between insulin resistance and cancer and between immune deregulation and cancer in obesity, as well as those areas where there remains a paucity of data. It is anticipated that issues discussed in this paper will also recover new therapeutic targets that can assist in diagnostic screening and novel approaches to controlling tumor development.

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Section: Insulin Resistance Immune Response Alterations and Cancer:mentioning

confidence: 99%

Insulin resistance and cancer: the role of insulin and IGFs

Djiogue¹,

Kamdje²,

Vecchio³

et al. 2012

Endocrine-Related Cancer

223

188

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“…5,6 Similar to obese men, obese mice fed a high fat diet also results in increased adiposity, circulating growth factors and inflammation when compared with control mice and may contribute to prostate cancer progression. [7][8][9][10] Studies suggest that cancer cells undergo an epithelialmesenchymal-transition (EMT) program at the initiation of invasion, which is a critical process for metastasis. 11,12 Hallmarks of EMT include loss or decreased protein expression of e-cadherin, increased vimentin and deregulation of b-catenin.…”

Section: Introductionmentioning

confidence: 99%

Obesity-related systemic factors promote an invasive phenotype in prostate cancer cells

Price

Cavazos

Angel

et al. 2012

Prostate Cancer Prostatic Dis

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BACKGROUND: Obesity is associated with larger tumors, shorter time to PSA failure, and higher Gleason scores. However, the mechanism(s) by which obesity promotes aggressive prostate cancer remains unknown. We hypothesize that circulating factors related to obesity promote prostate cancer progression by modulating components of the metastatic cascade.METHODS: Male C57BL/6 mice (6 weeks) were fed an ad libitum diet-induced obesity (60% fat) or control diet (10% fat) for 12 weeks. Serum was collected, metabolic and inflammatory proteins were measured by an antibody array. Sera were used to measure, in vitro, characteristics of a metastatic phenotype. RESULTS:Comparable to obese men, obese sera contained higher levels or leptin, vascular endothelial growth factor, PAI-1, interleukin-6 (IL-6) and lower levels of testosterone. In prostate cells, serum was used to assess: proliferation, invasion, migration, epithelial-mesenchymal-transition (EMT) and matrix metalloproteinase (MMP) activity. LNCaP and PacMetUT1 cells exposed to obese sera increased proliferation, whereas PrEC and DU145 were unaffected. LNCaP, PacMetUT1 and DU145 cancer cells exposed to obese sera resulted in increased invasion, migration and MMP-9 activity. Prostate cancer cells exposed to obese sera showed increased vimentin, dispersion of e-cadherin and b-catenin from the plasma membrane. CONCLUSION:We report, prostate cancer cells exposed to sera from obese mice increases proliferation, invasion, migration, MMP activity and induces changes in proteins critical for EMT.

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“…Th1 immune responses are also related to food intake. Furthermore, Fenton et al (2009) reported that Il12 concentration is closely associated with nutritional status in C57BL/6N mice. Reiss et al (1996) also showed that Il12 up-regulates the production of NO in the CNS.…”

Section: Discussionmentioning

confidence: 99%

“…Interleukin 12 (Il12)-mediated functions are impaired in Stat4 KO mice Thierfelder et al, 1996). Il12 concentration in blood significantly increases in 30% calorie-restricted animal relative to control (Fenton et al, 2009). It is also known that Il12 activates macrophages and up-regulates nitric oxide (NO) production in response to infection (Reiss et al, 1996).…”

Section: Introductionmentioning

confidence: 99%