Insulin resistance in patients with cancer: relationships with tumor site, tumor stage, body-weight loss, acute-phase response, and energy expenditure

Yoshikawa, Takaki; Noguchi, Yoshikazu; Doi, Chiharu; Makino, Tatsuo; Nomura, K

doi:10.1016/s0899-9007(01)00561-5

Cited by 74 publications

(56 citation statements)

References 14 publications

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“…The role of resistin in pathogenesis of insulin resistance remains questionable, with conflicting data in animal models and negative findings in clinical observation [13,14] . The role of insulin resistance in cancer cachexia occurrence is not fully understood [1,2] . From this point of view, it came to mind whether resistin can have effect in gastric cancer cachexia occurrence.…”

Section: Resistin Ghrelin Leptin Adiponectin Igf-ⅰmentioning

confidence: 99%

“…These hormones are strongly anabolic and increase muscle protein synthesis [1,2] . IGF-Ⅰ concentrations increase with growth hormone and testosterone administration, thereby accounting for some of the effects of these hormones on muscle bulk and strength.…”

Section: Resistin Ghrelin Leptin Adiponectin Igf-ⅰmentioning

confidence: 99%

“…As major mediators of metabolism; growth hormone (GH) and insulin-like growth factor-Ⅰ (IGF-Ⅰ) have attracted many researchers in the field of cachexia associated gastrointestinal cancer [2,3] . Recent evidence suggests that an intricate interplay between multiple hypothalamic effector pathways and afferent hormonal signals of diverse systemic origin (resistin, leptin and adiponectin from adipocytes, ghrelin and polypeptides from the gastrointestinal tract, and insulin from the pancreas) is important in the regulation of energy intake and expenditure [4] .…”

Section: Introductionmentioning

confidence: 99%

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Adipokines and ghrelin in gastric cancer cachexia

Kerem

Ferahköşe²,

Yılmaz³

et al. 2008

WJG

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AIM:To investigate the roles of the adipocytokines, ghrelin and leptin in gastric cancer cachexia. METHODS: Resistin, ghrelin, leptin, adiponectin, insulin and insulin-like growth factor (IGF-Ⅰ), were measured in 30 healthy subjects, and 60 gastric cancer patients of which 30 suffered from cancerinduced cachexia and 30 served as a control group. The relationships between hormones, body mass index (BMI) loss ratio, age, gender, and Glasgow Prognostic Score (GPS) were investigated. RESULTS: Cachexia patients had higher tumor stage and GPS when compared with non-cachexia patients (P < 0.05). Ghrelin, resistin, leptin, adiponectin and IGF-Ⅰ, showed a significant correlation with BMI loss ratio and GPS (P < 0.05). A strong correlation was seen between GPS and BMI loss (R = -0.570, P < 0.0001). Multivariate analysis indicated that BMI loss was significantly independent as a predictor of ghrelin, resistin, leptin and IGF-Ⅰ (P < 0.05). Existence of an important significant relationship between resistin and insulin resistance was also noted. CONCLUSION: These results showed that serum ghrelin, leptin, adiponectin, and IGF-Ⅰ play important roles in cachexia-related gastric cancers. No relationship was found between resistin and cancer cachexia. Also, because of the correlation between these parameters and GPS, these parameters might be used as a predictor factor.

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Section: Resistin Ghrelin Leptin Adiponectin Igf-ⅰmentioning

confidence: 99%

Section: Resistin Ghrelin Leptin Adiponectin Igf-ⅰmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Adipokines and ghrelin in gastric cancer cachexia

Kerem

Ferahköşe²,

Yılmaz³

et al. 2008

WJG

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“…Normally, insulin binds to its receptor to initiate signal transduction. Insulin resistance (IR) can be induced by any of the following events: reduction in the number and affinity of insulin receptors, mutations of encoding genes, downregulation of the glucose transporter, and defects in insulin signal transduction (Yoshikawa et al, 2001;Wilcox, 2005;Draznin, 2006;Leclercq et al, 2007). IR refers to a decrease in the sensitivity of the whole organism, organs, tissues, or cells to insulin stimulation.…”

Section: Introductionmentioning

confidence: 99%

Insulin Resistance Reduces Sensitivity to Cis-Platinum and Promotes Adhesion, Migration and Invasion in HepG2 Cells

Li²,

Wei³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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The liver is normally the major site of glucose metabolism in intact organisms and the most important target organ for the action of insulin. It has been widely accepted that insulin resistance (IR) is closely associated with postoperative recurrence of hepatocellular carcinoma (HCC). However, the relationship between IR and drug resistance in liver cancer cells is unclear. In the present study, IR was induced in HepG2 cells via incubation with a high concentration of insulin. Once the insulin-resistant cell line was established, the stability of HepG2/ IR cells was further tested via incubation in insulin-free medium for another 72h. Afterwards, the biological effects of insulin resistance on adhesion, migration, invasion and sensitivity to cis-platinum (DDP) of cells were determined. The results indicated that glucose consumption was reduced in insulin-resistant cells. In addition, the expression of the insulin receptor and glucose transportor-2 was downregulated. Furthermore, HepG2/IR cells displayed markedly enhanced adhesion, migration, and invasion. Most importantly, these cells exhibited a lower sensitivity to DDP. By contrast, HepG2/IR cells exhibited decreased adhesion and invasion after treatment with the insulin sensitizer pioglitazone hydrochloride. The results suggest that IR is closely related to drug resistance as well as adhesion, migration, and invasion in HepG2 cells. These findings may help explain the clinical observation of limited efficacy for chemotherapy on a background of IR, which promotes the invasion and migration of cancer cells.

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“…However, although defects in anabolism may encourage and maintain this deleterious state of catabolism, few studies have addressed the relationship between the systemic inflammatory response and anabolic mediators of metabolism in patients with advanced cancer [15][16][17] . The insulin-like growth factor-1 (IGF-1) axis is an important regulator of anabolism, which may be deregulated in advanced cancer 15,18 .…”

Section: Introductionmentioning

confidence: 99%

The relationship between the insulin-like growth factor-1 axis, weight loss, an inflammation-based score and survival in patients with inoperable non-small cell lung cancer

et al. 2010

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Methods: 56 patients with inoperable NSCLC were studied. The plasma concentrations of IGF-1, IGFBP-3 and leptin were measured using ELISA and RIA. Results:The patients were predominantly male (61%), over 60 years old (80%), with advanced (stage III or IV) disease (98%), with a BMI >20 (84%), an ECOG-ps of 0 or 1 (79%), a haemoglobin (59%) and white cell count (79%) in the reference range. On followup 43 patients died of their cancer. On univariate analysis, BMI (p<0.05), Stage (p<0.05), ECOG-ps (p<0.05), haemoglobin (p<0.05), white cell count (p<0.05) and mGPS (p<0.05)were associated with cancer specific survival. There was no association between age, sex, treatment, IGF-1, IGFBP-3, IGF-1:IGFBP-3 ratio, or leptin and cancer specific survival.With an increasing mGPS concentrations of haemoglobin (p<0.005) and decreased. mGPS was not associated with either IGF-1(p>0.20), or leptin (p>0.20). Conclusions:In summary, the results of this study suggest that anabolism (IGF-1 axis) does not play a significant role in the relationship between nutritional and functional decline, systemic inflammation and poor survival in patients with inoperable NSCLC.

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Insulin resistance in patients with cancer: relationships with tumor site, tumor stage, body-weight loss, acute-phase response, and energy expenditure

Cited by 74 publications

References 14 publications

Adipokines and ghrelin in gastric cancer cachexia

Adipokines and ghrelin in gastric cancer cachexia

Insulin Resistance Reduces Sensitivity to Cis-Platinum and Promotes Adhesion, Migration and Invasion in HepG2 Cells

The relationship between the insulin-like growth factor-1 axis, weight loss, an inflammation-based score and survival in patients with inoperable non-small cell lung cancer

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