Association between fasting serum glucose levels and incidence of colorectal cancer in Korean men: The Korean Cancer Prevention Study-II

Kim, Yeon Jung; Linton, John A.

doi:10.1016/j.metabol.2014.07.006

Cited by 40 publications

(34 citation statements)

References 33 publications

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“…This finding was consistent with those of several previous studies [2,8], although the specific classification and study designs differed between the studies. In the Framingham Heart Study offspring cohort, the incidence of CRC was found to be higher in subjects with IFG.…”

Section: Hyperglycemiasupporting

confidence: 93%

“…Of these individuals, 159,844 provided informed consent and were followed prospectively, forming the cohort of participants in the Korean Cancer Prevention Study-II (KCPS-II). A full description of KCPS-II has been previously published [2]. Of the 159,844 participants, 156,836 donated a blood specimen for genetic studies.…”

Section: Study Subjectsmentioning

confidence: 99%

“…In Korea, the standardized incidence of CRC has increased from 21.2/100,000 people in 1999 to 57.6/ 100,000 people in 2012 [1]. A steady increase in the incidence of CRC is expected in the future, partly as a result of factors such as the increase in Western dietary patterns, the increase in diabetes [2], and interaction between these factors and genetic factors [3]. In particular, an association with several common single-nucleotide polymorphisms (SNPs) has been reported, with high replicability.…”

Section: Introductionmentioning

confidence: 99%

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Impaired fasting glucose, single-nucleotide polymorphisms, and risk for colorectal cancer in Koreans

2016

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OBJECTIVES:Numerous studies have demonstrated that fasting serum glucose (FSG) levels and certain single-nucleotide polymorphisms (SNPs) are related to an increased risk of colorectal cancer (CRC); however, their combined effects are still unclear. METHODS:Of a total of 144,527 men and women free of cancer at baseline, 317 developed CRC during 5.3 years of follow-up. A case-cohort study (n = 1,691) was used, consisting of participants with a DNA sample available. Three well-known SNPs (rs3802842, rs6983267, rs10795668) were genotyped. Hazard ratios (HR) and 95% confidence intervals (CI) of CRC, colon and rectal cancer were calculated, with the Cox proportional hazard models. RESULTS:The crude incidence rates per 100,000 person-years were 41.1 overall, 48.4 for men, and 29.3 for women. Among participants with dysglycemia, SNPs rs3802842 and rs6983267 were both associated with an increased risk of CRC (HR, 3.2; 95% CI, 1.9 to 5.5 and HR, 1.8; 95% CI, 1.1 to 3.1, respectively) and rectal cancer (HR, 3.4; 95% CI, 1.8 to 6.6 and HR, 3.3; 95% CI, 1.6 to 7.1, respectively). The interaction effect of dysglycemia and SNPs was positive, that is, resulted in an elevated risk of CRC, but was not statistically significant. CONCLUSIONS:This study demonstrates that both high FSG and certain SNPs are major risk factors for CRC and rectal cancer but that they did not interact synergistically. The difference in effect size of the SNPs according to CRC subtype (i.e., colon or rectal cancer) and presence of dysglycemia merits further research.

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Section: Hyperglycemiasupporting

confidence: 93%

Section: Study Subjectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impaired fasting glucose, single-nucleotide polymorphisms, and risk for colorectal cancer in Koreans

2016

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“…Therefore, the autocrine/paracrine produced IGF-2 will have a strong mitogenic effect on the tumor (c) IR-A hemireceptors form hybrid receptors with IGF-1R hemireceptors These hybrids stimulate cell growth not only in response to IGF-1, but also in response to IGF-2 and insulin endometrium, and stomach/colorectum cancers [56][57][58]. The duration of IFG exposure (>10 years) may be important to increase the cancer risk [58,59].…”

Section: Therefore Malignant Cells Are Overstimulated By Insulin In Cmentioning

confidence: 99%

Insulin, insulin receptors, and cancer

Vigneri

Goldfine

Frittitta

2016

J Endocrinol Invest

179

147

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Insulin is a major regulator of cell metabolism but, in addition, is also a growth factor. Insulin effects in target cells are mediated by the insulin receptor (IR), a transmembrane protein with enzymatic (tyrosine kinase) activity. The insulin receptor, however, is represented by a heterogeneous family of proteins, including two different IR isoforms and also hybrid receptors resulting from the IR hemireceptor combination with a hemireceptor of the cognate IGF-1 receptor. These different receptors may bind insulin and its analogs with different affinity and produce different biologic effects. Since many years, it is known that many cancer cells require insulin for optimal in vitro growth. Recent data indicate that: (1) insulin stimulates growth mainly via its own receptor and not the IGF-1 receptor; (2) in many cancer cells, the IR is overexpressed and the A isoform, which has a predominant mitogenic effect, is more represented than the B isoform. These characteristics provide a selective growth advantage to malignant cells when exposed to insulin. For this reason, all conditions of hyperinsulinemia, both endogenous (prediabetes, metabolic syndrome, obesity, type 2 diabetes before pancreas exhaustion and polycystic ovary syndrome) and exogenous (type 1 diabetes) will increase the risk of cancer. Cancer-related mortality is also increased in patients exposed to hyperinsulinemia but other factors, related to the different diseases, may also contribute. The complexity of the diseases associated with hyperinsulinemia and their therapies does not allow a precise evaluation of the cancer-promoting effect of hyperinsulinemia, but its detrimental effect on cancer incidence and mortality is well documented.

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“…Hyperglycemia is one of the most direct internal environmental alterations in patients with T2DM (5,6). It has previously been demonstrated that hyperglycemia is a key factor in the mechanisms underlying diabetes-associated increased cancer risk (7). Furthermore, hyperglycemia activates numerous pathways to promote the progression of cancer; for example, it increases the levels of insulin-like growth factor 1 (IGF1), upregulates protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling and enhances WNT/β-catenin signaling (8).…”

Section: Introductionmentioning

confidence: 99%

Effects of β-caryophyllene on arginine ADP-ribosyltransferase 1-mediated regulation of glycolysis in colorectal cancer under high-glucose conditions

et al. 2018

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Type 2 diabetes mellitus (T2DM) is associated with an increased risk of the development of colorectal cancer (CRC). A previous study revealed that the levels of arginine-specific mono-ADP-ribosyltransferase 1 (ART1) in CRC tissues from patients with T2DM were higher than in non-diabetic patients. Hyperglycemia, which is a risk factor of cancer, is a common feature of T2DM; however, the effects of ART1 on glycolysis and energy metabolism in CRC cells under high-glucose conditions remains to be elucidated. β-caryophyllene (BCP) has been reported to exert anticancer and hypoglycemic effects. In the present study, CT26 cells were cultured under a high-glucose conditions and the expression levels of relevant factors were detected by western blotting. Cell Counting Kit-8 assay, ﬂow cytometry, Hoechst 33258 staining, ATP assay and lactic acid assay were used to detect the proliferation, apoptosis and energy metabolism of CT26 cells. To observe the effects of ART1 and BCP on tumor growth in vivo, CT26 cell tumors were successfully transplanted into BALB/c mice with T2DM. The results demonstrated that overexpression of ART1 may increase glycolysis and energy metabolism in CT26 CRC cells under high glucose conditions by regulating the protein kinase B/mammalian target of rapamycin/c‑Myc signaling pathway and the expression of glycolytic enzymes. BCP inhibited the effects induced by ART1, which may be due to a BCP-induced reduction in the expression levels of ART1 via nuclear factor-κB. Therefore, ART1 may be considered a therapeutic target for the treatment of diabetic patients with CRC.

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Association between fasting serum glucose levels and incidence of colorectal cancer in Korean men: The Korean Cancer Prevention Study-II

Cited by 40 publications

References 33 publications

Impaired fasting glucose, single-nucleotide polymorphisms, and risk for colorectal cancer in Koreans

Impaired fasting glucose, single-nucleotide polymorphisms, and risk for colorectal cancer in Koreans

Insulin, insulin receptors, and cancer

Effects of β-caryophyllene on arginine ADP-ribosyltransferase 1-mediated regulation of glycolysis in colorectal cancer under high-glucose conditions

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