Serum insulin level, HOMA-IR and prostate cancer risk: A systematic review and meta-analysis

Saboori, Somayeh; Rad, Esmaeil Yousefi; Birjandi, Mehdi; Mohiti, Sara; Falahi, Ebrahim

doi:10.1016/j.dsx.2018.08.031

Cited by 23 publications

(16 citation statements)

References 31 publications

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“…In spite of the prevalence of obesity and its privileged place in public health discourse, the metabolic and molecular mechanisms underpinning the relationship between obesity and cancer remain contentious. Hyperinsulinemia has emerged as a focal point of research on obesity-related tumors, with increased plasma insulin concentrations independently predicting increased risk and mortality in prostate [1, 2], colon [3–7], breast [8–13], endometrial [12, 14, 15], and pancreatic cancer [16, 17], as well as several other tumor types. The idea that hyperinsulinemia may promote cancer risk is bolstered by the fact that biguanides such as metformin and phenformin, the most commonly prescribed class of diabetes drug worldwide, slow tumor growth associated with reductions in plasma insulin concentrations [18–30], although this class of agents has also shown efficacy in vivo independent of changes in plasma insulin concentrations in a minority of studies [31–33].…”

Section: Introductionmentioning

confidence: 99%

Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation

et al. 2019

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Obesity is associated with increased incidence and worse prognosis of more than one dozen tumor types; however, the molecular mechanisms for this association remain under debate. We hypothesized that insulin, which is elevated in obesity-driven insulin resistance, would increase tumor glucose oxidation in obesity-associated tumors. To test this hypothesis, we applied and validated a stable isotope method to measure the ratio of pyruvate dehydrogenase flux to citrate synthase flux (V PDH /V CS , i.e. the percent of total mitochondrial oxidation fueled by glucose) in tumor cells. Using this method, we found that three tumor cell lines associated with obesity (colon cancer [MC38], breast cancer [4T1], and prostate cancer [TRAMP-C3] cells) increase V PDH /V CS in response to physiologic concentrations of insulin. In contrast, three tumor cell lines that are not associated with obesity (melanoma [YUMM1.7], B cell lymphoma [BCL1 clone 5B1b], and small cell lung cancer [NCI-H69] cells) exhibited no oxidative response to insulin. The observed increase in glucose oxidation in response to insulin correlated with a dose-dependent increase in cell division in obesity-associated tumor cell lines when grown in insulin, whereas no alteration in cell division was seen in tumor types not associated with obesity. These data reveal that a shift in substrate preference in the setting of physiologic insulin may comprise a metabolic signature of obesity-associated tumors that differs from that of those not associated with obesity.

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Section: Introductionmentioning

confidence: 99%

Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation

et al. 2019

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“…In other hand, in ammatory markers such as TNF-α can cause insulin resistance in visceral tissues through activating c-Jun N-terminal kinase 1 and 2 (JNK1/2) [36]. Epidemiological studies have shown that insulin resistance could increase the risk of cardiovascular diseases [37,38] and also it is related to increased incidence of some neoplasms including breast, colorectal and prostate cancers [39,40]. PCOS is a low grade in ammatory disease and pro-in ammatory markers including interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) are increases in these patients which can induce hyperandrogenism seen in the PCOS patients [41,42].…”

Section: Discussionmentioning

confidence: 99%

Association of Dietary Inflammatory Index (DII) With the Risk of Poly Cystic Ovary Syndrome: a Case-control Study

Kavei

Rad

Akbari

et al. 2021

Preprint

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Objective: The aim of this case-control study was to investigate the association between Dietary Inflammatory Index (DII) and PCOS risk in the 120 newly-diagnosed cases of PCOS and 120 healthy controls aged between 18-45 years in Khorramabad of Iran. Results: Energy intake was significantly more in PCOS patients (p=0.01) and these people were less active than control women (p=0.001). The mean ± SD of DII in PCOS patients was 0.4±2.09 while it was 0.45±1.92 in control group (p=0.001). There was a positive association between increasing DII score and the risk of PCOS with the OR of 2.41(1.15, 5.02) in the crude model when we compared the fourth quartile with the lowest one. This association was still significant in several models after adjusting for age and energy intake in the model 1 (P- value for trend=0.001), in the second model and after adjusting for the level of activity, education, and family history of PCOS along with the first model (P- value for trend 0.003), and finally after additional adjustment for BMI in model 3 (P- value for trend 0.003). Results of present study showed that consuming more pro-inflammatory diets with higher DII scores are associated with increased risk of PCOS.

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“…Meta-analysis performed on a total of 1143 men in the prostate cancer group and 1692 men in the control group has shown that patients with prostate cancer had insulin level significantly higher in comparison with the control group. Sub-group analysis has pointed out that this correlation takes place only in older patients (>65 years old) [ 52 ]. In a prospective study examining 310 patients (54 of them died because of PC during 5-years follow-up), hyperinsulinemia and T2DM have been shown to have a statistically significant correlation with lethal prostate cancer [ 53 ].…”

Section: Insulinmentioning

confidence: 99%

The Influence of Anti-Diabetic Drugs on Prostate Cancer

Knura

Garczorz

Borek

et al. 2021

Cancers

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The incidences of prostate cancer (PC) and diabetes are increasing, with a sustained trend. The occurrence of PC and type 2 diabetes mellitus (T2DM) is growing with aging. The correlation between PC occurrence and diabetes is noteworthy, as T2DM is correlated with a reduced risk of incidence of prostate cancer. Despite this reduction, diabetes mellitus increases the mortality in many cancer types, including prostate cancer. The treatment of T2DM is based on lifestyle changes and pharmacological management. Current available drugs, except insulin, are aimed at increasing insulin secretion (sulfonylureas, incretin drugs), improving insulin sensitivity (biguanides, thiazolidinediones), or increasing urinary glucose excretion (gliflozin). Comorbidities should be taken into consideration during the treatment of T2DM. This review describes currently known information about the mechanism and impact of commonly used antidiabetic drugs on the incidence and progression of PC. Outcomes of pre-clinical studies are briefly presented and their correlations with available clinical trials have also been observed. Available reports and meta-analyses demonstrate that most anti-diabetic drugs do not increase the risk during the treatment of patients with PC. However, some reports show a potential advantage of treatment of T2DM with specific drugs. Based on clinical reports, use of metformin should be considered as a therapeutic option. Moreover, anticancer properties of metformin were augmented while combined with GLP-1 analogs.

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Serum insulin level, HOMA-IR and prostate cancer risk: A systematic review and meta-analysis

Cited by 23 publications

References 31 publications

Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation

Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation

Association of Dietary Inflammatory Index (DII) With the Risk of Poly Cystic Ovary Syndrome: a Case-control Study

The Influence of Anti-Diabetic Drugs on Prostate Cancer

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