Type 2 Diabetes Prevention Diet and Hepatocellular Carcinoma Risk in US Men and Women

Luo, Xiao; Sui, Jing; Yang, Wanshui; Sun, Qi; Ma, Yanan; Simon, Tracey G.; Liang, Geyu; Meyerhardt, Jeffrey A.; Chan, Andrew T.; Giovannucci, Edward; Zhang, Xuehong

doi:10.14309/ajg.0000000000000450

Cited by 40 publications

(35 citation statements)

References 63 publications

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“…This is the first study in which the DRRD was examined in association with endometrial cancer. An inverse association of the DRRD with breast cancer [ 39 , 40 ], pancreatic cancer [ 41 ], and hepatocellular carcinoma [ 38 ] has previously been observed.…”

Section: Discussionmentioning

confidence: 99%

“…The original version of the DRRD was characterized by high intakes of cereal fiber, coffee and nuts, high polyunsaturated:saturated fats ratio, low glycemic index (GI), and low intakes of red and processed meat, sugar-sweetened beverages, and trans fats. Higher adherence to the original DRRD was found to decrease the risk of hepatocellular carcinoma [ 38 ]. More recently, a new version of the DRRD was developed, where fruit was added as a favorable component and fruit juices were included in the sugar-sweetened beverage unfavorable component.…”

Section: Introductionmentioning

confidence: 99%

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Diabetes Risk Reduction Diet and Endometrial Cancer Risk

et al. 2021

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Diabetes increases endometrial cancer risk. We investigated the role of a diabetes risk reduction diet (DRRD) on the risk of endometrial cancer using data from a multicentric, Italian hospital-based case–control study (1992–2006) enrolling 454 histologically confirmed cases of endometrial cancer and 908 controls matched by age and center. We derived a DRRD score assigning higher scores for higher intakes of cereal fiber, fruit, coffee, polyunsaturated:saturated fatty acid ratio, and nuts and for lower glycemic load and lower intakes of red/processed meat and sugar-sweetened beverages/fruit juices. The odds ratios (OR) of endometrial cancer according to the DRRD score were derived by multiple conditional logistic regression models. The OR for high (DRRD score >24, i.e., third tertile) versus medium–low adherence to the DRRD was 0.73 (95% confidence interval, CI, 0.55–0.97). Similar results were observed after the exclusion of diabetic women (OR 0.75; 95% CI, 0.56–1.00) and allowance for total vegetable consumption (OR 0.80; 95% CI, 0.60–1.07). Inverse associations were observed in most of the analyzed subgroups. The OR for high DRRD combined with high vegetable consumption was 0.45 (95% CI, 0.28–0.73). Our results suggest that diets able to reduce diabetes risk may also reduce endometrial cancer risk. High vegetable consumption combined with high adherence to the DRRD may provide additional benefit in endometrial cancer prevention.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Diabetes Risk Reduction Diet and Endometrial Cancer Risk

et al. 2021

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“…2,4 In recent years, there are abundant evidences showing that diabetes mellitus (DM) is a confirmed risk factor for HCC and diabetic patients have a higher incidence of HCC. 5,6 According to the 8th IDF Atlas, 425 million people have suffered from diabetes in 2007 and the number will rise to 629 million by 2045. 7 Metformin (1,1-dimethylbiguanide hydrochloride), a biguanide derivative, is one of the most used first-line anti-hyperglycemic drugs for type 2 DM.…”

Section: Introductionmentioning

confidence: 99%

<p>Metformin Induces Autophagy via the AMPK-mTOR Signaling Pathway in Human Hepatocellular Carcinoma Cells</p>

Gao¹,

Long²,

Zhang³

et al. 2020

CMAR

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Background Metformin may exert the anticancer effect on multiple types of cancers and some potential mechanisms have been suggested. Our study was designed to determine the effect of metformin on the cell autophagy and autophagic flux via the AMPK-mTOR signaling pathway in human hepatocellular carcinoma (HCC) cells. Methods MHCC97H and HepG2 cell lines were cultured and treated without and with metformin at various concentrations (2, 5, 10 and 20 mM) for 48 h. Then, 10 mM was determined as the optimal concentration and the HCC cells were treated with metformin for 12, 24, 48, and 72 h. MTT assay was used to assess the cell viability and Western blotting was used to determine the expression of proteins (LC3-II, p62, phospho-AMPKα, phospho-mTOR, mTOR, phospho-p70 S6 Kinase, p70 S6 Kinase, PARP1, Caspase-9 and Caspase-3). Autophagy inhibitor 3-methyladenine, EGFP-LC3 and mCherry-GFP-LC3B plasmid transfection were used for further study. Results Metformin inhibited significantly the viability of MHCC97H and HepG2 cells in a dose- and time-dependent manner. For the apoptotic properties, activation of Caspase-9 and Caspase-3 and PARP cleavage were not observed after treatment with metformin. MHCC97H cells were transfected with a EGFP-LC3 plasmid and treatment with metformin could lead to the increased level of LC3-II and decreased level of p62. In metformin-induced autophagy, AMPK expression was activated, and the phosphorylation levels of mTOR and p70 S6 Kinase were inhibited. Metformin treatment and mCherry-GFP-LC3B plasmid transfection showed that metformin could induce the autophagic flux. 3-Methyladenine (3-MA) partly abolished this effect. Conclusion Metformin could induce the autophagy, autophagic flux, and activate the AMPK-mTOR signaling pathway in human HCC cells.

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“… 14 Moreover, a greater adherence to a T2DM prevention diet is associated with a lower risk of developing HCC among US men and women. 15 …”

Section: Epidemiologymentioning

confidence: 99%

Mechanisms Underlying Hepatocellular Carcinoma Progression in Patients with Type 2 Diabetes

Shi¹,

Kobara²,

Oura³

et al. 2021

JHC

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Hepatocellular carcinoma (HCC) ranks third in cancer-related deaths from solid tumors worldwide. The incidence of type 2 diabetes mellitus (T2DM) has increased worldwide in conjunction with the expansion of the Western lifestyle. Furthermore, patients with T2DM have been documented to have an increased risk of HCC, as well as bile tract cancer. Growing evidence shows that T2DM is a strong additive metabolic risk factor for HCC, but how diabetes affects the incidence of HCC requires additional investigation. In this review, we discuss the underlying mechanisms of HCC in patients with T2DM. Topics covered include abnormal glucose and lipid metabolism, hyperinsulinemia, and insulin resistance; the effect of activated platelets; hub gene expression associated with HCC; inflammation and signaling pathways; miRNAs; altered gut microbiota and immunomodulation. The evidence suggests that reducing obesity, diabetes, and nonalcoholic fatty liver disease/nonalcoholic steatohepatitis through efficient measures of prevention may lead to decreased rates of T2DM-related HCC.

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Type 2 Diabetes Prevention Diet and Hepatocellular Carcinoma Risk in US Men and Women

Cited by 40 publications

References 63 publications

Diabetes Risk Reduction Diet and Endometrial Cancer Risk

Diabetes Risk Reduction Diet and Endometrial Cancer Risk

<p>Metformin Induces Autophagy via the AMPK-mTOR Signaling Pathway in Human Hepatocellular Carcinoma Cells</p>

Mechanisms Underlying Hepatocellular Carcinoma Progression in Patients with Type 2 Diabetes

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