The influence of obesity on folate status, DNA methylation and cancer-related gene expression in normal breast tissues from premenopausal women.

Epidemiological studies have established obesity as a critical risk factor for postmenopausal breast cancer (post-BC), whereas a reverse association holds prior to menopause. A significant scientific gap exists in understanding the mechanism(s) underpinning this epidemiological phenomenon, particularly the reverse association between obesity and premenopausal breast cancer (pre-BC). This study aimed to understand how folate metabolism and DNA methylation inform the association between obesity and pre-BC.

Genetic ablation of tumor necrosis factor-alpha attenuates the promoted colonic Wnt signaling in high fat diet-induced obese mice.

Obesity is an established risk factor for colorectal cancer, but the mechanisms responsible for this relationship are not adequately delineated. Using a TNF-α mouse model, the present study aimed to test the causal role of TNF-α in mediating the promotion of tumorigenic Wnt signaling by high-fat diet-induced obesity. A 2×2 factorial study was performed with wild-type and TNF-α mice on a 60 kcal% high-fat diet or a 10 kcal% low-fat diet.

The Prevention of a High Dose of Vitamin D or Its Combination with Sulforaphane on Intestinal Inflammation and Tumorigenesis in Apc Mice Fed a High-Fat Diet.

Scope: The previous study shows that obesity-promoted inflammation is responsible for the activation of the intestinal tumorigenic Wnt-signaling. The present study aims to test a dietary strategy, dietary supplementation with a high dose of vitamin D (VD) or its combination with sulforaphane (SFN) to inhibit intestinal inflammation and obesity-associated tumorigenesis.

Methods And Results: Apc mice are randomly divided into four groups: LF, a low-fat diet (10 kcal% fat) with 200 IU VD; HF, a high-fat diet (60 kcal% fat) with 200 IU VD; HFD, a high-fat diet with 5000 IU VD; and HFDS, a high-fat diet plus 5000 IU VD and 0.