Docosahexaenoic Acid in Combination with Dietary Energy Restriction for Reducing the Risk of Obesity Related Breast Cancer.

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obesity 30 endocrinologydiseases
pioglitazone 1 endocrinologydiseasesdrugs

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pioglitazone 13721 estrogen production via inhibition of aromatase activity/expression [[51]]. In support of this contention, pioglitazone , a recognized inducer of PPARγ transcriptional activation, has indeed been reported to inhibit aromatase
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obesity 822 henry.thompson@colostate.eduPublication date (epub): 12/2017Publication date (collection): 1/2018AbstractThere is strong evidence that obesity poses a significant risk factor for postmenopausal breast cancer. There are multiple mechanisms by which
obesity 935 a significant risk factor for postmenopausal breast cancer. There are multiple mechanisms by which obesity can predispose to breast cancer, prominent among which is the creation of a pro-inflammatory milieu
obesity 1471 omega-3 fatty acids, and among them docosahexaenoic acid (DHA) in particular, may reduce the risk of obesity related breast cancer primarily because of their pleotropic effects which target many of the systemic
obesity 1890 protective effect of DHA because of its complementary mechanisms of action and its ability to reverse the obesity -induced alterations in fatty acid metabolism predisposing to carcinogenesis. We believe that the combination
obesity 2082 believe that the combination of DER and DHA is a promising safe and effective intervention for reducing obesity -related breast cancer risk which needs to be validated in appropriately designed prospective, randomized
obesity 4465 that n-3FA and docosohexaenoic acid (DHA) in particular maybe particularly effective in preventing obesity related breast cancer, a highly prevalent phenotype due to the obesity epidemic in western societies.
obesity 4536 particularly effective in preventing obesity related breast cancer, a highly prevalent phenotype due to the obesity epidemic in western societies. We will also review the evidence to suggest that IWL secondary to dietary
obesity 4984 overweight (body mass index (BMI) 25.0–29.9 kg/m2) or obese (BMI ≥ 30 kg/m2) [[4]]. After smoking, obesity is now considered to be the most important modifiable cause of cancer as it has been associated with
obesity 5183 associated with increased risk of many cancers including postmenopausal breast cancer [[5],[6]]. Although obesity in postmenopausal women has been primarily associated with estrogen receptor positive tumors, an increased
obesity 5462 reported in both pre- and postmenopausal obese women compared to lean subjects [[7],[8]]. In addition, obesity has been associated with worse prognosis, including increased mortality in women diagnosed with breast
obesity 5626 increased mortality in women diagnosed with breast cancer [[9]]. There are multiple mechanisms by which obesity predisposes to breast cancer such as altering the production and bioavailability of critical mitogens
obesity 5995 as a result of the high circulating level of insulin acting as a growth factor [[12]]. In addition, obesity induces changes in circulating adipokines such as leptin [[13]] and adiponectin [[14]] which are protumorigenic.
obesity 6302 associated with an increase in breast cancer risk [[15]]. Conversely, adiponectin levels are reduced in obesity and in inverse association between serum adiponectin and breast cancer risk has been observed [[16]].
obesity 6598 fat [[17],[18]] and locally in the breast [[19]] has been recognized as a major mechanism by which obesity promotes the development of breast cancer. Typical inflammatory foci called crown-like structure have
obesity 7382 increased aromatase expression and estrogen production [[22]]. These findings highlight the link between obesity , inflammation and the creation of a hyperestrogenic milieu promoting the development of hormone responsive
obesity 7605 postmenopausal breast cancer. It is also recognized that a state of inflammation frequently associated with obesity may also be present in a subset of lean subjects while it may be absent in some obese women [[23]].
obesity 8692 activity which has received limited attention in the literature [[26]].Although the association between obesity and breast cancer is well established, it is unclear whether losing excess weight will lower the risk
obesity 12666 women.From a mechanistic point of view, n-3FA inhibit several of the oncogenic pathways activated by obesity as summarized by us in a recent review [[45]]. Preclinical studies have suggested that n-3FA reduce
obesity 12774 as summarized by us in a recent review [[45]]. Preclinical studies have suggested that n-3FA reduce obesity related inflammation and insulin resistance [[46],[47]]. In addition, fish oil rich in n-3FA has been
obesity 13082 plasma leptin concentrations [[48]] thus reversing the protumorigenic adipokine profile induced by obesity . A major mechanism by which n-3FA reduce the risk of obesity related breast cancer is through suppression
obesity 13143 protumorigenic adipokine profile induced by obesity. A major mechanism by which n-3FA reduce the risk of obesity related breast cancer is through suppression of inflammation [[42],[49]]. Our data, obtained in a preclinical
obesity 13943 induction by PGE2 [[52]]. Particularly supportive of a preferential protective effect of n-3FA against obesity -related breast cancer is a report by Ford, N.A. et al. [[53]]. Using two mouse models of postmenopausal
obesity 14323 effect only in obese mice. In addition, this treatment blocked many of the protumorigenic effects of obesity .2.2. DHA, Breast Density, and Obesity Related Breast Cancer RiskSupport for a preferential protective
obesity 14457 and Obesity Related Breast Cancer RiskSupport for a preferential protective effect of n-3FA against obesity related breast cancer is provided by the results of our recently published clinical trial [[54]]. In
obesity 16391 SFA to Monounsaturated fatty acids (MUFA) is potentially a critical factor both in the development of obesity [[58]] and cancer including breast cancer [[59]]. Epidemiological studies have indeed shown a positive
obesity 18182 in the literature to suggest that the combination of n-3FA and DER may lead to optimal inhibition of obesity related breast cancer which is characterized by a high degree of inflammation. As we discussed above,
obesity 19909 the rationale for combining DER specifically with the n-3FA DHA is strengthened by the finding that obesity may diminish the antitumor effect of DHA against breast cancer by increasing sEH which hydrolyzes and
obesity 20193 epoxygenases [[24]]. Therefore, DER may potentiate the antitumor action of DHA by reversing the effects of obesity on sEH and thus restoring the levels of these tumor protective compounds.3. Conclusions and Future DirectionsBased
obesity 20485 offers the promise of being a health-promoting and effective approach to inhibiting the development of obesity related breast cancer. The effectiveness of this intervention in the clinical setting will need to be
obesity 22852 among individuals since it is regulated both by genetic [[73]] and by environmental factors such as obesity [[24]].In conclusion, we believe that the inconclusive results reported in the literature over the last

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