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201 KiB

Open AccessArticle

Association between Alcohol Consumption, Folate Intake, and Risk of Pancreatic Cancer: A Case-Control Study

by Winta Yallew, William R. Bamlet, Ann L. Oberg, Kristin E. Anderson, Janet E. Olson, Rashmi Sinha, Gloria M. Petersen, Rachael Z. Stolzenberg-Solomon and Rick J. Jansen

Nutrients 2017, 9(5), 448; https://doi.org/10.3390/nu9050448 - 01 May 2017

Cited by 7 | Viewed by 3577

Abstract

Pancreatic cancer is one of the most fatal common cancers affecting both men and women, representing about 3% of all new cancer cases in the United States. In this study, we aimed to investigate the association of pancreatic cancer risk with alcohol consumption [...] Read more.

Pancreatic cancer is one of the most fatal common cancers affecting both men and women, representing about 3% of all new cancer cases in the United States. In this study, we aimed to investigate the association of pancreatic cancer risk with alcohol consumption as well as folate intake. We performed a case-control study of 384 patients diagnosed with pancreatic cancer from May 2004 to December 2009 and 983 primary care healthy controls in a largely white population (>96%). Our findings showed no significant association between risk of pancreatic cancer and either overall alcohol consumption or type of alcohol consumed (drinks/day). Our study showed dietary folate intake had a modest effect size, but was significantly inversely associated with pancreatic cancer (odds ratio (OR) = 0.99, p < 0.0001). The current study supports the hypothesis that pancreatic cancer risk is reduced with higher food-based folate intake. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

3687 KiB

Open AccessArticle

Engineered Resistant-Starch (ERS) Diet Shapes Colon Microbiota Profile in Parallel with the Retardation of Tumor Growth in In Vitro and In Vivo Pancreatic Cancer Models

by Concetta Panebianco, Kaarel Adamberg, Signe Adamberg, Chiara Saracino, Madis Jaagura, Kaia Kolk, Anna Grazia Di Chio, Paolo Graziano, Raivo Vilu and Valerio Pazienza

Nutrients 2017, 9(4), 331; https://doi.org/10.3390/nu9040331 - 27 Mar 2017

Cited by 47 | Viewed by 7460

Abstract

Background/aims: Pancreatic cancer (PC) is ranked as the fourth leading cause of cancer-related deaths worldwide. Despite recent advances in treatment options, a modest impact on the outcome of the disease is observed so far. We have previously demonstrated that short-term fasting cycles have [...] Read more.

Background/aims: Pancreatic cancer (PC) is ranked as the fourth leading cause of cancer-related deaths worldwide. Despite recent advances in treatment options, a modest impact on the outcome of the disease is observed so far. We have previously demonstrated that short-term fasting cycles have the potential to improve the efficacy of chemotherapy against PC. The aim of this study was to assess the effect of an engineered resistant-starch (ERS) mimicking diet on the growth of cancer cell lines in vitro, on the composition of fecal microbiota, and on tumor growth in an in vivo pancreatic cancer mouse xenograft model. Materials and Methods: BxPC-3, MIA PaCa-2 and PANC-1 cells were cultured in the control, and in the ERS-mimicking diet culturing condition, to evaluate tumor growth and proliferation pathways. Pancreatic cancer xenograft mice were subjected to an ERS diet to assess tumor volume and weight as compared to mice fed with a control diet. The composition and activity of fecal microbiota were further analyzed in growth experiments by isothermal microcalorimetry. Results: Pancreatic cancer cells cultured in an ERS diet-mimicking medium showed decreased levels of phospho-ERK1/2 (extracellular signal-regulated kinase proteins) and phospho-mTOR (mammalian target of rapamycin) levels, as compared to those cultured in standard medium. Consistently, xenograft pancreatic cancer mice subjected to an ERS diet displayed significant retardation in tumor growth. In in vitro growth experiments, the fecal microbial cultures from mice fed with an ERS diet showed enhanced growth on residual substrates, higher production of formate and lactate, and decreased amounts of propionate, compared to fecal microbiota from mice fed with the control diet. Conclusion: A positive effect of the ERS diet on composition and metabolism of mouse fecal microbiota shown in vitro is associated with the decrease of tumor progression in the in vivo PC xenograft mouse model. These results suggest that engineered dietary interventions could be supportive as a synergistic approach to enhance the efficacy of existing cancer treatments in pancreatic cancer patients. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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5985 KiB

Open AccessArticle

Inhibition of Cell Survival by Curcumin Is Associated with Downregulation of Cell Division Cycle 20 (Cdc20) in Pancreatic Cancer Cells

by Yu Zhang, Ying-bo Xue, Hang Li, Dong Qiu, Zhi-wei Wang and Shi-sheng Tan

Nutrients 2017, 9(2), 109; https://doi.org/10.3390/nu9020109 - 04 Feb 2017

Cited by 39 | Viewed by 7010

Abstract

Pancreatic cancer is one of the most aggressive human tumors in the United States. Curcumin, a polyphenol derived from the Curcuma longa plant, has been reported to exert its antitumor activity in pancreatic cancer. However, the molecular mechanisms of curcumin-mediated tumor suppressive function [...] Read more.

Pancreatic cancer is one of the most aggressive human tumors in the United States. Curcumin, a polyphenol derived from the Curcuma longa plant, has been reported to exert its antitumor activity in pancreatic cancer. However, the molecular mechanisms of curcumin-mediated tumor suppressive function have not been fully elucidated. In the current study, we explore whether curcumin exhibits its anti-cancer function through inhibition of oncoprotein cell division cycle 20 (Cdc20) in pancreatic cancer cells. We found that curcumin inhibited cell growth, enhanced apoptosis, induced cell cycle arrest and retarded cell invasion in pancreatic cancer cells. Moreover, we observed that curcumin significantly inhibited the expression of Cdc20 in pancreatic cancer cells. Furthermore, our results demonstrated that overexpression of Cdc20 enhanced cell proliferation and invasion, and abrogated the cytotoxic effects induced by curcumin in pancreatic cancer cells. Consistently, downregulation of Cdc20 promoted curcumin-mediated anti-tumor activity. Therefore, our findings indicated that inhibition of Cdc20 by curcumin could be useful for the treatment of pancreatic cancer patients. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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Review

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475 KiB

Open AccessReview

Nutrients and the Pancreas: An Epigenetic Perspective

by Andee Weisbeck and Rick J. Jansen

Nutrients 2017, 9(3), 283; https://doi.org/10.3390/nu9030283 - 15 Mar 2017

Cited by 24 | Viewed by 6224

Abstract

Pancreatic cancer is the fourth most common cause of cancer-related deaths with a dismal average five-year survival rate of six percent. Substitutional progress has been made in understanding how pancreatic cancer develops and progresses. Evidence is mounting which demonstrates that diet and nutrition [...] Read more.

Pancreatic cancer is the fourth most common cause of cancer-related deaths with a dismal average five-year survival rate of six percent. Substitutional progress has been made in understanding how pancreatic cancer develops and progresses. Evidence is mounting which demonstrates that diet and nutrition are key factors in carcinogenesis. In particular, diets low in folate and high in fruits, vegetables, red/processed meat, and saturated fat have been identified as pancreatic cancer risk factors with a proposed mechanism involving epigenetic modifications or gene regulation. We review the current literature assessing the correlation between diet, epigenetics, and pancreatic cancer. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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482 KiB

Open AccessReview

Nutritional and Metabolic Derangements in Pancreatic Cancer and Pancreatic Resection

by Taylor M. Gilliland, Nicole Villafane-Ferriol, Kevin P. Shah, Rohan M. Shah, Hop S. Tran Cao, Nader N. Massarweh, Eric J. Silberfein, Eugene A. Choi, Cary Hsu, Amy L. McElhany, Omar Barakat, William Fisher and George Van Buren II

Nutrients 2017, 9(3), 243; https://doi.org/10.3390/nu9030243 - 07 Mar 2017

Cited by 151 | Viewed by 14062

Abstract

Pancreatic cancer is an aggressive malignancy with a poor prognosis. The disease and its treatment can cause significant nutritional impairments that often adversely impact patient quality of life (QOL). The pancreas has both exocrine and endocrine functions and, in the setting of cancer, [...] Read more.

Pancreatic cancer is an aggressive malignancy with a poor prognosis. The disease and its treatment can cause significant nutritional impairments that often adversely impact patient quality of life (QOL). The pancreas has both exocrine and endocrine functions and, in the setting of cancer, both systems may be affected. Pancreatic exocrine insufficiency (PEI) manifests as weight loss and steatorrhea, while endocrine insufficiency may result in diabetes mellitus. Surgical resection, a central component of pancreatic cancer treatment, may induce or exacerbate these dysfunctions. Nutritional and metabolic dysfunctions in patients with pancreatic cancer lack characterization, and few guidelines exist for nutritional support in patients after surgical resection. We reviewed publications from the past two decades (1995–2016) addressing the nutritional and metabolic status of patients with pancreatic cancer, grouping them into status at the time of diagnosis, status at the time of resection, and status of nutritional support throughout the diagnosis and treatment of pancreatic cancer. Here, we summarize the results of these investigations and evaluate the effectiveness of various types of nutritional support in patients after pancreatectomy for pancreatic adenocarcinoma (PDAC). We outline the following conservative perioperative strategies to optimize patient outcomes and guide the care of these patients: (1) patients with albumin < 2.5 mg/dL or weight loss > 10% should postpone surgery and begin aggressive nutrition supplementation; (2) patients with albumin < 3 mg/dL or weight loss between 5% and 10% should have nutrition supplementation prior to surgery; (3) enteral nutrition (EN) should be preferred as a nutritional intervention over total parenteral nutrition (TPN) postoperatively; and, (4) a multidisciplinary approach should be used to allow for early detection of symptoms of endocrine and exocrine pancreatic insufficiency alongside implementation of appropriate treatment to improve the patient’s quality of life. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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877 KiB

Open AccessReview

Pancreatic Exocrine Insufficiency in Pancreatic Cancer

by Miroslav Vujasinovic, Roberto Valente, Marco Del Chiaro, Johan Permert and J.-Matthias Löhr

Nutrients 2017, 9(3), 183; https://doi.org/10.3390/nu9030183 - 23 Feb 2017

Cited by 92 | Viewed by 10215

Abstract

Abstract: Cancer patients experience weight loss for a variety of reasons, commencing with the tumor’s metabolism (Warburg effect) and proceeding via cachexia to loss of appetite. In pancreatic cancer, several other factors are involved, including a loss of appetite with a particular [...] Read more.

Abstract: Cancer patients experience weight loss for a variety of reasons, commencing with the tumor’s metabolism (Warburg effect) and proceeding via cachexia to loss of appetite. In pancreatic cancer, several other factors are involved, including a loss of appetite with a particular aversion to meat and the incapacity of the pancreatic gland to function normally when a tumor is present in the pancreatic head. Pancreatic exocrine insufficiency is characterized by a deficiency of the enzymes secreted from the pancreas due to the obstructive tumor, resulting in maldigestion. This, in turn, contributes to malnutrition, specifically a lack of fat-soluble vitamins, antioxidants, and other micronutrients. Patients with pancreatic cancer and pancreatic exocrine insufficiency have, overall, an extremely poor prognosis with regard to surgical outcome and overall survival. Therefore, it is crucial to be aware of the mechanisms involved in the disease, to be able to diagnose pancreatic exocrine insufficiency early on, and to treat malnutrition appropriately, for example, with pancreatic enzymes. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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1102 KiB

Open AccessReview

Black‐Box Gastrointestinal Tract—Needs and Prospects of Gaining Insights of Fate of Fat, Protein, and Starch in Case of Exocrine Pancreatic Insufficiency by Using Fistulated Pigs

by Anne Mößeler and Josef Kamphues

Nutrients 2017, 9(2), 150; https://doi.org/10.3390/nu9020150 - 16 Feb 2017

Cited by 6 | Viewed by 6496

Abstract

Exocrine pancreatic insufficiency (EPI) results in the maldigestion and malabsorption of nutrients. The digestive processes in humans and other monogastric species like rat and pig are characterized by a predominantly enzymatic digestion within the small intestine and microbial fermentation located in the hindgut. [...] Read more.

Exocrine pancreatic insufficiency (EPI) results in the maldigestion and malabsorption of nutrients. The digestive processes in humans and other monogastric species like rat and pig are characterized by a predominantly enzymatic digestion within the small intestine and microbial fermentation located in the hindgut. For protein, it is doctrine that only prececally absorbed amino acids can be transferred to the amino acid pool of the host, while postileal absorption of nitrogen‐containing compounds occurs mainly in the form of ammonia, being a burden rather than a benefit for the organism. The pig is an established animal model for humans to study digestive processes. As digestion is markedly impaired in case of EPI the use of an appropriate animal model to study the effects of this disease and to optimize treatment and dietetic measures is of special interest. By using an animal model of experimentally‐induced EPI allowing differentiating between digestive processes in the small as well as in the large intestine by use of ileo‐cecal fistulated animals, marked effects of EPI on prececal digestion of starch and protein could be shown. The data indicatethat estimation of digestibility of nutrients over the entire digestive tract results in a distinct overestimation of enzymatic digestion of starch and protein. Therefore, this model clearly shows that protein and starch digestion are significantly reduced in case of EPI although this cannot be detected on a fecal level. As postileal fermentation of starch is associated not only with energy losses but also with intensive gas production, this is of special interest to minimize meteorism and improve wellbeing of patients. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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1104 KiB

Open AccessReview

Dietary Patterns and Pancreatic Cancer Risk: A Meta-Analysis

by Pei-Ying Lu, Long Shu, Shan-Shan Shen, Xu-Jiao Chen and Xiao-Yan Zhang

Nutrients 2017, 9(1), 38; https://doi.org/10.3390/nu9010038 - 05 Jan 2017

Cited by 47 | Viewed by 8509

Abstract

A number of studies have examined the associations between dietary patterns and pancreatic cancer risk, but the findings have been inconclusive. Herein, we conducted this meta-analysis to assess the associations between dietary patterns and the risk of pancreatic cancer. MEDLINE (provided by the [...] Read more.

A number of studies have examined the associations between dietary patterns and pancreatic cancer risk, but the findings have been inconclusive. Herein, we conducted this meta-analysis to assess the associations between dietary patterns and the risk of pancreatic cancer. MEDLINE (provided by the National Library of Medicine) and EBSCO (Elton B. Stephens Company) databases were searched for relevant articles published up to May 2016 that identified common dietary patterns. Thirty-two studies met the inclusion criteria and were finally included in this meta-analysis. A reduced risk of pancreatic cancer was shown for the highest compared with the lowest categories of healthy patterns (odds ratio, OR = 0.86; 95% confidence interval, CI: 0.77–0.95; p = 0.004) and light–moderate drinking patterns (OR = 0.90; 95% CI: 0.83–0.98; p = 0.02). There was evidence of an increased risk for pancreatic cancer in the highest compared with the lowest categories of western-type pattern (OR = 1.24; 95% CI: 1.06–1.45; p = 0.008) and heavy drinking pattern (OR = 1.29; 95% CI: 1.10–1.48; p = 0.002). The results of this meta-analysis demonstrate that healthy and light–moderate drinking patterns may decrease the risk of pancreatic cancer, whereas western-type and heavy drinking patterns may increase the risk of pancreatic cancer. Additional prospective studies are needed to confirm these findings. Full article

(This article belongs to the Special Issue Nutrition and Pancreatic Health)

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