Dataset Information

Saturated, Monounsaturated and Polyunsaturated Fatty Acids Intake and Risk of Pancreatic Cancer: Evidence from Observational Studies.

ABSTRACT:

Background

Although the relationship between dietary monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs), and saturated fatty acids (SFAs) intake and pancreatic cancer risk has been reported by several studies, the evidence is controversial. We firstly conducted this comprehensive meta-analysis to summarize the aforementioned evidence from observational studies.

Methods

The MEDLINE (PubMed), Embase, and ISI Web of Science databases were used to search for epidemiological studies of dietary SFA, MUFA, and PUFA and pancreatic cancer risk that were published until the end of June 2014. Random- or fixed-effects models were used to estimate the relative risks (RRs) and 95% confidence intervals (CIs). We also carried out subgroup, sensitivity, and publication bias analyses.

Results

We identified 13 case-control studies and 7 prospective studies which including 6270 pancreatic cancer cases in the meta-analysis of SFA, MUFA, and PUFA and risk of pancreatic cancer. The summary RR was 1.13 (95%CI = 0.94-1.35, I2 = 70.7%) for SFA, 1.00 (95%CI = 0.87-1.14, I2 = 43.4%) for MUFA, and 0.87 (95%CI = 0.75-1.00, I2 = 55.3%) for PUFA for high versus low intake categories. We found no evidence of publication bias.

Conclusion

In summary, findings of this study supports an inverse association between diets high in PUFA and pancreatic cancer risk. Further large prospective studies are warranted to report the results stratified by the subtypes of MUFA and PUFA and adjust for other potential risk factors to eliminate residual confounding.

SUBMITTER: Yao X

PROVIDER: S-EPMC4481405 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Publications

Saturated, Monounsaturated and Polyunsaturated Fatty Acids Intake and Risk of Pancreatic Cancer: Evidence from Observational Studies.

Yao Xu X Tian Zhong Z

PloS one 20150625 6

<h4>Background</h4>Although the relationship between dietary monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs), and saturated fatty acids (SFAs) intake and pancreatic cancer risk has been reported by several studies, the evidence is controversial. We firstly conducted this comprehensive meta-analysis to summarize the aforementioned evidence from observational studies.<h4>Methods</h4>The MEDLINE (PubMed), Embase, and ISI Web of Science databases were used to search for epid ...[more]

PMID: 26110621

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Project description:Obesity is a recognized epidemic worldwide, and the accumulation of excess free saturated fatty acids (SFAs) in cells induces cellular lipotoxic damage and increases the risk of a wide spectrum of metabolic diseases including type 2 diabetes (T2D) and nonalcoholic fatty liver disease (NAFLD). Monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) have been reported to combat SFA-induced cellular damage. However, the comparative studies of the two types of unsaturated fatty acids (UFAs) are still limited. We investigated the effects of different MUFAs and PUFAs in the human hepatocyte line L-02 cells in vitro, and in high-fat-diet (HFD)-induced obese C57BL/6 mice in vivo. The results of the in vitro study showed that SFAs induced significant cellular lipotoxic damage, but the combination of MUFAs/PUFAs with SFAs significantly improved the impaired cell viability. Particularly, oleic acid (OA) was superior to eicosapentaenoic acid (EPA), Docosahexaenoic acid (DHA), and arachidonic acid (AA) in terms of its anti-apoptotic effect and inhibition of endoplasmic reticulum (ER) stress. In vivo, both olive-oil-enriched (HFD + OO) and fish-oil-enriched high-fat diets (HFD + FO) reduced hepatic steatosis and improved insulin sensitivity in obese mice. However, FO induced an abnormal increase in serum aspartate aminotransferase (AST) and an increase in the oxidative stress indicator Malondialdehyde (MDA). Liver-targeted lipidomic analysis showed that liver lipid metabolites under the two types of UFA dietary interventions differed from the HFD group, modulating the abundance of some lipid metabolites such as triglycerides (TGs) and glycerophospholipids. Furthermore, the FO diet significantly increased the abundance of the associated FA 20:5 long-chain lipid metabolites, whereas the OO diet regulated the unsaturation of all fatty acids in general and increased the abundance of FA 18:1 in the overall lipid metabolites, especially TGs, which may primarily contribute to the FO, and OO drove protection in NAFLD.

Project description:Neuropathy is the most common complication of prediabetes and diabetes and presents as distal-to-proximal loss of peripheral nerve function in the lower extremities. Neuropathy progression and disease severity in prediabetes and diabetes correlates with dyslipidemia in man and murine models of disease. Dyslipidemia is characterized by elevated levels of circulating saturated fatty acids (SFAs) that associate with the progression of neuropathy. Increased intake of monounsaturated fatty acid (MUFA)-rich diets confers metabolic health benefits; however, the impact of fatty acid saturation in neuropathy is unknown. This study examines the differential effect of SFAs and MUFAs on the development of neuropathy and the molecular mechanisms underlying the progression of the complication. Male mice Mus musculus fed a high-fat diet rich in SFAs developed robust peripheral neuropathy. This neuropathy was completely reversed by switching the mice from the SFA-rich high-fat diet to a MUFA-rich high-fat diet; nerve conduction velocities and intraepidermal nerve fiber density were restored. A MUFA oleate also prevented the impairment of mitochondrial transport and protected mitochondrial membrane potential in cultured sensory neurons treated with mixtures of oleate and the SFA palmitate. Moreover, oleate also preserved intracellular ATP levels, prevented apoptosis induced by palmitate treatment, and promoted lipid droplet formation in sensory neurons, suggesting that lipid droplets protect sensory neurons from lipotoxicity. Together, these results suggest that MUFAs reverse the progression of neuropathy by protecting mitochondrial function and transport through the formation of intracellular lipid droplets in sensory neurons.SIGNIFICANCE STATEMENT There is a global epidemic of prediabetes and diabetes, disorders that represent a continuum of metabolic disturbances in lipid and glucose metabolism. In the United States, 80 million individuals have prediabetes and 30 million have diabetes. Neuropathy is the most common complication of both disorders, carries a high morbidity, and, despite its prevalence, has no treatments. We report that dietary intervention with monounsaturated fatty acids reverses the progression of neuropathy and restores nerve function in high-fat diet-fed murine models of peripheral neuropathy. Furthermore, the addition of the monounsaturated fatty acid oleate to sensory neurons cultured under diabetic conditions shows that oleate prevents impairment of mitochondrial transport and mitochondrial dysfunction through a mechanism involving formation of axonal lipid droplets.

Dataset Information

Saturated, Monounsaturated and Polyunsaturated Fatty Acids Intake and Risk of Pancreatic Cancer: Evidence from Observational Studies.

Background

Methods

Results

Conclusion

Publications

Saturated, Monounsaturated and Polyunsaturated Fatty Acids Intake and Risk of Pancreatic Cancer: Evidence from Observational Studies.

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