Cheek cell fatty acids reflect n 3 PUFA in blood fractions during linseed oil supplementation: a controlled human intervention study
Cheek cell fatty acids reflect n 3 PUFA in blood fractions during linseed oil supplementation: a controlled human intervention study
Year: 2013
Authors: Grindel, A. Staps, F. Kuhnt, K.
Publication Name: Lipids Health Dis.
Publication Details: Volume 14; Issue 12; Page 173
Abstract:
Background: Adequate biomarkers for the dietary supply of fatty acids (FA) are FA of adipose tissue and blood fractions. In human studies, invasive sample collection is unpleasant for subjects. In contrast, cheek cell sampling can be considered as a non invasive alternative to investigate FA status. The aim of this study was to analyze whether cheek cell FA composition reflect the supplementation of alpha linolenic acid (ALA) using a linseed oil mixture compared to olive oil supplementation. Additionally, it was investigated if cheek cell FA composition correlates with the FA composition of plasma, red blood cells (RBC) and peripheral blood mononuclear cells (PBMC) before and during both interventions. Methods: During a 10 week randomized, controlled, double blind human intervention study, 38 subjects provided cheek cell and blood samples. After a two week run in period, the test group (n of 23) received 17 g per d of an ALA rich linseed oil mixture, while the control group (n of 15) received 17 g per d of an omega 3 (n 3) polyunsaturated FA (PUFA) free olive oil. Cheek cells and blood were collected on days 0, 7 and 56 of the 8 week intervention period. Results: Compared to olive oil, the linseed oil intervention increased ALA and also the endogenously converted long chain n 3 metabolites eicosatetraenoic , eicosapentaenoic and docosapentaenoic acid in cheek cells (P less 0.05). Docosahexaenoic acid remained unchanged. Reflecting the treatment, the n6 to n3 ratio decreased in the test group. In general, cheek cell FA reflected the changes of FA in blood fractions. Independent of treatment, significant correlations (P less 0.05) of n 6 PUFA and n 3 PUFA between cheek cells and plasma, RBC and PBMC were found, except for linoleic acid and ALA. Conclusions: The changes in FA composition of cheek cells confirmed that ALA from linseed oil increased endogenously derived n 3 PUFA in cheek cell lipids. These changes in cheek cells and their correlation to the respective FA in blood fractions indicate the cheek cell FA profile as an adequate non invasive biomarker for short term n 3 PUFA intake and metabolism. Therefore, cheek cell FA can be used in human intervention studies or large scale epidemiological studies, especially for assessment of the n 3 PUFA status. (Authors abstract)
The n 3 index which can be determined from red blood cells (RBC) is considered a biomarker, or even a risk factor, for CVD. The use of cheek cells as an alternative material reflecting dietary FA composition has been proposed. Along with its noninvasive nature, utilizing cheek cells is cost effective and can be applied in a non clinical environment without medicinal personal on a large scale. To validate the method’s significance, the aim of the present study was to detect the FA composition of cheek cells with focus on n 3 PUFA without intervention and during supplementation with either alpha linolenic acid (ALA) rich linseed oil mixture or with n 3 PUFA free olive oil. Additionally, it was of interest if the cheek cell FA composition correlates to the FA composition of plasma, RBC and peripheral blood mononuclear cells
(PBMC). Cheek cells were collected by rotary scraping with one brush at the inside of each cheek, followed by a mouth rinse to collect remaining cells. The results confirmed PL as the major lipid class (57 percent) of cheek cells. In the present study, the additional dietary intake of about 5 g per d ALA increased ALA portion of cheek cell lipids. Besides the increase of the supplemented ALA, the long chain n 3 PUFA metabolites such as ETA, EPA, and DPA also significantly increased in the cheek cell lipids after eight weeks of linseed oil intervention. Based on this study’s dietary n 3 PUFA restriction (no fish, fish oil, other n 3 PUFA containing oils) these long chain n 3 PUFA derived from the endogenous conversion of ALA. No changes occurred in DHA. Cheek cells are known as a tissue with a fast regeneration time of approximately five days. Therefore cheek cell FA are thought to be a biomarker detecting short term changes in the diet, as it is known from plasma. This assumption was confirmed by the present results. Successfully absorbed ALA was incorporated in cheek cell membranes and was detectable after already 7 days of a linseed oil intervention. Moreover, after only one week of linseed oil free washout period (n of 7), ALA almost returned to its baseline values. The supplementation of linseed oil led to an enrichment of n 3 PUFA in all four analyzed materials and thus decreased the ratios of n6 to n3 PUFA and AA to EPA. Therefore, linseed oil consumption could contribute to beneficial health effects such as a reduction of the CVD risk by improving the n 3 PUFA status in the body. A general use of linseed oil as a replacement for the commonly used high n 6 PUFA plant oils of the Western diet can be recommended to improve the n6 to n 3 PUFA ratio in the diet. The present results indicate cheek cell FA as a noninvasive biomarker for both dietary n 3 PUFA supply and endogenously derived n 3 PUFA metabolites. The present results indicated that ALA intake by linseed oil increased EPA and lowered the n6 to n3 PUFA ratio in cheek cell lipids. Cheek cell FA can used as alternative to FA of plasma and RBC to determine dietary FA intake, with special regard to n 3 PUFA. In general, the FA profile of cheek cells mainly reflected short term changes. Furthermore, the non invasive sampling procedure is an advantage to study participants and can be performed independently of clinical personnel. Therefore, the assessment of cheek cell FA can be considered for human intervention studies and large scale epidemiological studies where the n 3 PUFA supply and its metabolism are of interest. (Editors comments)
The n 3 index which can be determined from red blood cells (RBC) is considered a biomarker, or even a risk factor, for CVD. The use of cheek cells as an alternative material reflecting dietary FA composition has been proposed. Along with its noninvasive nature, utilizing cheek cells is cost effective and can be applied in a non clinical environment without medicinal personal on a large scale. To validate the method’s significance, the aim of the present study was to detect the FA composition of cheek cells with focus on n 3 PUFA without intervention and during supplementation with either alpha linolenic acid (ALA) rich linseed oil mixture or with n 3 PUFA free olive oil. Additionally, it was of interest if the cheek cell FA composition correlates to the FA composition of plasma, RBC and peripheral blood mononuclear cells
(PBMC). Cheek cells were collected by rotary scraping with one brush at the inside of each cheek, followed by a mouth rinse to collect remaining cells. The results confirmed PL as the major lipid class (57 percent) of cheek cells. In the present study, the additional dietary intake of about 5 g per d ALA increased ALA portion of cheek cell lipids. Besides the increase of the supplemented ALA, the long chain n 3 PUFA metabolites such as ETA, EPA, and DPA also significantly increased in the cheek cell lipids after eight weeks of linseed oil intervention. Based on this study’s dietary n 3 PUFA restriction (no fish, fish oil, other n 3 PUFA containing oils) these long chain n 3 PUFA derived from the endogenous conversion of ALA. No changes occurred in DHA. Cheek cells are known as a tissue with a fast regeneration time of approximately five days. Therefore cheek cell FA are thought to be a biomarker detecting short term changes in the diet, as it is known from plasma. This assumption was confirmed by the present results. Successfully absorbed ALA was incorporated in cheek cell membranes and was detectable after already 7 days of a linseed oil intervention. Moreover, after only one week of linseed oil free washout period (n of 7), ALA almost returned to its baseline values. The supplementation of linseed oil led to an enrichment of n 3 PUFA in all four analyzed materials and thus decreased the ratios of n6 to n3 PUFA and AA to EPA. Therefore, linseed oil consumption could contribute to beneficial health effects such as a reduction of the CVD risk by improving the n 3 PUFA status in the body. A general use of linseed oil as a replacement for the commonly used high n 6 PUFA plant oils of the Western diet can be recommended to improve the n6 to n 3 PUFA ratio in the diet. The present results indicate cheek cell FA as a noninvasive biomarker for both dietary n 3 PUFA supply and endogenously derived n 3 PUFA metabolites. The present results indicated that ALA intake by linseed oil increased EPA and lowered the n6 to n3 PUFA ratio in cheek cell lipids. Cheek cell FA can used as alternative to FA of plasma and RBC to determine dietary FA intake, with special regard to n 3 PUFA. In general, the FA profile of cheek cells mainly reflected short term changes. Furthermore, the non invasive sampling procedure is an advantage to study participants and can be performed independently of clinical personnel. Therefore, the assessment of cheek cell FA can be considered for human intervention studies and large scale epidemiological studies where the n 3 PUFA supply and its metabolism are of interest. (Editors comments)
